Practice Parameter

Contact Dermatitis: A Practice ParametereUpdate 2015

Luz Fonacier, MD, David I. Bernstein, MD, Karin Pacheco, MD, D. Linn Holness, MD, Joann Blessing-Moore, MD,
David Khan, MD, David Lang, MD, Richard Nicklas, MD, John Oppenheimer, MD, Jay Portnoy, MD,
Christopher Randolph, MD, Diane Schuller, MD, Sheldon Spector, MD, Stephen Tilles, MD, and Dana Wallace, MD

This parameter was developed by the Joint Task Force on Allergy & Immunology are available at http://www.JCAAI.org or
Practice Parameters, which represents the American Academy of http://www.allergyparameters.org. 2015 American Academy
Allergy, Asthma & Immunology (AAAAI); the American College of Allergy, Asthma & Immunology (J Allergy Clin Immunol
of Allergy, Asthma & Immunology (ACAAI); and the Joint Pract 2015;3:S1-S39)
Council of Allergy, Asthma & Immunology. The AAAAI and the
Key words: Allergic contact dermatitis; patch testing; allergen;
ACAAI have jointly accepted responsibility for establishing
parameter; guideline; contact dermatitis; occupational; sensitizer
Contact Dermatitis: A Practice ParametereUpdate 2015. This
is a complete and comprehensive document at the current time.
The medical environment is changing and not all PREFACE
recommendations will be appropriate or applicable to all The Practice Parameter on Contact Dermatitis (CD) was last
patients. Because this document incorporated the efforts of many updated in 2006, and focused primarily on the basics of CD and
participants, no single individual, including members serving on patch testing for the allergist. In the ensuing years, there has been
the Joint Task Force, are authorized to provide an ofcial AAAAI considerable interest by the allergist in allergic skin diseases due
or ACAAI interpretation of these practice parameters. Any to increasing numbers of referrals for CD. With the ease of
request for information or interpretation of this practice application, the use of the preloaded commercially available
parameter by the AAAAI or ACAAI should be directed to the T.R.U.E. Test patch testing method has increased among aller-
Executive Ofces of the AAAAI, the ACAAI, and the Joint gists, as has the use of patch testing with individually loaded
Council of Allergy, Asthma & Immunology. These parameters chambers. The T.R.U.E. Test has also been expanded to include
are not designed for use by the pharmaceutical industry in drug 35 antigens and a negative control, improving their sensitivity to
development or promotion. Previously published practice detect inclusive allergens. There have also been advances in the
parameters of the Joint Task Force on Practice Parameters for eld in many areas including our basic understanding of type IV
hypersensitivity reactions, emerging contact allergens, irritant
contact dermatitis (ICD), systemic contact dermatitis (SCD),
patch testing in children, occupational dermatitis, and reactions
See Appendix A for members of the Joint Task Force Contact Dermatitis Parameter
to biomedical devices. Improved diagnosis and management of
Workgroup, reviewers of this Practice Parameter, and members of the Joint Task
Force on Practice Parameters. CD and availability of more comprehensive databases of causa-
Disclosure of potential conict of interest: L. Fonacier has received research and tive contact allergens enable physicians to manage allergic contact
educational grants (made to Winthrop University Hospital) from Genentech, dermatitis (ACD) with avoidance of allergens the patient is
Merck, and Baxter; is in the Speakers Bureau/Honoraria of Baxter; and is on the sensitized to and availability of lists of safe products that do not
Board of Directors, Joint Council of Allergy, Asthma and Immunology (JCAAI)
2012-2015. D. Bernstein is the consultant in Merck, Genentech, Proctor and
contain these allergens. Given the many advances in the eld, the
Gamble, Sano, and TEVA; and has received research grants from Amgen, Joint Task Force on Practice Parameters (JTF) appointed a
GlaxoSmithKline, Greer, Johnson & Johnson, Merck, Teva, Pzer, Genentech, working group to review and update the standing practice
Array, Cephalon, Novartis, Boeringer Ingelheim, and Medimmune. The rest of the parameters.
authors declare that they have no relevant conicts of interest.
The Contact Dermatitis: A Practice ParametereUpdate 2015
The Joint Task Force recognizes that experts in a eld are likely to have interests that
could come into conict with the development of a completely unbiased and workgroup was commissioned by the JTF to develop a practice
objective practice parameter. To take advantage of that expertise, a process has parameter that addresses recent advances in the eld of CD and
been developed to prevent potential conicts from inuencing the nal document the optimal methods of diagnosis and management based on an
in a negative way. assessment of the most current literature. The Chair (Luz
At the workgroup level, members who have a potential conict of interest either do
not participate in discussions concerning topics related to the potential conict or
Fonacier, MD) invited workgroup members to participate in the
if they do write a section on that topic, the workgroup completely rewrites it parameter development who are considered to be experts in the
without their involvement to remove potential bias. In addition, the entire docu- eld of CD. Workgroup members have been vetted for conict
ment is then reviewed by the Joint Task Force and any apparent bias is removed at of interest (COI) by the JTF and their COIs have been listed in
that level. Finally, the practice parameter is sent for review both by invited re-
this document and are posted on the JTF web site at http://www.
viewers and by anyone with an interest in the topic by posting the document on the
web sites of the ACAAI and the AAAAI. allergyparameters.org.
Corresponding author: Joint Task Force on Practice Parameters, 59 N Brockway St, The charge of the workgroup was to develop current practice
#304, Palatine, IL 60067. E-mail: [email protected]. guidelines based on an up-to-date systematic literature review.
Received for publication February 25, 2015; accepted for publication February 26, Consensus expert opinion and workgroup-identied supplementary
2015.
2213-2198
documents were utilized when published evidence was lacking.
2015 American Academy of Allergy, Asthma & Immunology A search of the medical literature on PubMed was performed
http://dx.doi.org/10.1016/j.jaip.2015.02.009 for a variety of terms that were considered to be relevant to this

S1
S2 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

practice parameter. All reference types were included in the re-

Abbreviations used sults. References identied as being relevant were searched for
AA- Amidoamine other relevant references. Published clinical studies were rated by
AAAAI- American Academy of Allergy, Asthma and Immunology category of evidence and utilized to establish the strength of the
ACAAI- American College of Allergy, Asthma and Immunology
recommendations (see Appendix B). The parameter was subse-
ACC- Allergic contact cheilitis
ACD- Allergic contact dermatitis
quently appraised by reviewers designated by the AAAAI and
ACDS- American Contact Dermatitis Society ACAAI. Based on this process, this parameter represents an ev-
AD- Atopic dermatitis idence-based, broadly accepted consensus document.
AGEP- Acute generalized exanthematous pustulosis Search terms include contact dermatitis, eczema, cosmetic
APT- Atopy patch test allergy, contact allergen, patch testing, and each of the specic
BOP- Balsam of Peru conditions reviewed in this parameter.
BTM- Betamethasone
CAMP- Contact Allergen Management Program
CAPB- Cocoamidopropyl betaine GLOSSARY
CARD- Contact Allergen Replacement Database Angry back syndrome or excited skin syndrome: dened
CD- Contact dermatitis as false-positive patch test (PT) reactions usually adjacent to large
CLO- Clobetasol true-positive reactions that induce contiguous skin inammation
COI- Conict of interest and irritability.
CS- Corticosteroid
Ectopic allergic contact dermatitis: contact allergy lesions
CU- Contact urticaria
manifested in locations distant from or indirectly in contact with
DMAPA- Dimethylaminopropylamine
DRESS- Drug rash with eosinophilia and systemic symptoms the original skin sites directly exposed to allergens due to inad-
ELISA- Enzyme-linked immunosorbent assay vertent transfer by the patient (eg, transfer of sensitizers in nail
EliSPOT- Enzyme-linked immunospot polish to the eyelids) or others (eg, mother transferring allergen
ENDA- European Network on Drug Allergy to the child or a partner transferring the allergen by contact).
ESCD- European Society of Contact Dermatitis Contact sensitization: evidence of sensitization such as pos-
FDA- Food and Drug Administration itive PT reaction is not denitive of an allergy but simply a
FM- Fragrance mix conrmation of immunologic sensitization that must then be
FM I- Fragrance mix I conrmed as clinically relevant by history and clinical ndings
FM II- Fragrance mix II
analysis.
GCDG- German Contact Dermatitis Group
Contact urticaria: dened as the development of a wheal-
HC- Hydrocortisone
ICD- Irritant contact dermatitis and-are reaction at a site where an external agent contacts the
IM- Intramuscular skin or mucosa.
IPPD- Isopropyl-para-phenylenediamine Late patch test reading: late PT reading is performed at or
IUDs- Intrauterine devices after 7 days after application of a PT as opposed to the standard
IV- Intravenous of care reading that is performed between day 3 and 7.
LPTs- Lymphocyte proliferation tests Photo-allergic contact dermatitis: it is a delayed contact
MCI- Methychloroisothiazolinone hypersensitivity reaction to an allergen activated by exposure to
MELISA- Memory Lymphocyte Immuno Stimulation Assay UV radiation.
MI- Methylisothiazolinone
Repeated open application test (ROAT): several open PT
MPL- Methylprednisolone
techniques have been used to test substances with the potential for
MSDS- Material safety data sheets
NACDG- North American Contact Dermatitis Group irritation, and are especially suitable for cosmetics and other per-
NHIS- National Health Interview Survey sonal care products such as makeup foundation and skin lotions.
NS- Nasal spray The more commonly used provocative open use test involves the
NSAIDs- Nonsteroidal anti-inammatory drugs repeated application of a suspected allergen to the antecubital fossa
OCD- Occupational contact dermatitis twice daily for up to 1 to 2 weeks, and observation for the local
OHS- Occupational health supplement development of dermatitis at the application site.
PABA- Para-aminobenzoic acid Usage test: use of a product highly suspected of containing a
PPD- Para-phenylenediamine sensitizer under real world conditions to prove causation. An
PT- Patch test
example is for a patient to use eye mascara daily on 1 eye and not
PTDS- Para-toluenediamine sulfate
the other to observe for the development of local dermatitis at the
ROAT- Repeated open application test
SCD- Systemic contact dermatitis exposed site. This is often used when PT with suspected com-
SJS- Stevens Johnson syndrome mercial allergens is negative but the suspicion of ACD is high.
TCI- Topical calcineurin inhibitors Systemic allergic contact dermatitis: a generalized ACD rash
TCL- Triamcinolone from systemic administration of a drug, chemical, or food to
TCS- Topical corticosteroids which the patient previously experienced ACD.
TEN- Toxic epidermal necrolysis
UK- United Kingdom
UVA- Ultraviolet A INTRODUCTION
UVB- Ultraviolet B Contact dermatitis (CD) is dened as any skin disorder caused
by contact with an exogenous substance that elicits an allergic
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S3
VOLUME 3, NUMBER 3S

and/or irritant response. The vast majority of cases are attribut- evidence is impossible to obtain, and the anticipated benets
able to irritant ICD. CD is also a signicant cause of workplace strongly outweigh the harms.
disability. Overall, this is a practical, clinically pertinent, and user-
Contact urticaria (CU) is dened as the development of a wheal- friendly parameter that has attempted to address important
and-are reaction, or hives, at a site where an external agent contacts clinical questions pertaining to the evaluation and management
the skin or mucosa. CU can be divided in 2 broad categories: of ACD. This document, although not intended to replace an
nonimmunologic CU and immunologic CU (caused by an IgE- authoritative textbook, is a valuable updated evidence-based
mediated hypersensitivity reaction). Symptoms of CU range from resource for the practicing allergist.
pruritic, localized wheal-and-are reactions to generalized urticaria
and anaphylaxis. Aside from the need to differentiate between ACD
and CU, this parameter will not discuss CU in detail. COMPILATION OF SUMMARY STATEMENTS
This CD practice parameter, updated from the original docu- Summary Statement 1: Consider ACD in the differential
ment published in 2006, is intended as a useful guide for the diagnosis of patients with chronic eczematous or noneczematous
practicing allergist in the evaluation and management of ACD in dermatitis. [Strength of Recommendation: Strong; C Evidence]
adults and children. This updated parameter has been restructured Summary Statement 2: In patients suspected of ACD, patch
around action-based and patient-centered summary statements that testing is the gold standard to conrm the diagnosis. [Strength of
provide specic evidence-based recommendations for assessing and Recommendation: Strong; C Evidence]
treating ACD. In contrast to the original 2006 parameter, the Summary Statement 3: In addition to personal products used
pathophysiology, susceptibility, and clinical background are not by a patient suspected of ACD, review the home and workplace
reviewed here. The evidence-based summary statements in this for other sources of contact allergens. [Strength of Recommen-
document provide specic recommendations pertaining to the dation: Moderate; D Evidence]
approach to medical history, physical examination, patch testing, Summary Statement 4: Evaluate patients for both irritant and
and management of patients suspected of ACD. allergic causes, especially in those presenting with hand derma-
As in the 2006 parameter, action-based summary statements titis. [Strength of Recommendation: Strong; C Evidence]
provide guidance for identication of potential causative sensi- Summary Statement 5: Allergic CD should be suspected and
tizers based on clinical presentation in specic geographical skin evaluated in the patient with both generalized and anatomically
locations. Patch testing is emphasized in this updated parameter, localized skin eruptions (such as the hands, face, eyelids) that
with action-based statements that address selection of PT anti- come in contact with the substances in the environment.
gens; testing to personal products when necessary; different patch [Strength of Recommendation: Moderate; C Evidence]
testing devices; timing of readings; late PT reactions; false-posi- Summary Statement 6: In a patient with a facial rash involving
tive, false-negative, and true-negative responses; and photo-patch the periorbital areas (eg, eyelids), evaluate for ACD caused by
testing. Lists of sensitizers encountered in different settings or in components of cosmetics, such as fragrances, preservatives, and
specic types of products (eg, cosmetics, sunscreens, joint pros- excipients, because these are common sensitizers of the facial
theses) are presented as tables in the appendices. skin. [Strength of Recommendation: Moderate; C Evidence]
Since the publication of the original parameter, new questions Summary Statement 7: Evaluate patients presenting with lip
have been addressed in summary statements related to emerging dermatitis (cheilitis) and perioral dermatitis for both irritant and
clinical problems including preoperative screening for and post- allergic causes of contact dermatitis. [Strength of Recommen-
implantation patch testing for metal allergy in patients who have dation: Moderate; C Evidence]
undergone joint replacement surgery. In this updated practice Summary Statement 8: Evaluate patients with chronic oral
parameter, summary statements have been added that more mucosal inammatory conditions for disorders other than ACD.
comprehensively address evaluation and management of occupa- [Strength of Recommendation: Moderate; C Evidence]
tional contact dermatitis (OCD). The potential benets and limi- Summary Statement 9: In patients presenting with dermatitis
tations of drug patch testing in patients with maculopapular rashes, that involves the scalp and neck, consider patch testing for
erythroderma, and nonimmediate cutaneous reactions are addressed common causative sensitizers in cosmetics, hair products, and
in a summary statement. New summary statements have been jewelry. [Strength of Recommendation: Moderate; C Evidence]
included that make recommendations pertaining to the overall Summary Statement 10: Consider irritant and ACD in all
management of CD, focusing on avoidance and prevention. patients presenting with acute or chronic hand eczema. All such
The majority of summary statements in this document are patients suspected of CD should undergo patch testing.
based on descriptive and retrospective studies, representative [Strength of Recommendation: Moderate; C Evidence]
of the current published CD literature. Because the treat- Summary Statement 11: Evaluate patients with axillary
ment of choice for CD is avoidance, there are limited dermatitis for ACD caused by local contact sensitivity to allergens
numbers of published placebo-controlled studies of other in topically applied products found in deodorants and textiles. In
therapeutic interventions (eg, drugs). The absence of a vali- some cases, axillary dermatitis could be a manifestation of systemic
dated positive control to conrm a diagnosis of ACD is a contact dermatitis (SCD) (ie, the baboon syndrome). [Strength
major limitation of studies reporting patch testing data. For of Recommendation: Moderate; C Evidence]
these reasons, the categories of evidence supporting the Summary Statement 12: Evaluate patients presenting with
summary statements in this document are relatively low. anogenital dermatitis for possible ACD to antigens contained in
Therefore, the strength of recommendation for most of the topically applied products. [Strength of Recommendation:
statements in this parameter is Moderate even if in some Moderate; C Evidence]
clearly identied circumstances, Strong recommendations Summary Statement 13: Consider a diagnosis of SCD
may be made based on lesser evidence because high-quality following systemic exposure (eg, ingestion, infusion, or
S4 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

transcutaneous exposure) to a known contact sensitizer in a pa- Summary Statement 23: Determine the relevance of a PT result
tient who presents with generalized dermatitis, intertriginous and based on the clinical and exposure history when interpreting the
exural exanthema (Baboon syndrome), and/or a are at previ- PT. [Strength of Recommendation: Moderate; D Evidence]
ous cutaneous sites of exposure [Strength of Recommendation: Summary Statement 24: Consult physicians with expertise in
Moderate; C Evidence]. patch testing to household cleaning or industrial products if
Summary Statement 14: Consider PT to rubber chemicals, testing to the actual product suspected of containing the relevant
adhesives, and leather components of footwear in patients pre- allergen(s) is necessary, because false-positive and severe irritant
senting with unexplained chronic dermatitis involving the lower reactions can occur. [Strength of Recommendation: Moderate; C
extremities, feet and/or soles. [Strength of Recommendation: Evidence]
Moderate; C Evidence] Summary Statement 25: Consult physicians with expertise in
Summary Statement 15: In addition to avoiding irritants in UV radiation and photo-patch testing to conrm a suspected
patients with atopic dermatitis (AD), evaluate for ACD, if sus- diagnosis of photo-allergic CD. [Strength of Recommendation:
pected, as the 2 dermatologic conditions often coexist in the Strong; C Evidence]
same patient. [Strength of Recommendation: Moderate; C Summary Statement 26: Although in vitro tests for delayed
Evidence] hypersensitivity to contact allergens (ie, metals and bone cement)
are available, routine use of such assays is not currently recom-
Patch testing recommendations mended as their sensitivity and specicity for diagnosing ACD
Summary Statement 16: Avoid or reduce doses of immuno- has not been determined and should be considered investiga-
suppressant medications such as systemic corticosteroids (CS) tional. [Strength of Recommendation: Moderate; C Evidence]
and systemic immunosuppressants before patch testing. Avoid Summary Statement 27: Use the repeated open application
application of topical corticosteroids (TCS), topical calcineurin test (ROAT) to further evaluate a patient suspected of ACD who
inhibitors (TCI), or ultraviolet radiation to the PT site, because exhibits doubtful or negative PT responses, to conrm that the
these may reduce allergic PT responses. [Strength of Recom- patient is reacting to that particular product or to determine
mendation: Moderate; C Evidence] clinical tolerability to new cosmetic products. [Strength of
Summary Statement 17: In addition to using a core or base- Recommendation: Moderate; C Evidence]
line series of PT allergens in evaluating ACD, consider using
supplemental series of PT allergens based on specic patient Sources of exposure to clinically relevant allergens
exposures, and the patients personal products to increase the Summary Statement 28: Evaluate patients who present with
probability of identifying relevant sensitizers. [Strength of recurrent dermatitis on exposed skin surfaces during airborne
Recommendation: Moderate; C Evidence] pollen seasons for contact sensitization to seasonal pollen aller-
Summary Statement 18: Patch testing can be performed either gens. [Strength of Recommendation: Moderate; C Evidence]
using a preloaded thin-layer rapid use epicutaneous testing kit of Summary Statement 29: The clinician should consider cos-
36 chambers or with a panel of antigens loaded individually in a metics and personal hygiene products that are directly applied to
chamber system recommended by the North American Contact involved skin or ectopically transferred from uninvolved skin as
Dermatitis Group (NACDG) Research Group or the American potential sources of allergens in patients with ACD. [Strength of
Contact Dermatitis Society (ACDS). [Strength of Recommen- Recommendation: Strong; C Evidence]
dation: Moderate; C Evidence] Summary Statement 30: When evaluating ACD from cos-
Summary Statement 19: Read and interpret PT conforming to metics and personal care products that contain many different
the scoring system developed by the International Contact chemical ingredients, consider that the most common causes are
Dermatitis Research Group. [Strength of Recommendation: due to a few important chemical classes, including fragrances,
Moderate; D Evidence] preservatives, excipients, nickel, and sun screening agents.
Summary Statement 20: Remove and read PT at approxi- [Strength of Recommendation: Moderate; C Evidence]
mately 48 hours after application. A second reading should be Summary Statement 31: Patients suspected to have allergy to
done between 3 and 7 days after application. [Strength of hair products should be evaluated for PT reactions to cocoami-
Recommendation: Moderate; C Evidence] dopropyl betaine (CAPB), para-phenylenediamine (PPD), fra-
Summary Statement 21: Consider that a possible false-positive grances, preservatives, and glycerol thioglycolate. [Strength of
reaction can result with the use of irritants or allergic substances Recommendation: Moderate; C Evidence]
at potentially irritating higher concentrations, pressure reaction Summary Statement 32: Suspect allergy to nail products when
from the lling chamber, an angry back syndrome, or patch the dermatitis presents locally at the distal digit or ectopically on
testing on skin with active dermatitis. [Strength of Recommen- the eyelids and face. [Strength of Recommendation: Moderate; C
dation: Moderate; D Evidence] Evidence]
Summary statement 22: Recognize the possibility that Summary Statement 33: Suspect the diagnosis of photo-
false-negative reactions could be due to inadequate allergen allergic CD to cosmetics when eczema occurs in a light-exposed
concentration needed to elicit a response; inability of the distribution following the use of a skin care product or cosmetic,
vehicle to release sufcient allergen; reduced skin respon- including sunscreens. [Strength of Recommendation: Strong; C
siveness because of prior ultraviolet light exposure (ie, sun, Evidence]
tanning bed); concomitant immunosuppressive therapies; or
methodological testing errors such as insufcient occlusion, Topical medicinal CD
failure to perform delayed readings, and failure to perform a Summary Statement 34: If an eruption worsens, rather than
photo PT. [Strength of Recommendation: Moderate; C improves, after the topical application of certain medications, or
Evidence] fails to respond to TCS, PT should be performed to the
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S5
VOLUME 3, NUMBER 3S

suspected product and/or ingredients known to be contact sen- these should be considered in the differential diagnosis. The
sitizers. [Strength of Recommendation: Moderate; C Evidence] suspicion of ACD is the rst step in making the diagnosis. Patch
Summary Statement 35: The clinician may use the drug PT testing is indicated in any patient with acute or chronic, often
for the diagnosis of some drug hypersensitivity reactions, recog- pruritic, dermatitis if underlying or secondary ACD is suspected.
nizing that there is no standardized approach to dene the The history is important for the diagnosis and subsequent
population, clinical manifestation, drug to PT, and PT materials management of this disease. Although medical history can
to make patch testing to drugs a standard of care. [Strength of strongly suggest the cause of ACD, it has moderate sensitivity
Recommendation: Weak; D Evidence] (76%) and specicity (76%) in establishing the diagnosis. In
Summary statement 36: Consider preoperative patch testing for addition, the occupational, avocational, and environmental his-
metal sensitization in patients with a signicant history of metal tory must all be carefully reviewed. Chronologic exposure his-
allergy. [Strength of Recommendation: Moderate; C Evidence] tories that include hobbies and specic activities relative to onset
Summary Statement 37: In patients with joint replacement of the dermatitis should be obtained. Because the worker may be
failure, patch testing to components of the implant may be unaware of specic chemicals to which he or she is exposed,
helpful after infection and biomechanical causes have been material safety data sheets (MSDS) obtained from the manu-
excluded. [Strength of Recommendation: Moderate; C Evidence] facturer may be helpful. Hobbies and nonwork activity such as
gardening, macram, painting, ceramic work, carpentry, and
Special populations photography may be sources of exposure to culprit contactants.
Contact dermatitis in children. Summary Statement 38: In addition to exposure to a single agent, simultaneous exposure
ACD and ICD are signicant clinical problems in children. to multiple irritants and contact allergens may produce additive,
Patch testing should be performed and remains the gold standard synergistic, or antagonistic responses. Simultaneous exposure to
for the diagnosis of ACD in children. [Strength of Recommen- both an irritant and a contact allergen or 2 contact allergens can
dation: Strong; C Evidence] reduce the clinical threshold concentration for elicitation of
response to a given allergen due to irritant disruption of the skin
Occupational contact dermatitis. Summary Statement barrier and immunologic activation of the skin.
39: In a patient who presents with dermatitis associated with There is conicting evidence as to whether patients with AD
workplace exposures (ie, OCD), consider ICD as well as ACD. are at heightened overall risk of contact sensitization compared
[Strength of Recommendation: Strong; C Evidence] with nonatopic individuals. Because AD is associated with an
Summary Statement 40: In patients with suspected occupa- impaired skin barrier, it is plausible that this impairment is likely
tion-related CD, the examining physician should verify the to increase absorption of topically applied chemicals and enhance
diagnosis by conrming that the dermatitis was caused or the risk of subsequent sensitization, resulting in ACD and
aggravated by workplace exposures. [Strength of Recommenda- worsening of the underlying dermatitis. In children with severe
tion: Moderate; C Evidence] recalcitrant AD and concomitant ACD, avoidance of offending
Summary Statement 41: Consider botanical-related ACD in allergens in topically applied products can result in marked
outdoor workers, or others exposed to plants, including orists, improvement of eczema.
gardeners, landscapers, maintenance workers, park, and wildlife The latest NACDG lists the top 3 most common body lo-
ofcials. [Strength of Recommendation: Moderate; C Evidence] cations of contact dermatitis as scattered and/or generalized
distribution, the hands, and the face. In addition, attention
Treatment of contact dermatitis. Summary Statement should be given to specic anatomical sites, particularly the
42: Once the allergen or irritant has been identied, the patient eyelids, neck, scalp, axillae, lower extremities, and anogenital
should be counseled on avoidance of contact with the offending area. Facial ACD may present as a generalized facial eruption or
agent and informed of any cross-reactivity concerns. [Strength of in specic regions such as the forehead, periorbital, or perioral
Recommendation: Strong; B Evidence] areas. Sensitizers in commercial facial products that are in direct
Summary Statement 43: In addition to avoidance of exposure, skin contact are the most common causes of facial ACD.
the physician should prescribe appropriate adjunct medical Patients presenting with acute or chronic hand eczema should
treatment. [Strength of recommendation: Strong; B Evidence] undergo patch testing. Although most cases of CD involving the
Summary Statement 44: To prevent CD, avoid exposure to hands are caused by irritants, allergic contact sensitization is a
irritants and allergens and use appropriate skin protection. common cause of chronic hand dermatitis. The prevalence of
[Strength of Recommendation: Strong; B Evidence] ACD in patients presenting with hand dermatitis or hand eczema
Summary Statement 45: Education of the workers with ACD varies according to exposure history and occupation. Thus, it is
or ICD should include prognosis, and information that their strongly recommended to evaluate all patients with chronic hand
disease may persist and need long-term management even after eczema for ACD by obtaining a medical history of contact allergy
treatment and workplace modications. [Strength of Recom- and performing patch testing.
mendation: Moderate; C Evidence] Acute or chronic inammation of the lips manifested as
eczematous cheilitis can be characterized by itching, burning,
EXECUTIVE SUMMARY redness, edema, and ssuring. This is most commonly caused by
Contact dermatitis may be suspected on the basis of the physical (eg, cold, dryness, wind) or chemical irritants (eg, saliva,
clinical appearance of the cutaneous lesions, the distribution of lip cosmetics, or other oral products). Fragrance mix (FM),
the dermatitis, and the absence of other etiologies. Acute CD is balsam of Peru (BOP, Myroxylon pereirae), and nickel are the
characterized by erythematous papules, vesicles, and crusted le- most common positive allergens on PT. Sources of fragrances
sions. There are other dermatological conditions that may include oral hygiene products (eg, toothpastes, mouthwashes,
resemble the clinical and/or histological appearance of CD, and avorings, compounds used for dental impressions), cosmetics,
S6 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

and lip products (including lipsticks, glosses, and lip balms). Oral Patch testing is indicated in any patient suspected of ACD.
contact sensitization is considered to be uncommon. Persistent Patch testing can be performed using either a preloaded thin-
oral complaints or gingivitis has been associated with positive PT layer rapid use epicutaneous testing kit of 36 chambers or with a
reactions to allergens in dental components, including mercury, panel of antigens individually loaded in a chamber system rec-
methacrylate, and beryllium. Chemical and traumatic injury may ommended by the NACDG Research Group or the ACDS. The
be the most common causes of contact reactions involving mu- T.R.U.E. Test (panel of 35 antigens and a negative control) (see
cous membranes. Other conditions that should be considered in Appendix H) is standardized across lot numbers and is highly
patients with oral mucosal inammation include burning mouth reproducible. Depending on the test antigen, the T.R.U.E. Test
syndrome, lichenoid tissue reactions, stomatitis, gingivitis, oro- method has moderate concordance (62% to 63%) with indi-
facial granulomatosis, recurrent aphthous stomatitis, precancer- vidually loaded chamber systems (eg, Finn chamber system).
ous and cancerous lesions, viral and fungal infections and lichen Reliance on a core or baseline series of PT antigens such as those
planus. used by the NACDG Research Group or in the T.R.U.E. Test
In patients presenting for patch testing for evaluation of CD, panel for assessing all patients is likely to lead to underdiagnoses
nickel remains the most common contact sensitizer and is found of ACD. Selection of allergens to be patch tested will be more
more frequently in women than it is in men. The gender dif- accurate when selection is based on the clinical history. One can
ference is likely due to greater exposure of the neck, hands, and use PT panels based on the specic industry or exposure group.
ears to nickel in jewelry and body piercing practices. Females are Frequently, especially in the eyelid, lip, and facial dermatitis, it
twice as likely as males to have ACD involving the head and neck may be necessary to include personal products and substances
due to cosmetics. Among patients with cosmetic allergies, fra- specic to the patients exposure history.
grances, preservatives, and emulsiers are the most common Commercially available panels of supplemental allergens that
causative allergens. In addition to the most common hair dye are constituents of personal care products or encountered in
sensitizer, PPD, there are sensitizers in shampoos, including specic occupational environments are listed in the Appendices
fragrances, CAPB, and preservatives. ACD involving the scalp is B, C, and D.
frequently caused by allergens in personal hygiene and medical The International Contact Dermatitis Research Groups
products (eg, neomycin, benzocaine), hair tint and/or dyes, hair scoring system listed below is widely used:
cleansing products, and bleaches. (-) Negative reaction
ACD involving the axillary region is often due to contact (?) Doubtful reaction with faint erythema only
sensitivity to fragrance chemicals in deodorants; antiperspirant (1) Weak positive reaction with nonvesicular erythema,
chemicals are uncommon causes of ACD. Allergic CD due to inltration, possibly papules
disperse dyes in clothing can elicit eczematous eruptions in the (2) Strong positive reaction with vesicular erythema, inl-
axillae, feet, and groin. Axillary dermatitis may be a manifestation tration, and papules
of SCD, specically the baboon syndrome, a diffuse eruption (3) Extreme positive reaction with intense erythema and
involving exural and intertriginous areas following oral, inltration, coalescing vesicles, bullous reaction
intravenous, or transcutaneous exposure to the allergen in a (IR) Irritant reaction
contact-sensitized individual. Three groups of allergens are most (NT) Not tested
common causes of SCD: (i) metals such as mercury, nickel, and In the evaluation of delayed hypersensitivity reactions, the
gold; (ii) medications including aminoglycoside antibacterials, initial reading of PT should be done approximately 48 hours
CS, and aminophylline; and (iii) plants and herbal products after their application following patch removal. Tests may need
including Compositae and Anacardiaceae families and BOP (also to be read 30 minutes after removal of the patches to allow er-
known as Myroxylon pereirae). ythema from the occluding pressure of the tape and/or chamber
Patients presenting with anogenital dermatoses have been to resolve. A second reading must be done; this is often done at
diagnosed with conrmed ACD to allergens contained in topi- day 3 to 7 after the initial application. A collaborative study
cally applied products such as cosmetics, medications, feminine demonstrated that 30% of relevant allergens were positive at 96
hygiene and contraceptive products. The most common sources hours and were negative at the 48-hour reading, which suggests
of antigens were topical medications, including TCS, fragrances, that 96 hours may be optimal for a second reading. Occasionally,
BOP, nickel sulfate, cinnamic aldehyde, and neomycin sulfate. an additional late reading after 7 days may be needed for certain
The preservative methylisothiazolinone (MI) and benzocaine contactants such as metals, some antibiotics, and TCS that may
were frequently identied as contact allergens in patients with yield late reactions. Oral CS exceeding 20 mg/day of prednisone
anogenital complaints. or its equivalent have been shown to diminish skin test reactivity
The pattern of foot dermatitis due to ACD varies according to to 5% nickel sulfate at 48 hours. There is minimal evidence to
the type of footwear used. Para-tertiary butylphenol formaldehyde guide the duration of steroid reduction or withdrawal before
resin (in adhesives), potassium dichromate, cobalt chloride, and performing patch testing. If the clinical suspicion is high despite
carbamates are among the most common allergens. Allergic CD a negative PT in a patient receiving immunosuppressive medi-
involving the feet is commonly caused by sensitization to common cations, consider repeat testing when the immunosuppressant
rubber allergens (carbamates, thiurams, and mercaptobenzothia- doses are lowered or discontinued. The test site where the PT are
zole). Children presenting with sole dermatitis should be evaluated applied should have no topical potent CS or TCI applied for 5 to
by patch testing to rule out ACD caused by rubber additives, ad- 7 days before testing. UV irradiation of PT sites before testing
hesives, and/or chromates. The majority of patients with chronic can suppress PT responses.
leg ulcers and leg dermatitis have contact sensitization to chemical Doubtful (?) or weakly positive (1) questionable or irre-
sensitizers found in topically applied preparations including BOP, producible reactions on PT can be easily misinterpreted. The
FMs, antibacterial agents, CS, and lanolin. timing of the response may also affect its clinical signicance,
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S7
VOLUME 3, NUMBER 3S

with a weak reaction at day 7 more likely to be clinically relevant When evaluating ACD from cosmetics and personal care
than one at day 3. The inability to separate nonspecic from true products that contain many different chemical ingredients,
allergic responses may be due to the angry back or excited consider that the most common causes are due to a few
skin syndrome, which is dened as false-positive reactions important chemical classes, including fragrances, preservatives,
adjacent to large true-positive reactions that induce contiguous excipients, nickel, and sun blocks. Fragrances are complex sub-
skin inammation and irritability. The frequency of false-nega- stances and are the most common cause of ACD from cosmetic
tive results is not known, but has been estimated to occur in up in the United States. Previous studies suggest that the standard
to 30% of patch-tested patients. The ROAT is used to further FM and BOP will detect approximately 60% to 70% of
evaluate a patient suspected of ACD who exhibits doubtful or fragrance-allergic individuals. The addition of other commonly
suspected false-negative PT responses, to conrm that the patient used fragrance ingredients (FM II, lyral, ylang ylang oil, narcissus
is reacting to that particular product or to determine clinical oil, and sandalwood oil) may increase the yield up to 96%.
tolerability to new cosmetic products. The threshold concen- However, it should be noted that fragrances in PT have marginal
tration for a positive reaction for the ROAT is lower than the irritant potential and weak positive reactions may not be regar-
threshold concentration for a positive PT, although the accu- ded as proof of contact sensitization (low specicity of the test).
mulated ROAT dose was very similar to the PT. Preservatives and antibacterials are used to prevent rancidity
The clinical relevance of positive PT reactions to ACD can and microbial contamination. Preservatives tend to be grouped
only be established by carefully correlating the history, which into 2 broad categories: formaldehyde releasers (products that
includes exposure to the allergen, with the PT results. A positive emit formaldehyde) and nonformaldehyde releasers. It is rec-
PT may be clinically relevant depending on current or past ex- ommended that patients allergic to formaldehyde be advised to
posures. Current relevance is dened as denite if the PT or use avoid stay-on cosmetics preserved with formaldehyde releasers.
test with the suspected material is positive; probable if the PT is Among nonformaldehyde releaser preservatives, methlydibromo
positive and the antigen is present in known skin contactants and gluteronitrile and methychloroisothiazolinone/methyl-
the clinical presentation is consistent with that exposure; or isothiazolinone (MCI/MI) (trade name: Kathon CG) have
possible if the PT is positive, and skin contact with materials emerged as an important cosmetic and toiletry allergen with
known to contain the allergen was likely. increasing prevalence. The use of MI alone as a preservative in
If photo-allergic CD is suspected, physicians should be con- personal care and cosmetic products has increased in the past few
sulted with expertise in UV radiation and photo-patch testing to years especially in rinse-off products such as shampoos, condi-
conrm a suspected diagnosis. Photo-allergic CD typically affects tioners, baby soaps and detergents, and wet wipes. Although
sun-exposed areas such as the face, the V of the anterior neck, parabens formulated in cosmetics are infrequent causes of ACD,
the dorsal hands, and forearms. It typically spares the upper they can induce ACD when used as antibacterial in topical
eyelids, upper lip, and submental and postauricular areas. The medications especially those used on damaged skin, such as in
more common cause of sunscreen sensitization is the chemical long-standing dermatitis and stasis ulcers. The rate of sensitiza-
sunscreens. Titanium dioxide and zinc oxide (physical UV tion to parabens in patients with chronic leg ulcers is higher than
blockers) have not been reported to cause ACD or photo-allergy, that of the general population.
although there are a few reports of titanium in implants causing Botanicals (such as tea tree oil, propolis, and other essential
ACD. Testing requires duplicate application of allergen with oils) are plant extracts that are increasingly used as additives to
subsequent occlusion, and irradiation of one side to compare to skin care products and are potential causes of CD. It is important
the other, nonirradiated application. that patients who are allergic to fragrance also be made aware of
Although in vitro tests for delayed hypersensitivity to contact the potential dangers of cosmetic products that may contain
allergens (ie, metals and bone cement) are available, routine use of plant extracts and patients should also be counseled that natural
such assays is not currently recommended as their sensitivity and products does not equate with safety.
specicity for diagnosing ACD has not been determined and should In patients suspected to have allergy to hair products, CAPB,
be considered investigational. In vitro tests for assessing antigen PPD, fragrances, preservatives and glycerol thioglycolate should
specic sensitization are based on measuring lymphocyte prolifera- be considered. CAPB is an amphoteric surfactant that is often
tion (lymphocyte proliferation testsLPTs) or cytokine production found in shampoos, bath products, and cleaners. Allergy to
(ELISA or EliSPOT) after incubation with antigens. Some in vitro CAPB typically presents as eyelid, facial, scalp, and/or neck
tests have been validated against patch testing, whereas others have dermatitis. Paraphenylenediamine is the active ingredient in
not. The clinical relevance of in vitro testing to the diagnosis of CD many hair dyes, and is a very common cause of CD in hair-
has not been established and is still investigational. dressers. Other routes of exposure include body painting and
Identifying sources of exposure to clinically relevant allergens temporary tattooing. ACD from PPD can be severe, sometimes
is challenging. Dermatitis present on the face, hands, and mimicking angioedema. Cross-reactivity of PPD with other
exposed chest may be triggered by airborne protein allergens such para-amino compounds, such as benzocaine, para-amino-
as grass pollen, house dust mite, and cat dander; and diagnosed benzoic acid (PABA), sulfa drugs, aminoazobenzene, isopropyl-
by the application of the allergen by patch testing. CD caused by para-phenylenediamine (IPPD), and azo dyes has been reported
cosmetics is noted predominantly at the site of application; and may require avoidance. Glycerol thioglycolate is the active
however, occasionally personal care products and cosmetics ingredient in permanent wave solution and tends to cause more
manifest the contact allergy lesions in locations distant from the occupational dermatitis in hair dressers than consumers. Thi-
original skin sites. This phenomenon termed ectopic CD can be oglycolates may remain allergenic in the hair long after it has
caused by nickel transferred to the eyelid by ngers that have been rinsed out.
been exposed to a nickel source or toluene sulfonamide formal- Allergy to nail products is suspected when dermatitis presents
dehyde resin in nail polish. locally at the distal digit or ectopically on the eyelids and face.
S8 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

Most allergic reactions to nail polish and articial nail products to experience the same symptoms. Similarly, a group of patients
are to tosylamide and/or formaldehyde resin found in nail polish with implant-related eczema who were metal sensitized, and then
enamel, in addition to nail hardeners and setting lacquers. Up to underwent revision with a different metal alloy implant, had a
80% of the reactions appear on the neck, face, lips, and eyelids. higher incidence of eczema resolution. Anecdotal case reports
Alkyl polyester resin may be a suitable alternative for sensitive suggest that patients with skin or systemic manifestations of
patients. sensitization to components of implantable debrillators, pace-
Topical medicinal CD commonly develops after exposure to makers, arterial stents, dentures, and intrauterine devices (IUDs)
topical medications, including lanolin, para-aminobenzoic acid appeared to improve once the sensitizing agent was replaced.
(in sunscreens), caines (anti-itch preparations), topical antibi- There are no current guidelines or recommendations for
otics (neomycin, bacitracin), topical antihistamines, nonsteroidal symptomatic patients with positive PT to metals or bone cement
anti-inammatory drugs (NSAIDs), and/or TCS. Lanolin is used components. The decision regarding implant revision following
as the base of many topical medications, including TCS and positive PT results can only be made after a thorough discussion
moisturizers. Allergy to TCS affects 0.5% to 5.8% of patients between the patient, the allergist or dermatologist, and the or-
suspected of ACD. PT to CS is complicated by the inherent, thopedic surgeon. In addition to the possibility of metal sensi-
anti-inammatory nature of the drug itself, which results in tization as a potential cause of joint replacement failure, there are
frequent false-negative results if tested at too high concentration also reports of implant failure related to bone cement or its
or late PT readings (7-10 days following application) are not components including benzoyl peroxide, hydroquinone, methyl
done. Coopman et al classied 4 major groups of CS prepara- methacrylate, and n,n-dimethyl para-toluidine.
tions based on 2 immune recognition sites with considerable In considering special populations, both ACD and ICD are
cross-reactivity within the groups. Testing should include tix- signicant clinical problems in children. Patch testing should be
ocortol pivalate, budesonide, triamcinolone, the patients com- performed and remains the gold standard for the diagnosis of
mercial steroid, the vehicle, and the preservatives in the ACD in children. In children, a careful, age-appropriate history
preparations. Although rare, patients sensitized to TCS can should include exposure to diapers, hygiene products, personal
develop SCD with administration of the CS by an oral, IV, IM, care products, cosmetics, sunscreens, textiles with dyes and re
or inhalation route. retardant materials, medications, pets and pet products, school
PT to drugs may have a role in delayed hypersensitivity drug projects, sports, and so on. A US-based study showed nickel,
reactions and have a higher positivity in patients presenting with fragrance, cobalt, thimerosal, BOP, potassium dichromate,
maculopapular rashes, erythroderma, and nonimmediate cuta- neomycin, lanolin, thiuram mix, and PPD to be common al-
neous reactions including drug rash with eosinophilia and sys- lergens in children. In addition, there are highly relevant aller-
temic symptoms (DRESS), acute generalized exanthematous gens that have signicant frequency in children because of their
pustulosis (AGEP), Stevens Johnson syndrome/toxic epidermal unique exposure such as MCI/MI, dialkyl thiourea, p-tert-butyl
necrolysis (SJS/TEN), and xed drug eruptions. The utility of formaldehyde resin, CAPB, and disperse dyes.
the PT depends on various factors including the type and Contact dermatitis is one of the most common types of
formulation of the drug being tested, the vehicle used, as well as occupational illness, with estimated annual costs exceeding $1
the immunopathogenesis eliciting the eruption. Currently, there billion. OCD is classically divided into ICD and ACD. ICD
is no standardized approach to dene the population likely to represents approximately 80% of all cases of OCD and most
benet and validated PT materials to make PT to drugs a stan- commonly involves the hands. Common irritant exposures
dard of care. include wet work, solvents and alcohols, cutting oils, coolants,
Indications for pre-operative patch testing in patients with a degreasers, soaps, detergents, and other cleaning agents and
history of metal allergy are still being studied. However, pre- disinfectants. The major chemical groups associated with ACD
operative PT may help guide the selection of implant alloys in include metals, rubber-related materials, epoxies, resins and
patients with a high suspicion of metal allergy, and such patients acrylics, organic dyes, plants, foods, medications, biocides, and
demonstrate improved outcomes. This testing is not recom- germicides. The most common causes of plant dermatitis in
mended for patients without such a history of metal sensitivity. outdoor workers include poison ivy, poison oak, and poison
There is no information regarding pre-operative PT in patients sumac. Patch testing is not recommended to poison ivy because
with a prior history of methacrylate or antibiotic sensitivity. it can cause sensitization or large bullous reactions.
The clinician should recognize that contact sensitization to Accepted and validated criteria such as those proposed by
metals or bone cement that are used in orthopedic, cardiac, Mathias should be used to conrm the diagnosis of OCD. These
dental, and gynecological implants have been associated with include (1) the clinical appearance that is consistent with CD; (2)
both dermatitis and noncutaneous complications. These com- potential culprit cutaneous irritants and/or allergens are present
plications may include localized pain, swelling, erythema, in the workplace; (3) the anatomic distribution of dermatitis is
warmth, implant loosening, decreased range of motion, stent consistent with workplace skin exposure; (4) the temporal rela-
stenosis, and pericardial effusions in the case of cardiac implants. tionship between exposure and onset of symptoms is consistent
Patch testing to implant or device components is recommended with CD; (5) nonoccupational exposures are excluded as prob-
to help determine the etiology of the postimplantation adverse able causes of the dermatitis; (6) the dermatitis improves when
reaction. absent from work exposure, and re-exposure results in exacer-
Patients who experienced failed joint replacements and un- bation; and (7) PT performed according to established guidelines
derwent revision using components dictated by a positive metal demonstrates positive and relevant reactions.
PT reported resolution of their joint symptoms, most frequently Management of CD begins with avoidance of contact with the
joint pain, joint loosening, and localized dermatitis. Those pa- conrmed offending agent and the patient is informed of any
tients with a positive metal PT who were not revised continued cross-reactivity concerns. The identication and avoidance of
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S9
VOLUME 3, NUMBER 3S

contact with the offending agent(s) is the key to successful lymphohistiocytic inltrates. Features on physical examination or
treatment of ICD and ACD. For cosmetic products, the patients histological ndings are unable to differentiate ACD from ICD.
should be given not only a list of what they are allergic to but also Patch testing and environmental history of exposure to contact
a list of products that they can use, that are free of the suspected allergens is required. There are other dermatological conditions
allergens. Several databases are currently available in the United that may resemble the clinical and/or histological appearance of
States. CD, and these should be considered in the differential diagnosis
Components of medical management of ACD include TCS (Table I)1,2 that includes cutaneous T-cell lymphoma. The
with second line therapies including phototherapy, oral retinoids, cutaneous biopsy, if needed to differentiate CD from other forms
and immunosuppression. TCS are widely accepted as the treat- of dermatitis, should be interpreted by a pathologist with
ment of acute and chronic dermatitis, and selection of the TCS expertise in dermatopathology.
for efcacy, potency, and acceptability is determined by many Summary Statement 2: In patients suspected of ACD,
factors including the severity, the location, and the acuteness of patch testing is the gold standard to conrm the diagnosis.
the dermatitis. Key to the management of ACD is still the [Strength of Recommendation: Strong; C Evidence]
identication and avoidance of the allergen. Several topical T-cell The suspicion of ACD is the rst step in making the diag-
selective inhibitors (topical tacrolimus and pimecrolimus) have nosis. Patch testing is indicated in any patient with acute or
been used successfully in the treatment of AD, but their efcacy chronic, often pruritic, dermatitis if underlying or secondary
in ACD or ICD has not been established. Other treatments ACD is suspected. The history is important for the diagnosis and
including cyclosporin, azathioprine and psoralen plus ultraviolet subsequent management of this disease. Although medical his-
A (UVA) have been used for steroid-resistant ACD such as tory can strongly suggest the cause of ACD, it has moderate
chronic hand dermatitis. sensitivity (76%) and specicity (76%) in establishing the
Primary prevention of ICD and ACD involves avoidance of diagnosis.3 Because the patient may be unaware of any relevant
exposure to possible irritants and allergens and appropriate skin exposure, virtually any eczematous lesion could be aggravated by
protection. Avoidance of exposure may be accomplished by several a contact sensitizer.4-8 Noneczematous eruptions such a prurigo
means including elimination of an irritant or an allergen, substi- nodularis may also be associated with clinically relevant positive
tution, training, and rotation of job task. The use of personal PT.9 Studies have demonstrated the utility of patch testing in
protective equipment such as gloves, goggles and/or face shields, children with chronic dermatitis.10
uniforms, and equipment to protect the skin from the exposure is The sensitivity and specicity of patch testing varies according
important. The use of cotton liners under gloves can be useful. Skin to the allergen. For example, it has been reported that a positive
care to protect the barrier function of the skin is important and PT to nickel sulfate is demonstrable in only 60% of patients with a
involves the use of moisturizers, particularly lipid-rich moisturizers. positive history of nickel allergy (ie, positive predictive value 60%),
In a review of 15 studies reporting prognosis in OCD between whereas 12.5% to 15% of persons reporting a negative history of
1958 and 2002, the range of complete clearance of the dermatitis metal allergy had a positive PT response to nickel sulfate.3,11
was 18% to 72%. Atopic dermatitis is associated with poorer Patch testing identies contact sensitizers in nearly 50% of
outcomes. The longer the duration between the onset and patients presenting with scattered generalized dermatitis.12 The
diagnosis of hand dermatitis, the poorer the outcome. There is experienced clinician can misclassify ACD as nonspecic eczema
signicant job disruption for workers with CD. There are a small or IgE-mediated CU if the assessment is based solely on the
percentage of individuals with occupational hand dermatitis who medical history without patch testing.13,14
do poorly even with removal from exposure. Although sensitization occurring after patch testing is rare, this
has been reported after testing to plant allergens such as poison
ivy or poison oak, as well as to p-aminoazobenzene, p-phenyl-
CONTACT DERMATITIS: A PRACTICE enediamine, diaminodiphenylmethane, cobalt, chromium,15 and
PARAMETEReUPDATE 2015 beryllium.16 The possibility of active sensitization can be mini-
Clinical evaluation mized by testing with dilute solutions.17
Summary Statement 1: Consider ACD in the differential Patch testing has been shown to be cost effective if performed
diagnosis of patients with chronic eczematous or non- early in the course of the disease in patients with chronic ACD
eczematous dermatitis. [Strength of Recommendation: by reducing prediagnosis costs of treatment. Treated patients
Strong; C Evidence] with CD conrmed by patch testing exhibit signicantly greater
Contact dermatitis may be suspected on the basis of the improvement in dermatology-specic quality of life than those
clinical appearance of the lesions, the distribution of the patients who were not patch tested.18 Skin prick testing has no
dermatitis, and the absence of other etiologies or lack of associ- role in the evaluation of ACD but is often useful in patients
ated systemic manifestations. Acute CD is characterized by presenting with allergic CU.
erythematous papules, vesicles, and crusted lesions. Recurrent or Summary Statement 3: In addition to personal products
persistent episodes of CD will change over time from acute skin used by a patient suspected of ACD, review the home and
inammation to skin thickening, hardening, scaling, and workplace for other sources of contact allergens. [Strength of
ssuring, with exaggeration of the normal markings known as Recommendation: Moderate; D Evidence]
lichenication. Pruritus is characteristic of both acute and Work and environmental history must be carefully reviewed.
chronic CDs, and constant skin rubbing contributes to the Chronologic exposure histories that include hobbies and spe-
lichenication. Histologically, CD demonstrates intercellular cic activities relative to onset of the dermatitis should be
edema of the epidermis known as spongiosis, with varying de- obtained.
grees of acanthosis (thickening of the epidermal stratum basale The exact nature of the work duration of each activity and
and stratum spinosum) and supercial perivascular, occurrence of similar skin effects in coworkers may provide clues
S10 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

TABLE I. Differential diagnosis of allergic contact dermatitis (ACD)

Dermatologic condition Differentiating features and clues to diagnosis

Irritant contact dermatitis  Glazed, parched, or scalded appearance

 Sharply circumscribed dermatitis
 Healing begins promptly on withdrawal of the offending agent
 Patch testing negative
Atopic dermatitis  Personal or family history of atopy
 Early age of onset
 Chronic and recurrent
 Dry, scaly very pruritic
 Typical distribution
Facial in infancy
Extensors in early childhood
Flexural areas in adolescence and adults
Seborrheic dermatitis  Distribution: areas with sebaceous glands
 Scalp, periauricular, face (medial eyebrows, glabella, nasolabial folds), presternal trunk, interscapular
 Blepharitis common
 Dandruff appears to be a precursor
 Distinctive morphology: dull, yellowish-red, sharply demarcated lesions covered with greasy-looking scales
Dyshidrotic eczema  Small (1-2 mm) vesicles, deep seated on nonerythematous base
 Palms, soles, and/or lateral aspects of ngers, often symmetrical
 Intensely pruritic and itching prodrome
 Persists for 2-3 weeks and then resolves by involution and desquamation
Psoriasis  Plaques typically have dry, thin, silvery-white, or micaceous scale
 Auspitz sign: removing scale reveals a smooth, red, glossy membrane with tiny punctate bleeding
Dermatitis herpetiformis  Genetic predisposition for gluten sensitivity
 Intensely pruritic
 Symmetrically grouped (herpetiform) papules and vesicles
 Elbows, knees, buttocks, scapula, scalp
 Direct immunouorescence of the skin shows granular IgA at dermal papillae and occasionally
along the dermo-epidermal border
Mycoses fungoides and  Patches with thin, wrinkled quality, often with reticulated pigmentation
cutaneous T-cell lymphoma  Pruritus varies from minimal or absent to common in premycotic phase and may precede MF by years
 Often on lower trunk and buttocks
 Cutaneous biopsy required for conrmation

as to potential causes of work-related ICD or ACD.19,20 Relevant not apply. Simultaneous exposure to both an irritant and a contact
changes in work environments that result in new direct chemical allergen or 2 contact allergens can reduce the clinical threshold
exposures to the skin, including vapors and fumes, must be concentration for elicitation of response to a given allergen. The 2
probed. Certain occupations (eg, hospital workers) require mechanisms have been suggested to explain the effect of exposure to
frequent hand washing, and the use of cleansing agents may an irritant on potentiation of contact sensitization, including effects
compromise the skin barrier and cause irritant hand dermatitis.21 on the immune response by upregulation of proinammatory
Because the worker may be unaware of specic chemicals to cytokines and/or enhanced penetration of the allergen.23
which he or she is exposed, MSDS obtained from the manu- Detergents are common causes of hand dermatitis because of
facturer may be helpful; however, key sensitizing ingredients their disruption of the skin barrier and are frequently associated
found at low concentrations are often omitted from product with ICD of the hand. Although there are some reports of ACD
descriptions.22 related to detergents, careful evaluation suggests that allergic re-
Hobbies and nonwork activity such as gardening, macram, sponses are rare.24 Irritants that disrupt the skin barrier may then
painting, ceramic work, carpentry, and photography may be penetrate into the epidermis resulting in injury to the keratino-
sources of exposure to culprit contactants. Obtaining a detailed cyte membranes and release of inammatory cytokines, and
history of animal and animal product exposure is essential. contribute to developing ICD. This disruption of the skin barrier
Summary Statement 4: Evaluate patients for both irritant and also allows for allergen penetration and resultant induction of
allergic causes, especially in those presenting with hand immunological responses.25
dermatitis. [Strength of Recommendation: Strong; C Evidence]
In addition to exposure to a single agent, simultaneous exposure to Physical examination
multiple irritants and contact allergens may produce additive, syn- Summary Statement 5: Allergic CD should be suspected
ergistic, or antagonistic responses. Although most research related and evaluated in the patient with both generalized and
to irritant and allergic effects comes from studies of single agents, anatomically localized skin eruptions (such as the hands,
individuals are often exposed to multiple irritants and allergens. In face, eyelids) that come in contact with the substances in the
some situations, accepted threshold concentrations for elicitation of environment. [Strength of Recommendation: Moderate; C
an allergic cutaneous PT response to a specic contact allergen may Evidence]
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S11
VOLUME 3, NUMBER 3S

The latest NACDG lists the top 3 most common body lo- lip dermatitis and 85% of these cases were women.34 Allergic
cations of CD as scattered and/or generalized distribution, the contact cheilitis (ACC) often involves the lip vermillion border
hands and the face.26 In addition, attention should be given to and extends to contiguous skin presenting with concomitant
specic anatomical sites, particularly the face, eyelids, lips, oral perioral dermatitis; with adjacent oral mucosa typically spared. In
mucosa, neck and scalp, hand, axillae, anogenital area, feet, and patients presenting to dermatologists with cheilitis, history
lower extremities. Each of these areas can be affected by ACD combined with patch testing was able to conrm ACC in only
and will be described in greater detail in Summary statements 6 34% to 38% of patients.34,35 FM, BOP, and nickel were the
through 14. A diagnosis of ACD based on the physical exami- most common positive allergens on PT. Sources of fragrances
nation and history alone, however, is not conclusive and should include oral hygiene products (eg, toothpastes, mouthwashes,
be conrmed by PT.27 avorings, compounds used for dental impressions), cosmetics,
Summary Statement 6: In a patient with a facial rash and lip products (including lipsticks, glosses, and lip balms). In
involving the periorbital areas (eg, eyelids), evaluate for ACD another study, lipsticks and lip balms were identied as the most
caused by components of cosmetics, such as fragrances, pre- common sources of allergens for ACC in females and toothpaste
servatives, and excipients, because these are common sensi- was the most commonly implicated allergen35 in males. In
tizers of the facial skin. [Strength of Recommendation: toothpastes, avoring chemicals are most frequent relevant al-
Moderate; C Evidence] lergens, including mint derivatives such as spearmint, menthol,
Facial ACD may present as a generalized facial eruption or in peppermint, carvone as well as cinnamal, and anethole.36 In lip
specic regions such as the forehead, periorbital, or perioral areas. balms, propolis produced by bees, lanolin, coconut oil, almond
Sensitizers in commercial facial products that are in direct skin oil, peppermint oil, and vitamin E are potential sensitizers.37 Less
contact are the most common causes of facial ACD.28 Facial common antigen sources of ACC are jewelry (ie, nickel by
ACD may also occur when contact allergens are transferred ectopic transfer) and topical medications (eg, neomycin, bude-
ectopically to the face by the hands from other regions of the sonide, tetracaine). Interestingly, relevant positive PT to allergens
body. Skin exposure to airborne plant-derived aeroallergens (eg, that were not part of the NACDG patch series have been
tree, weed pollens) may cause an eczematous dermatitis of the identied in 36% of patients with ACC.34 This suggests that a
exposed areas of the face, neck, and arms. These reactions typi- selected panel should be used that is based on the patients
cally occur on a seasonal basis during the summer months.29 personal products.
Compositae sensitizers are also found in many natural cosmetic Summary Statement 8: Evaluate patients with chronic oral
products and may cause facial ACD. mucosal inammatory conditions for disorders other than
Allergic CD is the most common cause of isolated periorbital ACD. [Strength of Recommendation: Moderate; C Evidence]
and eyelid dermatitis.28 Risk factors include female gender, AD, ACD is often considered in the differential diagnosis of
and age over 40 years. In one study, the most common sources burning mouth syndrome, lichenoid tissue reactions, stomatitis,
of causative allergens were found in cosmetic products (eg, gingivitis, orofacial granulomatosis, recurrent aphthous stomati-
facial cream, eye shadow) and ophthalmic therapeutics. The tis, precancerous and cancerous lesions, viral and fungal in-
most commonly identied sensitizers were FM (19%), BOP fections, lichen planus, especially in human immunodeciency
(10%), thimerosal (10%), and neomycin sulfate (8%).28 Nickel virus-infected patients and those with Melkersson-Rosenthal
has also been identied as a very common sensitizer associated syndrome. Nevertheless, the oral mucosa is considered an im-
with periorbital CD.30 Although it has been suggested that mune privileged site and oral contact sensitization is considered
preservatives in topical ophthalmic medications are important to be uncommon. Persistent oral complaints or gingivitis has
sensitizers, benzalkonium chloride (the most frequently used been associated with positive PT to allergens in dental compo-
today) has not been found to be a common sensitizer in patients nents including mercury, methacrylate, and beryllium.38
with periorbital CD.31 Thimerosal, a possible sensitizer, is less In a large study of 331 patients presenting with oral symp-
commonly used in ophthalmic products. A recent retrospective toms, PT was conducted to a comprehensive panel of avorings,
North American study of patients evaluated for periorbital preservatives, acrylates, medications, and metals.39 The mean age
dermatitis could not detect signicant sensitizers related to in this study was 58 years and 81% were women. The most
ophthalmic products, and found that nickel and fragrances were frequent positive PT was to potassium dicyanoaurate, nickel,
still the most common sensitizers identied by PT.32 ACD is gold sodium thiosulfate, FM, BOP, beryllium, cobalt, and
responsible for 81% of cases of eyelid dermatitis. Common acrylate. More than 50% of patients presenting with burning
sensitizers included nail product chemicals (tosylamide and/or mouth syndrome, lichenoid tissue reaction, cheilitis, stomatitis,
formaldehyde resin, acyrlates), botanicals in personal care and gingivitis exhibited at least one positive reaction considered
products, and nickel.33 to be relevant by the reporting physician. However, the term
Summary Statement 7: Evaluate patients presenting with relevant positive PT used in large retrospective PT studies is
lip dermatitis (cheilitis) and perioral dermatitis for both severely limited due to the lack of documentation of clinical
irritant and allergic causes of contact dermatitis. [Strength of improvement following avoidance to the suspected relevant
Recommendation: Moderate; C Evidence] allergens. Thus, based on available clinical data, there is insuf-
Eczematous cheilitis is an acute or chronic inammation of cient evidence to conrm a causative role of contact allergy in the
the lips and is characterized by itching, burning, redness, edema, aforementioned oral syndromes.
and ssuring. This is most commonly caused by physical (eg, Chemical and traumatic injury may be the most common
cold, dryness, wind) or chemical irritants (saliva, lip cosmetics, or causes of contact reactions involving mucous membranes. Many
other oral products). Other causes include atopic cheilitis that is of these reactions are caused by caustic chemical agents inad-
observed in patients with AD. In a series of more than 10,000 vertently applied during dental treatment. Lastly, one should be
patients reported by the NACDG, 2% of patients presented with aware that oral erosions and blistering lesions may be the initial
S12 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

presenting symptoms of autoimmune blistering diseases such as Summary Statement 11: Evaluate patients with axillary
pemphigus. dermatitis for ACD caused by local contact sensitivity to al-
Summary Statement 9: In patients presenting with lergens in topically applied products found in deodorants
dermatitis that involves the scalp and neck, consider patch and textiles. In some cases, axillary dermatitis could be a
testing for common causative sensitizers in cosmetics, hair manifestation of SCD (ie, the baboon syndrome).
products, and jewelry. [Strength of Recommendation: Mod- [Strength of Recommendation: Moderate; C Evidence]
erate; C Evidence] ACD involving the axillary region is often due to contact
Nickel remains the most common contact sensitizer and is sensitivity to fragrance chemicals in deodorants, including
found more frequently in women than it is in men. The gender hydroxyisohexyl-3-cyclohexene carboxaldehyde, isoeugenol,
difference is likely due to greater exposure of the neck, hands and hydroxycitronellal, as well as cinnamic aldehyde and sensitizers in
ears to nickel in jewelry,40,41 as well as piercing practices. natural botanical deodorants.47-52 Although ICD is more com-
Females are twice as likely as males to have ACD involving the mon, ACD has been rarely attributed to antiperspirants.53 Iso-
head and neck due to cosmetics.42 Among patients with cosmetic lated case reports of ACD causing axillary dermatitis have been
allergies, fragrances, preservatives, and emulsiers are the most attributed to propantheline bromide used as a treatment for
common causative allergens. Specically the most common in hyperhidrosis.54 Pretesting with a ROAT on the exor surface of
both genders are quaternium-15, FM and BOP. PPD (hair dye), the forearm and axilla is advised in any patient with a history of a
glyceryl thioglycolate (permanent wave solutions), tosylamide pre-existing axillary dermatitis before initiating use of a new
and/or formaldehyde resin (nail enamel products), and methyl product.
methacrylate (nail product adhesive) were common sensitizers in ACD due to disperse dyes in clothing can elicit eczematous
females. Sensitizers in hair care products affect 30% of females eruptions in the axillae, feet, and groin.55 In Sweden, 1.5% of all
and 22% of male patients who were evaluated for CD.42 In patients undergoing patch testing has positive reactions to a
addition to the most common hair dye sensitizer, PPD, more textile dye mix and the most common reactive dye was disperse
than 20 other potential sensitizers have been identied in hair orange 1, whereas a clinic in North America reported that
dye products.43 Frequent sensitizers contained in shampoos disperse blue 106 and disperse blue 124 were the most frequent
include fragrances, CAPB (a surfactant), preservatives such as sensitizers.56 Patients reacting to a textile dye mix more often
MCI/MI, and preservatives that are formaldehyde releasers (eg, reported dermatitis involving the axillary folds, arms, face, and
quaternium-15, imidazolidinyl urea). Other ingredients that are neck.57 In the axillae, the periphery is more often involved than
potential sensitizers include propylene glycol, vitamin E, para- the axillary vault due to greater contact of the garment to the skin
bens, benzophenones, iodopropynyl butylcarbamate, and meth- in this area.
yldibromo glutaronitrile/phenoxyethanol.44 Allergic CD Axillary dermatitis may be a manifestation of SCD, specically
involving the scalp is most frequently caused by sensitization to the baboon syndrome, a diffuse eruption involving exural and
medical products (eg, neomycin, benzocaine), hair tint, dyes, hair intertriginous areas following oral, intravenous, or trans-
cleansing products, and bleaches.45 cutaneous exposure to the allergen in a contact-sensitized indi-
Summary Statement 10: Consider irritant and ACD in all vidual.58 Allergens associated with SCD are listed in Appendix C.
patients presenting with acute or chronic hand eczema. All Summary Statement 12: Evaluate patients presenting with
such patients suspected of CD should undergo patch testing. anogenital dermatitis for possible ACD to antigens contained
[Strength of Recommendation: Moderate; C Evidence] in topically applied products. [Strength of Recommendation:
Allergic contact sensitization is a common cause of chronic Moderate; C Evidence]
hand dermatitis. The prevalence of ACD in patients pre- Allergic CD can cause anogenital dermatitis. A total of 17% to
senting with hand dermatitis or hand eczema varies according 74% of patients presenting with anogenital dermatoses have been
to exposure history and occupation. Hair dressers presenting diagnosed with conrmed ACD to allergens contained in topi-
with hand dermatitis had a high prevalence of ACD (75%) cally applied products such as cosmetics, medications, and
with 25% of the remaining cases being attributed to irri- feminine hygiene and contraceptive products. In a recent large
tants.40 In a multicenter collaborative study in Denmark, 508 retrospective study, 44% of patients with anogenital dermatitis
consecutive patients who presented with hand eczema were (including 41% of women and 50% of men) were identied with
evaluated. In these patients, ICD was diagnosed in 38%, ACD ACD. The most common sources of antigens were topical
in 24%, AD in 19%, and in 22%, nonspecic dermatitis was medications, including TCS, fragrances, BOP, nickel sulfate,
the diagnosis.46 Even in children, ACD is a common cause of cinnamic aldehyde, and neomycin sulfate. Cinnamic aldehyde,
hand dermatitis with one study reporting as high as 36% dibucaine, benzocaine, hydrocortisone-17-butyrate, and bude-
prevalence. Sensitizers deemed relevant to ACD involving the sonide were more common sensitizers in patients presenting
hands included the preservative quaternium-15 (16.5%), exclusively with anogenital dermatitis. A total of 21% patients
formaldehyde (13.0%), nickel sulfate (12.2%), FM (11.3%), were diagnosed with ICD; the most common irritants were
thiuram mix (10.2%), BOP (9.6%), carba mix (7.8%) used in cosmetics, soaps and cleansers, various health aides, and un-
rubber products, neomycin sulfate (7.7%), bacitracin (7.4%), known agents.59 In another patient series, the preservative MI
and methyldibromo glutaronitrile/phenoxyethanol 2.0% and benzocaine were frequently identied as contact allergens in
(7.4%). Thus, it is strongly recommended to evaluate all pa- patients with anogenital complaints.60 Methylisothiazolinone,
tients with chronic hand eczema for ACD by obtaining a used as a preservative in wet baby wipes has been identied as a
medical history of contact allergy and performing patch sensitizer and cause of ACD involving the buttocks and perianal
testing. In addition to ACD, chronic hand eczema may be a area in children.61
presenting symptom of psoriasis and should be considered in Summary Statement 13: Consider a diagnosis of SCD
the differential diagnosis. following systemic exposure (eg, ingestion, infusion, or
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VOLUME 3, NUMBER 3S

transcutaneous exposure) to a known contact sensitizer in a topical preparations containing fragrances and antiseptics should
patient who presents with generalized dermatitis, inter- be avoided in patients with leg ulcers and that they have the
triginous and exural exanthema (Baboon syndrome), and/or potential to become sensitized to components of products and
a are at previous cutaneous sites of exposure. [Strength of medications that are used to treat leg ulcers.70
Recommendation: Moderate; C Evidence] Summary Statement 15: In addition to avoiding irritants
The most common causes of SCD consist of 3 groups of al- in patients with AD, evaluate for ACD if suspected, as the 2
lergens: (i) metals such as mercury, nickel, and gold; (ii) medica- dermatologic conditions often coexist in the same patient.
tions including aminoglycoside antibacterials, CS, and [Strength of Recommendation: Moderate; C Evidence]
aminophylline; and (iii) plants and herbal products including the There is conicting evidence as to whether patients with AD
Compositae and Anacardiaceae plant families and BOP.58 Nickel are at heightened overall risk of contact sensitization compared
sulfate is ubiquitous in steel devices, jewelry, clothing, and food. with nonatopic individuals. One recent study showed an inverse
Systemic CD can result from ingestion of trace amounts of nickel relationship between contact sensitization and severe AD.73
in soy, chocolate, nuts, green beans, peas, and canned foods.62 Because AD is associated with an impaired skin barrier, it is
Other examples of systemic exposure to allergens that can trigger plausible that this impairment is likely to increase absorption of
diffuse SCD include systemic administration of aminoglycoside topically applied chemicals and enhance the risk of subsequent
antibiotics in a patient sensitized to topical neomycin; hydroxyzine sensitization. Atopic dermatitis has been diagnosed in 34% of
ingestion or administration of IV aminophylline in patients with children with clinically relevant PT reactions, although children
ACD to ethylenediamine, which cross-reacts with both medica- without AD are equally as likely as those with AD to exhibit
tions; oral estrogen triggering a systemic dermatitis after sensiti- clinically relevant positive PT.74
zation to estrogen patches63; or are of previously positive In a large population-based study of Danish adults, contact
budesonide PT sites after inhalation of nebulized budesonide.64 It sensitization to at least one allergen was observed in 14% of
is postulated that once the allergen has entered the blood stream, it patients who self-reported AD, whereas in 10% of those without
encounters and reactivates specic memory T cells that then home AD had ACD. This overall difference between atopics and
to the site of the previous dermatitis. nonatopics in this study was primarily attributed to a higher
Patients may also experience SCD after oral challenges with frequency of allergy to fragrances that may reect a greater cu-
fragrance-containing foods, Chinese herbs, or drugs. Patients mulative skin exposure to topical treatments containing fra-
who are contact sensitive to BOP are prone to SCD with grances.73 In this same study, the risks associated with laggrin
ingestion of foods or avoring agents that are constituents of mutations were also evaluated. Self-reported hand dermatitis as
BOP (eg, citrus products, ice cream, cinnamon, chutney, cola, well as AD combined with hand dermatitis was signicantly
vanilla, curry, ketchup, or tomatoes) or cross-react with those associated with contact sensitization in patients with a laggrin
constituent allergens. In addition, various spices, garlic, cashew gene mutation (R501X, 2282del4), whereas AD alone combined
nuts, and proteinaceous substances handled by grocers, meat and with laggrin mutations but without hand dermatitis was not
sh handlers, and bakers have been cited as causes of SCD. signicantly associated with contact sensitization.75 In a North
Summary Statement 14: Consider PT to rubber chemicals, American study, PT results compared between 300 patients with
adhesives, and leather components of footwear in patients AD and approximately 3000 patients without AD found that
presenting with unexplained chronic dermatitis involving the patients with AD were signicantly more likely to exhibit contact
lower extremities, feet and/or soles. [Strength of Recom- sensitization and this difference was attributable to sensitization
mendation: Moderate; C Evidence] to metals.76
The pattern of foot dermatitis due to ACD varies according to In a report by Jacob et al,77 comprehensive PT played a key
the type of footwear used. ACD rarely localizes between the toes role in the identication of relevant chemical allergens in per-
and typical sole involvement spares the instep and the toes sonal hygiene products and topical treatments used in manage-
exural creases. Patch testing studies have identied p-tertiary ment of 3 children with severe, recalcitrant AD. Avoidance of
butylphenol formaldehyde resin (in adhesives), potassium di- offending allergens resulted in marked improvement of eczema,
chromate, cobalt chloride, and carbamates as the most common which permitted reduction in TCS and subsequent discontinu-
allergens.27,65-72 Allergic CD involving the feet is commonly ation of systemic immunosuppressive therapy.
caused by sensitization to common rubber allergens (carbamates,
thiurams, and mercaptobenzothiazole). Patients suspected of Patch testing recommendations
rubber ACD should also be tested to mixed dialkyl thioureas Summary Statement 16: Avoid or reduce doses of immu-
(diethylthiourea and dibutylthiourea) because the majority of nosuppressant medications such as systemic CS and other
thiourea-sensitized patients do not react on PT to the more systemic immunosuppressants before patch testing. Avoid
common rubber allergens.67 Children presenting with sole application of TCS, TCI, or ultraviolet radiation to the PT
dermatitis should be evaluated by PT to rule out ACD caused by site, because these may reduce allergic PT responses.
rubber additives or chromates (from leather tanning).68 All the [Strength of Recommendation: Moderate; C Evidence]
aforementioned chemicals should be included in PT panels to The majority of adult patients treated with oral CS exceeding
evaluate patients with foot dermatitis. 20 mg/day of prednisone or its equivalent have been shown to
The vast majority of patients with chronic leg ulcers have diminish skin test reactivity at 48 hours to 5% nickel sulfate.78
positive PT to chemical sensitizers found in topically applied The effect of systemic CS on the results of PT is less understood
preparations. The most common of sensitizers were BOP, FM I, for children. Patch tests in patients on low doses of prednisone
antibacterial agents, CS, and lanolin.69,70 In a recent prospective and cyclosporine may still yield clinically relevant results.79
study of patients with leg ulcers, the number of positive PT There are no supporting data that guide the duration of ste-
correlated with duration of the leg ulcers. This suggests that roid reduction or withdrawal before performing PT. The
S14 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

suppression is not absolute, and if necessary, PT should be A study of the T.R.U.E. Test (panel of 35 antigens and a
performed while on the lowest possible dose of the immuno- negative control) (Appendix H) showed that it is highly repro-
suppressant medication.79,80 If the clinical suspicion is high ducible with only a 5% discordance between concomitant
despite a negative PT, consider repeat testing when the immu- duplicate tests in individual patients.89 Depending on the test
nosuppressant doses are lowered or discontinued. antigen, the T.R.U.E. Test method has moderate concordance
High/medium potency TCS (ie, betamethasone dipropi- with individually loaded chamber systems. In separate studies,
onate 0.05%) applied topically to PT sites for 3 successive 62% to 63% overall positive concordance rates were reported
days suppress 48-hour responses to contact allergens.81 The between the Finn chamber system and T.R.U.E. Test
test site where the PTs are applied should have no topical methods.90,91 The T.R.U.E. Test is widely used because of its
potent CS or TCI applied for 5 to 7 days before ease of application. However, it lacks exibility and has currently
testing.82,83 Topical tacrolimus (0.1%) pre-applied to skin a limited number of allergens available. The NACDG series
test sites for 48 hours suppressed 48-hour PT responses to comprises 65-70 allergens and is used as a screening research tool
5% nickel sulfate.84 Pretreatment of skin test sites with UV to track trends in delayed-type contact sensitization. It also tests
irradiation produced dose-related suppression of erythema established and newly marketed chemicals to determine preva-
measured at 48 hours after application of nickel sulfate PT lence and relevance in causing ACD. Thus, the NACDG may
in nickel-sensitized subjects.85 Protection from UV-induced contain allergens in different vehicles and concentrations. The
immunosuppression of allergic responses to nickel sulfate ACDS has outlined a Core Allergen Series of suggested 80 al-
was achieved by application of sunscreen products blocking lergens that can be scaled up or down depending on the needs of
UVA and UVB wavelengths.86 the physician and the patient being tested. The allergens are
Systemic antihistamines are generally not believed to interfere arranged with more likely allergens being higher in the tray.
with the PT readings. A study showed that treatment with 10 mg Appendix I is an example of a PT form listing the NACDG
loratadine for 4 days before patch testing was associated with a series. Exclusive reliance on the T.R.U.E. Test antigen panel as
signicant reduction in the size of the eczematous responses to opposed to an extended panel used by the NACDG or the
nickel sulfate. Recently, desloratadine given for 4 days at twice standard series outlined by the ACDS and personal products can
the normal daily dose (5 mg po bid) did not signicantly impact miss detection of sensitization to clinically relevant antigens.26
interpretation of positive patch responses to 10 contact aller- Currently, there are different loading chambers available; how-
gens.87 This would indicate that antihistamines do not need to ever, none have shown superiority over another.
be withheld for PT. Summary Statement 19: Read and interpret PT conform-
Summary Statement 17: In addition to using a core or ing to the scoring system developed by the International
baseline series of PT allergens in evaluating ACD, consider Contact Dermatitis Research Group. [Strength of Recom-
using supplemental series of PT allergens based on specic mendation: Moderate; D Evidence]
patient exposures and the patients personal products, to Patch testing techniques and scoring reactions by a grading
increase the probability of identifying relevant sensitizers. scale were rst standardized in the 1930s. The International
[Strength of Recommendation: Moderate; C Evidence] Contact Dermatitis Research Group published the following
Reliance on a core or baseline series of PT antigens such as nonlinear, descriptive grading scale in 1970,92 which continues
those used by the NACDG or in the T.R.U.E. Test panel for to be widely used.
assessing all patients is likely to lead to underdiagnoses of ACD. A (-) Negative reaction
recent multicenter North American study of over 4300 patients (?) Doubtful reaction with faint erythema only
published in 2013 revealed that 25% of patients exhibited a (1) Weak positive reaction with nonvesicular erythema,
clinically relevant positive test to an antigen not included in a inltration, possibly papules
standard 70-antigen panel, and 25% reacted to an allergen that (2) Strong positive reaction with vesicular erythema, inl-
was not part of the T.R.U.E. TEST panel.26 In 2009, the tration, and papules
NACDG reported that 23% of 4454 patients in a multicenter (3) Extreme positive reaction with intense erythema and
study exhibited at least one relevant positive test to a supple- inltration, coalescing vesicles, bullous reaction
mentary allergen and 5% reacted to a clinically relevant occupa- (IR) Irritant reaction
tional allergen not part of the standardized panel of 65.88 Many (NT) Not tested
PT companies provide kits with allergen panels selected for a The details of this rating system and corresponding clinical
specic industry such as machinists, cosmetologists, or dental interpretation with a visual key are given in Appendix H and
workers (Appendix D). There are other standardized panels for Figure 1.
exposure groups such as cosmetics, textiles, plastics, and glues Summary Statement 20: Remove and read PT at approx-
(Appendix E), and medications and topical treatments (Appendix imately 48 hours after application. A second reading should
F). Currently, such kits can only be obtained from the manufac- be done between 3 and 7 days following application.
turers listed in Appendix G. Frequently, especially in the eyelid, [Strength of Recommendation: Moderate; C Evidence]
lip, and facial dermatitis, it may be necessary to include personal In the evaluation of delayed hypersensitivity reactions, the
products and substances specic to the patients exposure history. initial reading of PT should be done approximately 48 hours
Summary Statement 18: Patch testing can be performed after their application following patch removal.93 However, if
either using a preloaded thin-layer rapid use epicutaneous CU is considered, the PT has to be checked at 20-30 minutes
testing kit of 36 chambers or with a panel of antigens loaded after application. Tests may need to be read 30 minutes after
individually in a chamber system recommended by the removal of the patches to allow erythema from the occluding
NACDG Research Group or the ACDS. [Strength of pressure or stripping of the tape and/or chamber to resolve. A
Recommendation: Moderate; C Evidence] second reading must be done, usually between day 3 and day 7
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S15
VOLUME 3, NUMBER 3S

allergens dissipated after the day 5 reading.96 With most al-

lergens, however, the gain in positive reactions was biggest
when a reading was performed at day 5.95,97 Table II lists al-
lergens with typical early and late reactivity. Reactions occur-
ring even as late as days 10 to 14 may be due to a delayed
irritant response and delayed allergic reactions such as for
metals and TCS, and very rarely represent sensitization from
the PT.97-99 Conversely, some irritant reactions appearing
within the rst 48 hours tend to disappear (decrescendo effect)
by 96 hours.100 In rare situations where patient circumstances
(ie, distance from the practice, insurance issues) do not permit 3
visits, the patches can be removed by the patient or local
physician at 48 hours and read by the treating physician in 72-
96 hours. Patients can be instructed to take a picture of the
back before removing the patch (to help the clinician determine
the integrity of the PT system, and to record any nonadherent
or loose patches), and another picture after removing the patch.
They should also re-label the PT sites after removal. However,
this approach is considered suboptimal.
Summary Statement 21: Consider that a possible false-
positive reaction can result with the use of irritants or allergic
substances at potentially irritating higher concentrations,
pressure reaction from the lling chamber, an angry back
syndrome, or patch testing on skin with active dermatitis.
[Strength of Recommendation: Moderate; D Evidence]
Many variables contribute to the strength of the PT reaction,
including the concentration and potency of the allergen, the de-
gree of subject sensitization, the length of application time, and
the timing of the readings.103 The greatest source of misinter-
pretation is due to questionable or irreproducible reactions in the
doubtful (?) or weakly positive (1) categories. The timing of
the response may also affect its clinical signicance; for example, a
weak reaction at day 7 is more likely to be clinically relevant than
one at day 3. The inability to separate nonspecic from true
allergic responses may be encountered in patients who exhibit the
angry back or excited skin syndrome, which is dened as false-
positive reactions adjacent to large true-positive reactions that
induce contiguous skin inammation and irritability. The longer
the duration of the primary dermatitis, the greater the risk for the
excited skin syndrome to occur with patch testing.104 This should
be suspected in cases with more than 5 reactions in close proximity
to each other. The underlying mechanisms are not fully
understood.
A pustular patch reaction should not be misinterpreted as a
FIGURE 1. Visual key for scoring patch test reactions. positive reaction in PT. A pustular reaction is common in atopic
individuals and in response to test of metals such as nickel,
copper, arsenic, and mercuric chloride. The test site is only
after the initial application.94 Occasionally, an additional late minimally pruritic and this type of pustular reaction is frequently
reading after 7 days may be needed for certain contactants such an irritant reaction.
as metals, some antibiotics, and TCS that may yield late re- The position of the allergen in a multiple allergen template
actions.95 A collaborative study documented that approximately may give rise to the false-positive results, especially if cross-
30% of relevant allergens that were negative at the 48-hour reacting or co-sensitizing substances are tested in too close
reading became positive at a 96-hour reading, suggesting that 96 proximity.105 Marginally irritating allergens may also trigger
hours may be optimal for a second reading. Consider a late false-positive reactions.106 Repeat the PT with greater separation
reading for allergens with negative early reactions, when the of allergens or sequentially if the initial reactions are not clinically
clinical history strongly supports sensitization. Four allergens relevant, because false-positive reactions are not reproducible
with the highest frequencies of delayed-positive reactions were when the triggering allergens are removed.106
gold sodium thiosulfate 0.5% (delayed-positive reactions in 22/ Summary Statement 22: Recognize the possibility that
353 patients), dodecyl gallate 0.25% (6/105), palladium chlo- false-negative reactions could be due to inadequate allergen
ride 2% (8/194), and neomycin sulfate 20% (10/253). In concentration needed to elicit a response; inability of the
contrast, reactions to certain preservatives and fragrance vehicle to release sufcient allergen; reduced skin
S16 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

TABLE II. Allergens associated with early and late reactions wrong carrier vehicle that resulted in insufcient penetration of
Allergens associated with early peak reactions (at 48 h) the allergen, or inclusion of the wrong salt or version of the
allergen. UV sunlight (eg, tanning), TCS, and TCI on the area of
Balsam of Peru resin (Myroxylon pereirae)95,101,102
PT and systemic CS (ie, >20 mg/day prednisone)78 and other
Benzoyl peroxide102
immunosuppressives can all inhibit a positive patch response.
Carba mix102 Also, the patient may need photo-patch testing if photo-allergic
Cinnamic alcohol102 CD is suspected.
Cocamidopropyl betaine95 Summary Statement 23: Determine the relevance of a PT
Fragrance mix95 result based on the clinical and exposure history when
Imidazolidinyl urea102 interpreting the PT. [Strength of Recommendation: Moder-
Thiuram mix102 ate; D Evidence]
Wool alcohols102 The clinical relevance of positive PT reactions to ACD can only
Allergens associated with reaction on day 5, resolved day 7
be established by carefully correlating the history, which includes
exposure to the allergen, with the PT test results. A positive PT
Fragrance mix101 may be clinically relevant depending on current or past exposures.
Methyl dibromo glutaronitrile phenoxy ethanol101 Current relevance is dened as denite if the PT or use test with
Octyl gallate101 the suspected material is positive; probable if the antigen is present
Balsam of Peru101 in known skin contactants and the clinical presentation is
Benzalkonium chloride101 consistent with that exposure; or possible if skin contact with
Benzoic acid101 materials known to contain the allergen was likely. Past relevance
Disperse blue #124101 is considered if the PT is positive but the exposure was in the past,
and not the present.109,110
Allergens associated with late peak reactions (days 6-7)
Summary Statement 24: Consult physicians with expertise
Dyes in patch testing to household cleaning or industrial products
Para-phenylenediamine95,102 if testing to the actual product suspected of containing the
Medications relevant allergen(s) is necessary, because false-positive and
Neomycin95,101,102 severe irritant reactions can occur. [Strength of Recommen-
Caine mix95 dation: Moderate; C Evidence]
Topical corticosteroids Household and industrial products should only be tested by
Tixocortol-21-pivalate95 physicians with expertise on this type of testing after determination
Budesonide95,101 of safety from MSDS information and using nonirritating PT
Metals based on an authoritative text.111 Some of these chemicals can be
Nickel sulfate95,101 extremely toxic to the skin and on rare occasions even produce
Gold sodium thiosulfate101 systemic effects. The PT concentration of these products must be
Palladium chloride101 based on established protocols when available. Nonirritant con-
Potassium dichromate95
centrations are established by testing groups of unaffected volun-
Cobalt chloride95
teer control subjects. Whenever possible, customized contactants
should be incorporated into a petrolatum base, but in some in-
Preservatives and glues
stances, a different vehicle should be used to increase exposure to
Dodecyl gallate101
the relevant antigen.112,113 It may be difcult to distinguish an
p-Tert-butyl phenol formaldehyde resin95,102
irritant from an allergic reaction. Examples of direct PT to prod-
Methylchloroisothiazolinone95
ucts at nonirritating concentrations found in Patch Testing 3rd
Epoxy resin95 Ed.,112 are bath products 1% aqua, shampoo 5% aqua, synthetic
Ethylenediamine dihydrochloride102 detergents 2% aqua, soap 1% or 2% aqua, and glues 1% to 20%
Mercapto mix95,102 in aqua, acetone, alcohol, or petrolatum. Antiperspirant, eau de
Thimerosol95,101,102 cologne, cosmetics that are leave on, and insect spray may be PT
without dilution. Agents that should not be patch tested include
benzene, toluene, and other solvents, such as gasoline, kerosene,
responsiveness because of prior ultraviolet light exposure (ie, lime, oor wax and polish, diesel oil, rust removers, and others.
sun, tanning bed); concomitant immunosuppressive thera- Furthermore, unknown substances should not be tested.
pies; or methodological testing errors such as insufcient Summary Statement 25: Consult physicians with expertise
occlusion, failure to perform delayed readings, and failure to in UV radiation and photo-patch testing to conrm a sus-
perform a photo PT. [Strength of Recommendation: Mod- pected diagnosis of photo-allergic CD. [Strength of Recom-
erate; C Evidence] mendation: Strong; C Evidence]
The strength of the reaction on the skin does not necessarily Photo-patch testing should be done in clinical settings with the
correlate with clinical relevance. For example, aminoglycosides expertise, materials, and equipment to perform the procedure. In
may cause weak reactions on PT that are nonetheless clinically brief, duplicate applications of the suspected photo-sensitizer(s) are
relevant.107 The frequency of false-negative results is not known, placed on either side of the upper back, and occluded for 24 to 48
but has been estimated to occur in up to 30% of patch-tested hours. A recent study suggests that 2 days of occlusion before
patients.108 Potential causes of false-negative reactions include irradiation of allergens is more sensitive at detecting photo-
too low a concentration of the allergen in the extract, use of the allergy.114 After PT removal, one side of the back is then irradiated
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S17
VOLUME 3, NUMBER 3S

with 5 J cm2 of UVA and the other side is left open but un- Patients with AD presenting in a pattern of airborne exposure
treated as the control. Both irradiated and unirradiated sides are (ie, present on face, hands, and exposed chest) may be triggered
then measured 48 hours after irradiation for a response. If the by airborne protein allergens such as grass pollen, house dust
patient has persistent photosensitivity, the minimum erythema mite, and cat dander. Although currently not standardized, this
dose (MED) must be determined rst and reduced to 1/2 of the can be diagnosed by the atopy patch test (APT), involving the
MED for the photo-patch test. Readings are recorded pre- application of intact protein allergens by PT and reading the site
irradiation, immediately postirradiation, and 48 hours post- after 24 to 72 hours. An APT reaction correlates frequently with
irradiation. Additional readings have been recommended.115 the skin prick test and serum IgE, but not always.123,124
Summary Statement 26: Although in vitro tests for delayed For some plants, both plant parts and pollen may contain the
hypersensitivity to contact allergens (ie, metals and bone same allergen, and have been reported to cause airborne CD.
cement) are available, routine use of such assays is not These include the weed Parthenium hysterophorus L. (a member
currently recommended as their sensitivity and specicity for of the Compositae family) in India and Australia,125,126 Japanese
diagnosing ACD has not been determined and should be cedar pollen conrmed by a positive scratch-patch test,127 and
considered investigational. [Strength of Recommendation: Ambrosia deltoidea, or triangle-leaf bursage, conrmed by PT
Moderate; C Evidence] with an oleoresinous extract of A. deltoidea leaves.128
In vitro tests for assessing antigen-specic sensitization are Mulberry pollen129 and Compositae pollen from dandelions,
based on measuring lymphocyte proliferation (LPTs) or cytokine blazing star, golden rod, yarrow, Aster ssp, chrysanthemums, or
production (ELISA or EliSPOT) after incubation with antigens. marguerite130 are reported to cause airborne CU that can be
Some in vitro tests have been validated by patch testing to conrmed by prick skin testing.
nickel,116,117 chromium,118 cobalt,119 and beryllium.120 Several Summary Statement 29: The clinician should consider
other in vitro tests are available, including the MELISA (Memory cosmetics and personal hygiene products that are directly
Lymphocyte Immuno Stimulation Assay), and LPTs from Or- applied to involved skin or ectopically transferred from un-
thopedic Analysis, but have not been validated against patch involved skin as potential sources of allergens in patients with
testing. The clinical relevance of in vitro testing in the diagnosis ACD. [Strength of Recommendation: Strong; C Evidence]
of contact dermatitis has not been established and is still The US Food and Drug Administration (FDA) denes
considered investigational. cosmetic as articles intended to be rubbed, poured, sprinkled,
Summary Statement 27: Use the ROAT to further evaluate or sprayed on, introduced into, or otherwise applied to the hu-
a patient suspected of ACD who exhibits doubtful or negative man body or any part thereof for cleansing, beautifying, pro-
PT responses, to conrm that the patient is reacting to that moting attractiveness, or altering the appearance, and articles
particular product or to determine clinical tolerability to new intended for use as a component of any such articles except soap
cosmetic products. [Strength of Recommendation: Moderate; (US FDA. The Federal Food, Drug, and Cosmetic Act, Sec. 201
C Evidence] [21 U.S.C. 321]; Chapter II, Denitions 1: www.fda.gov). Thus
Several open PT techniques have been used to test substances according to this broad denition, it is not unusual for in-
with the potential for irritation, and are especially suitable for dividuals to apply dozens of personal hygiene products to their
cosmetics and other personal care products such as make-up and skin on a daily basis including a plethora of cosmetics, each with
skin lotions. The ROAT involves the repeated application of a a unique formulation of synthetic or natural ingredients. Such
suspected allergen to the antecubital fossa twice daily for up to 1 products can include emollients for day and night use, hair care
to 2 weeks, and observing for the development of dermatitis. To products (shampoos, conditioners, pomade, relaxers, sprays, gels,
replicate the reactivity of the eyelid skin, the ROAT can also be mousses, foams), nail products (acrylic nails, polishes, hardeners,
performed on the back of the ear. Another provocative open use repair agents, extenders, wraps), traditional cosmetics (eye liners,
test involves the application of the product to the skin of the mascara, eye shadow, foundation, lipstick, lip liners), concealers,
forearm, which is then left untouched and observed for 5 to 10 shave creams and gels, antiperspirants and deodorants, tooth-
days for a reaction. A comparison of the ROAT with the PT for pastes, dentifrices, hand creams, and barrier creams.
nickel demonstrated that although the threshold concentration Although ACD caused by cosmetics is noted predominantly at
for a positive reaction for the ROAT per application was the site of application, occasionally personal care products and
signicantly lower than the threshold concentration for a positive cosmetics will manifest the contact allergy lesions in locations
PT, the accumulated ROAT dose was very similar to the PT.121 distant from the original skin sites. This phenomenon is termed
A usage test involves the daily direct application, under real world ectopic CD. Typical causes of ectopic ACD are allergens such as
conditions, of an undiluted product highly suspected of con- nickel transferred to the eyelid by ngers, toluene sulfonamide
taining a sensitizer, to prove causation. An example is for a pa- formaldehyde resin in nail polish (which may cause eyelid derma-
tient to apply mascara to one set of eyelashes and to leave the titis yet spare the periungual skin and distal ngers), and gold131
other eye bare, to observe for dermatitis. This is often used when (where dermatitis is reported in women who wear facial cosmetics
PT with suspected commercial allergens is negative but the that contain titanium dioxide that may adsorb or abrade the gold
suspicion of contact allergy is high.122 released from jewelry and make occasional contact with facial
skin).132 In addition, patients allergic to hair products that contain
Sources of exposure to clinically relevant allergens CAPB, a surfactant in shampoo, can present with eyelid dermatitis
Summary Statement 28: Evaluate patients who present without concurrent dermatitis on the scalp, neck, or ears.
with recurrent dermatitis on exposed skin surfaces during Consideration must also be given to dermatitis where the allergen is
airborne pollen seasons for contact sensitization to seasonal transferred between partners, parent or child.
pollen allergens. [Strength of Recommendation: Moderate; C Summary Statement 30: When evaluating ACD from
Evidence] cosmetics and personal care products that contain many
S18 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

different chemical ingredients, consider that the most com- positive reactions), and a positive PT to individual ingredients
mon causes are due to a few important chemical classes adds signicantly to the probability of a relevant test.
including fragrances, preservatives, excipients, nickel, and Current labeling laws do not always require manufacturers to
sun screening agents. [Strength of Recommendation: Mod- label a specic fragrance present in a product and regulation of
erate; C Evidence] fragrance ingredients in cosmetics exempts fragrance formulas as
In aggregate, the number of chemical contactants used by an trade secrets. Therefore, some manufacturers do not list essential
individual patient in a typical day can be more than 100. Despite oils that can also cause ACD such as tea tree oil (Melaleuca
this extensive use, typical contact allergens contained in these alternifolia), ylang-ylang oil (Cananga odorata), jasmine ower oil
products tend to be clustered in a few important classes, including (Jasminum ofcinale), peppermint oil (Mentha piperita), lavender
fragrances, preservatives, formulation excipients, nickel, and sun oil (Lavandula angustifolia), and citrus oil (limonene). Covert
blocks. The 15 most frequently positive allergens of the NACD fragrances that may be used for purposes other than for aroma, ie
2009-2010 PT were nickel sulfate (15.5%), neomycin (8.7%), preservatives, may be added to fragrance free products (benzal-
FM I (8.5%), bacitracin (8.3%), BOP (7.2%), cobalt chloride dehyde, benzyl alcohol, bisabolol, citrus oil, unspecied essential
(8.2%), formaldehyde (5.8%), quaternium-15 (5.8%), PPD oils) and may be problematic. In addition, new fragrance chem-
(5.5%), FM II (4.7%), carba mix (4.6%), iodopropynyl butyl- icals are constantly introduced. Use testing and slow reintro-
carbamate (4.3%), methyldibromo glutaronitrile/phenoxyethanol duction of some fragrance products may allow for the detection of
(3.8%), propylene glycol (3.2%), and thiuram mix (3.1%).26 intolerance to specic cosmetic agents. It may be possible to
Fragrances are complex substances that contain hundreds of identify the presence of specic fragrance ingredients by
different chemicals and are the most common cause of ACD communicating directly with product manufacturers.
from cosmetic in the United States. Fragrances are regularly Preservatives and antibacterials are present in most aqueous-
present in cosmetics and personal care products, household based cosmetics and personal hygiene products to prevent
products, and medicaments, either to achieve an appealing scent rancidity and microbial contamination. These preservatives are
or to mask unpleasant odors. However, the labeling of products important cosmetic allergens. Preservatives tend to be grouped
with regard to fragrance can be confusing.133-137 The use of the into 2 broad categories: formaldehyde releasers (products that
term unscented can erroneously suggest that a product does not emit formaldehyde) and nonformaldehyde releasers.145-148
contain fragrance when, in fact, a masking fragrance is present. Table III is a list of preservative systems commonly used in
Fragrance-free products are typically free of classic fragrance in- cosmetic and personal care products.
gredients and are generally acceptable for the allergic patient. In the United States, approximately 20% of cosmetics and
Caution should be exercised when substitute products, which are personal care products (stay-on and rinse-off products) contain a
labeled fragrance free, contain large numbers of botanical extracts formaldehyde releaser.149 The most recent data from the FDA
used for the purpose of improving odor characteristics.138 Allergy Voluntary Cosmetic Registration Program Database150 approxi-
to fragrances can be detected clinically when obvious contact sites mate that 1 in 6 stay-on cosmetics and 1 in 4 rinse-off products
of perfume are involved. Clear demarcation of eczematous contain a formaldehyde releaser, the most frequent of which is
dermatitis on the neck where perfume is sprayed may be an imidazolidinyl urea (7%), followed by DMDM hydantoin
obvious indication of fragrance allergy. (5.4%), diazolidinyl urea (4.5%), and quaternium-15 (1.4%).
It is necessary to PT to appropriate screening chemicals for De Groot et al149 recommend that patients allergic to form-
detection of delayed hypersensitivity to this group of aller- aldehyde be advised to avoid stay-on cosmetics preserved with
gens.139-143 The fragrance antigens in the current T.R.U.E. quaternium-15, diazolidinyl urea, DMDM hydantoin, or imi-
Test include BOP (a fragrant resinous natural product con- dazolidinyl urea. Provocation tests may also be performed to
taining a mixture of many substances), and FM I (cinnamyl determine relevance to this particular patient.
alcohol, cinnamaldehyde, a-amyl cinnamaldehyde [amyl cin- Among nonformaldehyde releaser preservatives, methlydi-
namal], hydroxycitronellal, geraniol, isoeugenol, eugenol, oak bromo gluteronitrile (also known as 1,2-dibromo-2,4-dicyano-
moss). Although there is a strong association between these butane and is the sensitizing ingredient in Euxyl K 400) has
fragrances, separated PT may still be warranted to identify the emerged as an important cosmetic allergen in recent years.151 In
specic offending fragrance so that not all fragrances need to North America, the prevalence of positive PT reactions to Euxyl
be avoided. K 400 increased from 1.5% between 1992 and 1994 to the
Previous studies suggest that the standard FM and BOP will current rate of 5.5% for 2007 and 2008.109 A total of 11.8% of
detect approximately 60% to 70% of fragrance-allergic in- hand dermatitis cases associated with Euxyl K 400 were occu-
dividuals. The addition of other commonly used fragrance in- pation related and were linked to solvents, oils, lubricants, fuels,
gredients (ylang ylang oil, narcissus oil, and sandalwood oil) may and cosmetics.152 In cosmetics, ACD from Euxyl K 400 or its
increase the yield up to 96%.141 In a recent study of patients components is most commonly reported in hand and face lo-
with eyelid dermatitis, PT to fragrance markers within the tions, hair products, and ultrasonic gels.152
standard series (ie, FM I, FM II, Myroxylon pereirae, and cin- Another nonformaldehyde releaser preservative MCI/MI
namic aldehyde) detected 73.2% of cases of fragrance allergy.144 (trade name: Kathon CG) is commonly used in cosmetics and
The elucidation of fragrance allergy should result in advising an toiletries in the United States. The NACDG data from 2009
avoidance protocol that eliminates all culprit fragranced cos- to201026 show that MCI/MI had a 2.5% frequency of positive
metics and personal hygiene products. However, it should be PT reactions, ranking it the fth most commonly positive pre-
noted that fragrances in PT have marginal irritant potential and servative. The combination of MCI/MI is tested at a 3:1 com-
weak positive reactions may not be regarded as proof of contact bination. Both MCI and MI can cause contact allergy with MCI
sensitization (low specicity of the test). The increased strength as the more potent allergen in this combination.153 However, the
of the test reaction, a positive reaction on retest to FM (repeated use of MI alone as a preservative in personal care and cosmetic
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S19
VOLUME 3, NUMBER 3S

TABLE III. Cosmetic preservatives CAPB is an amphoteric surfactant that is often found in
Formaldehyde releaser Nonformaldehyde releaser shampoos, bath products, eye and facial cleaners, liquid
detergents, surface cleaners, pet care products, and other skin
Formaldehyde Iodopropynyl butylcarbamate
and hair care products, and the incidence of sensitization is
Quaternium-15 Methychloroisothiazolinone/
increasing. Although it is less irritating than the older polar
methylisothiazolinone (MCI/MI)
surfactants such as sodium lauryl sulfate,161,162 it is more
Diazolidinyl urea Parabens
sensitizing. CAPB allergy typically presents as eyelid, facial,
Imidazolidinyl urea Methyldibromo glutaronitrile
scalp, and/or neck dermatitis.163 Consumers were sensitized
Bromonitropropane Chloroxylenol mainly through shampoos (including baby shampoo) and other
DMDM hydantoin Benzalkonium chloride toiletry products that include liquid shower gels, roll-on
Thimerosal deodorants, and facial cleansers.
Phenoxyethanol According to the NACDG data for 2007-2008, 1.1% of pa-
tients tested had a positive reaction to CAPB109 and positive PT
reactions to this allergen are often clinically relevant.
products has increased in the past few years. According to the US Commercial bulk production of CAPB may result in
Food and Drug Administration Voluntary Cosmetic Ingredient contamination of the nal product with 2 chemicals that are used
Registration Program, MI was used in a total of 1125 cosmetic in the synthesis of CAPB, such as amidoamine and
products in the United States in 2007.154 Of these, the majority dimethylaminopropylamine.163
are in rinse-off products: 24% were shampoos, 18% were con- Paraphenylenediamine is the active ingredient in many hair
ditioners, and 10% were baby soaps and detergents. Wet wipes dyes, both permanent and semipermanent, and is a very com-
(baby wipes, moist towelettes, and moist toilet paper) are a well- mon cause of CD in hairdressers. Although hair dye is the main
identied sensitization source for MI.155 source of exposure,164 other routes of exposure include body
The MCI/MI mix misses approximately 40% of allergy to MI painting and temporary tattooing. ACD from PPD can be severe,
likely because of the low concentration of MI in the MCI/MI sometimes mimicking angioedema. The skin sensitivity test
combination in the PT. In Europe, several groups have docu- recommended in the package insert of hair dyes has been vali-
mented frequency of allergy to this preservative of approximately dated as an effective method to predict a type IV hypersensitivity
1.5%.156 Patch testing to MI alone will likely diagnose more reaction and should be used by hairdressers.165 Nevertheless, PT
cases of MI contact allergy. may be needed to identify the active allergen in the consumer
Although parabens formulated in cosmetics are infrequent product.
causes of ACD, they can induce ACD when used as antibacterials It is difcult to nd alternative hair dyes for PPD-allergic
in topical medications. ACD has most commonly been reported individuals. Alternatives include henna (giving a reddish tint
when paraben-containing products are used on damaged skin for any hair color), lead oxide (which oxidizes to darken gray
such as in long-standing dermatitis and stasis ulcers. The rate of hair but has not been adequately evaluated for its toxicity),
sensitization to parabens in patients with chronic leg ulcers is and temporary coloring agents (which only last for a few
higher than that of the general population.157 washes). Semipermanent hair dyes containing F, D & C and
Botanicals are plant extracts that are increasingly used as D & C dyes appear to have very low cross-reactivity with
additives to skin care products either for their medicinal prop- PPD (examples: Elumen Hair Color from Goldwell Cos-
erties or as fragrances (such as essential oils). Unfortunately, in metics, Linthicum Heights, MD, and Clairol Basic Instincts-
cosmetics, product labeling may not list essential oils as fra- Loving Care from the Proctor & Gamble Company,
grances. These natural botanicals, plant extracts, and herbal Cincinnati, Ohio). However, semipermanent dyes may not
remedies are potential causes of CD. One study showed a be as cosmetically elegant and require more frequent appli-
sensitivity rate of 2.4% to testing with pure tea tree oil.158 Other cation. Scheman et al reported that PPD-sensitive individuals
studies showed that 1.2% to 6.6% of patients patch tested for who test negative to para-toluenediamine sulfate (PTDS)
dermatitis are sensitive to propolis,159 which is commonly used will very likely tolerate the newer permanent and demi-
in cosmetic and medicinal preparations because of its antiseptic, permanent PPD-free hair-dye products.166 However, this
anti-inammatory, and anesthetic properties. Propolis is found in study suggests that patients be tested for PTDS before using
many all natural products, including lip balms, cosmetics, lo- PPD contacting dyes. Examples of PPD-free hair dyes
tions and ointments, shampoos, conditioners, and toothpastes. include Wella Koleston Perfect (permanent), Wella Color
Synonyms for propolis include bee glue, bee bread, hive doss, Charm (demi-permanent), Schwarzkopf Igora Royal (per-
propolis balsam, propolis resin, and propolis wax. manent), Goldwell Color Chic (permanent), Goldwell
Thus, PT should be considered for propolis, tea tree oil, and ReShade for Men (demi-permanent), Sanotint Light (demi-
other essential oils in patients with cosmetic dermatitis. It is permanent), and LOreal Paris Excellence To-Go 10-Min.
important that patients who are allergic to fragrance also be made Crme Colorant (demi-permanent).26,167 Both physicians and
aware of the potential dangers of cosmetics containing plant patients should consult available databases like Contact
extracts and patients should be counseled that natural products Allergen Management Program (CAMP) and Contact Allergen
does not equate with safety.160 Replacement Database (CARD) regularly for updates.
Summary Statement 31: Patients suspected to have allergy Other sources of exposure to PPD include leather, fur, textiles,
to hair products should be evaluated for PT reactions to industrial rubber products, and black henna tattoos.167 Cross-
CAPB, PPD, fragrances, preservatives, and glycerol thio- reactivity with other para-amino compounds, such as benzocaine,
glycolate. [Strength of Recommendation: Moderate; C PABA, sulfa drugs, aminoazobenzene, IPPD, and azo dyes has
Evidence] been reported and may require avoidance.168
S20 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

Glycerol thioglycolate is the active ingredient in permanent more widespread. Allergic and photo-allergic reactions have been
wave solution. ACD to this chemical tends to cause more reported with several chemical sunscreen families.173,174
occupational dermatitis in hair dressers than consumers. Unlike Sunscreens have traditionally been divided into chemical
PPD, thioglycolates may remain allergenic in the hair long after it absorbers (UVB [290-320 nm], UVA II [321-340 nm], and
has been rinsed out. Hence, those individuals who are allergic to UVA I [341-400 nm]) and physical blockers.
it may continue to have skin eruptions weeks after application of Sunscreens are often overlooked as a cause of CD, because
the perm, and hairdressers allergic to it may be unable to cut or other excipients (fragrances, formaldehyde releasers, pre-
shape permanent waved hair.169 servatives, vitamin E, and lanolin alcohol)175 are more
Summary Statement 32: Suspect allergy to nail products frequently implicated. Sunscreen sensitization is much higher in
when the dermatitis presents locally at the distal digit or individuals referred for evaluation of photosensitivity.176 The
ectopically on the eyelids and face. [Strength of Recom- most common cosmetic sunscreen agents used are listed in
mendation: Moderate; C Evidence] Table IV.
Most allergic reactions to nail polish and articial nail
products are to tosylamide/formaldehyde resin105 found in Physical ultraviolet light blockers
nail polish enamel, in addition to nail hardeners and setting Titanium dioxide and zinc oxide are the most common
lacquers. Up to 80% of the reactions appear on the neck, physical UV blockers used today and have not been reported to
face, lips, and eyelids, although unusual locations including cause contact dermatitis or photo-allergy.
the gluteal, perianal, and genital areas have been reported.
Only 27% of reactions were reported in the periungual re- Topical medicinal CD
gion of the hands and feet. Some patients react to the polish Summary Statement 34: If an eruption worsens, rather
when it is still wet, but the majority of patients appear to than improves, after the topical application of certain med-
react to the water-soluble components (including monomers ications, or fails to respond to TCS, patch testing should be
and dimers) of tosylamide/formaldehyde resin found in dry performed to the suspected product and/or ingredients
polish.160 known to be contact sensitizers. [Strength of Recommenda-
As an alternative, some manufacturers may use an alkyl tion: Moderate; C Evidence]
polyester resin and label their products as hypoallergenic. CD may develop after exposure to topical medications,
These products would be suitable alternatives for sensitive including lanolin, para-aminobenzoic acid (in sunscreens),
patients.170 caines (anti-itch preparations), topical antibiotics, topical an-
Articial nails are increasingly used and are available as tihistamines, NSAIDs, and/or TCS.177-182 Neomycin, bacitra-
sculptured nails, photobonded nails, and preformed nails. Re- cin, and iodochlorhydroxyquin are well-known sensitizers.
actions to articial nails have included paronychia, onychody- Lanolin is used as the base of many topical medications including
strophies, and dermatitis at contact areas and at distant sites. TCS and moisturizers.
Acrylate monomers used for sculpting articial nails are impor- Allergy to TCS affects 0.5% to 5.8% of patients183 suspected
tant sensitizers for contact and occupational dermatitis. Pre- of ACD. Sensitization can occur by skin, airborne, oral, and IV
formed plastic nails may be glued over the natural nail plate using routes.184,185 Certain disorders predispose patients to an
ethyl cyanoacrylate, a potential sensitizer. increased risk of CS ACD. These include treatment of refractory
Certain guidelines for testing nail cosmetics are as follows: (1) eczema, chronic venous leg ulcers, stasis dermatitis, and CD (in
Nail polish should be tested as isundiluted. (2) Acrylate allergy particular, patients with a history of 2 or more positive PT results
should be screened with an acrylate test panel, including 2% and multiple medicament sensitivities).
methyl methacrylate, 1% bisphenol A, 2% tetraethylene glycol Patch testing to CS is complicated by the inherent, anti-in-
dimethacrylate, 2% bisphenol A dimethacrylate, 2% ethylene ammatory nature of the drug itself, which results in frequent
glycol dimethacrylate, 2% dimethyl-p-toluidine, and 1% benzoyl false-negative results if tested at too high concentration.
peroxide has been advocated.171 (3) Patch testing for nail polish Accordingly, PT readings should also be done 7-10 days
removers should be an open PT, at a concentration of 10% in following application because approximately 30% of ACD to
olive oil. (4) Cuticle removers are tested as an open PT at a 2% TCS could be missed by conventional readings.186,187
aqueous concentration.172 Patch testing substances for TCS allergy that are commer-
Summary Statement 33: Suspect the diagnosis of photo- cially available include amcinonide, betamethasone-17,21-
allergic CD to cosmetics when eczema occurs in a light- dipropionate, betamethasone-17-valerate, budesonide,
exposed distribution following the use of a skin care product clobetasol-17-propionate, desoximetasone, dexamethasone,
or cosmetic, including sunscreens. [Strength of Recommen- hydrocortisone, hydrocortisone 17-butyrate, prednisolone,
dation: Strong; C Evidence] tixocortol-21-pivalate, and triamcinolone acetonide. The pa-
Some cosmetic ingredients may only cause an ACD after tients own commercial steroid,184 as well as the vehicle and
exposure to UV radiation. Photo-allergic CD typically affects preservatives in the preparations,188,189 must also be tested.
sun-exposed areas such as the face, the V of the anterior neck, Coopman et al190 suggested that 4 major groups of CS prep-
the dorsal hands, and forearms. It typically spares the upper arations should sufce, because there is considerable cross-
eyelids, upper lip, and submental and postauricular areas. Before reactivity within the groups and possible cross-reactivity
evaluation for photo-allergic CD, one should rule out phototoxic between them. Ninety percent of ACD to CS should be
drug eruption, photo-allergic drug eruption, and systemic disease detected by using tixocortol pivalate, budesonide, triamcino-
such as lupus erythematosus. lone, and the patients commercial steroid.191,192 Although
The prevalence of allergic reactions to sunscreens may rare, patients sensitized to CS by skin contact can develop SCD
continue to increase as the use of sunscreen continues to become with administration of the CS by an oral, IV, IM, or inhalation
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S21
VOLUME 3, NUMBER 3S

TABLE IV. The most common cosmetic sunscreen agents Summary Statement 37: In patients with joint replacement
Cinnamates Octyl dimethyl failure, patch testing to components of the implant may be
para-aminobenzoic acid helpful after infection and biomechanical causes have been
Salicylates Benzophenones excluded. [Strength of Recommendation: Moderate; C Evidence]
Titanium dioxide Anthranilates The clinician should recognize that contact sensitization to metals
Butyl methoxydibenzoylmethane Zinc oxide or bone cement that is used in orthopedic, cardiac, dental, and gy-
or avobenzone (Parsol 1789) necological implants has been associated with both dermatitis and
noncutaneous complications. These complications may include
localized pain, swelling, erythema, warmth, implant loosening,
route.193 Cross-reactivity based on 2 immune recognition sites decreased range of motion, stent stenosis, and pericardial effusions in
has been reported,194 and the avoidance of TCS within each the case of cardiac implants. Patch testing to implant or device
class is recommended once allergy to TCS has been conrmed components has been recommended to help determine the etiology
by PT (Appendix J). of the adverse reaction (Tables V and VI).208-210
Summary Statement 35: The clinician may use the drug In a meta-analysis, the rates of sensitization to metals were
PT for the diagnosis of some drug hypersensitivity re- signicantly higher in patients with a failed implant than in pa-
actions, recognizing that there is no standardized approach tients with a well-functioning implant (P .002) or without an
to dene the population, clinical manifestation, drug to implant (P < .001).209 Patients who experienced failed joint re-
PT, and PT materials to make patch testing to drugs a placements and underwent revision using components dictated by
standard of care. [Strength of Recommendation: Weak; D a positive metal PT reported resolution of their joint symptoms,
Evidence] most frequently joint pain, joint loosening, and localized derma-
Patch testing to drugs may have a role in delayed hypersen- titis. Those patients with a positive metal PT who were not revised
sitivity drug reactions177 and have a higher positivity in patients continued to experience the same symptoms.204 Similarly, a group
presenting with maculopapular rashes, erythroderma, and non- of patients with implant-related eczema who were metal sensitized,
immediate cutaneous reactions,195 including DRESS,196 and then underwent revision with a different metal alloy implant,
AGEP,197 SJS/TEN, and xed drug eruptions. The utility of the had a higher incidence of eczema resolution.211 Anecdotal case
PT depends on various factors including the type and formula- reports suggest that skin or systemic manifestations of sensitization
tion of the drug being tested, the vehicle used, as well as the to components of implantable debrillators,212 pacemakers,213
immunopathogenesis eliciting the eruption. arterial stents,214 dentures,215 and IUDs,216 appeared to improve
PT may be helpful with aromatic anticonvulsants and various once the sensitizing agent was replaced.
antibiotics, but it is not consistently helpful for a wide range of At present, the recommendation for implant removal remains
drugs. Patients with a history of drug exanthem from antibiotics controversial. Indeed there are reports of individual patients with
are more likely to have a positive PT (10% to 46%) compared documented metal allergy who have tolerated implants of the
with those with a history of a drug exanthem from nonantibiotic same metal without adverse reactions. An older study reported
medications (w10% to 11%).198-200 that 18 patients with documented metal allergy did well for over
Within antibiotic classes, there are higher rates of positive PT 6 years following a joint replacement that contained the aller-
reactions to aminopenicillins, cephalosporins, pristinamycin, and genic metal.217 Gawkrodger stated in 1993 that there was no
clindamycin compared with macrolides, tetracyclines, and evidence that nickel-sensitive patients, when given a plastic-to-
quinolones.195 stainless-steel hip implant, developed cutaneous reactions or
PT can be performed for a wide variety of medications in loosening of their prostheses,218 although he has since identied
multiple concentrations and vehicles.201 The European Society an association between metal sensitization, peri-implant hyper-
of Contact Dermatitis (ESCD) and the European Network on sensitivity reactions, and implant loosening and failure. The
Drug Allergy (ENDA) have guidelines for performing PT for overall risk, however, was low.219 Other patients with docu-
medication-induced cutaneous eruptions.202,203 However, the mented metal sensitization have tolerated cardiac implants with
limitations of these studies include the lack of standardized test the same metal without adverse reaction.220
materials, the absence of information as to the ideal test con- As in all cases of PT, results must be interpreted within the clinical
centration and vehicle to use, and the differences in the inter- history and physical examination. If an implant is functioning well,
pretation of the tests. then a positive PT to an implant component is not clinically rele-
Summary Statement 36: Consider pre-operative patch vant.210 The likelihood that an allergy to implant components is the
testing for metal sensitization in patients with a signicant cause of implant failure is higher when other causes of implant failure
history of metal allergy. [Strength of Recommendation: (infection and biomechanical issues) have been ruled out. There are
Moderate; C Evidence] no current guidelines or recommendations for symptomatic patients
Indications for pre-operative PT in patients with a history of with positive PT to metals or bone cement components. The de-
metal allergy are still being developed. However, pre-operative cision regarding implant revision following positive relevant PT
PT may help guide the selection of implant alloys in patients results can only be made after a thorough discussion between the
with a high suspicion of metal allergy, and such patients patient, the allergist or dermatologist, and the orthopedic surgeon.
demonstrate improved outcomes.204-207 This testing is not rec- In addition to the possibility of metal sensitization as a po-
ommended for patients without such a history of metal sensi- tential therapeutic cause of joint replacement failure, there are
tivity. There is no information regarding pre-operative PT in also reports of implant failure related to bone cement or its
patients with a prior history of methacrylate or antibiotic components, including benzoyl peroxide, hydroquinone, methyl
sensitivity. methacrylate, and n,n-dimethyl para-toluidine.221-223
S22 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

TABLE V. Components of selected alloys used in metal implants

316L Stainless Cobalt-chromium-molybdenum Vitallium Titanium Nitinol Oxinium
Alloy Steel w% content steel (ASTM F75) w% content w% content w% content w% content w% content

Nickel 8.3-35 <0.5 Trace 45 None

Chromium 20 27-30
Manganese 2 <1 0.5
Molybdenum 2-3 5-7 5.6
Nitrogen 0.1 <0.25
Carbon 0.003 <0.35 0.02
Sulfur 0.03 <0.01
Silicon 0.75 <1 0.5
Phosphorus 0.045 <0.02
Iron Balance <0.75 None
Tungsten <0.2
Aluminum <0.1 5.5-6.5
Titanium <0.1 89.9 55
Boron <0.01 0.1
Cobalt Balance 61
Chromium 32
Vanadium 3.5-4.5
Zirconium (oxidized) 97.5
Niobium 2.5

Special population The NACDG compared results of PT in children and adults

ACD in children. Summary Statement 38: ACD and ICD and found no signicant difference in the overall frequency of at
are signicant clinical problems in children. Patch testing least one relevant positive PT reaction in children (51.2%)
should be performed and remains the gold standard for the compared with adults (54.1%).34 Additionally, there are highly
diagnosis of ACD in children. [Strength of Recommendation: relevant allergens that have signicant frequency in children
Strong; C Evidence] because of their unique exposure such as MCI/MI, a preservative
Although ACD was historically considered to occur less in infant wet wipes, liquid soaps, and shampoos. Also, exposures
frequently in children, recent studies show that positive PT re- to dialkyl thiourea and p-tert-butyl formaldehyde resin in rubber
actions range from 14% to 70% of children patch tested.224 products are seen in shin guards, wet suits, and protective pads.
ACD is considered rare in the rst few months of life with A US-based study showed nickel, fragrance, cobalt, thimer-
increased reports suggesting an early peak around age 3, and an osal, BOP, potassium dichromate, neomycin, lanolin, thiuram
increasing rate of occurrence through the teen years, attaining mix, and PPD to be common allergens in children.77 Eight of
and even exceeding that observed in adults.225-227 these are also in the top 10 allergens in adults suggesting that the
In children, a careful, age-appropriate history should include sensitization prole for children does not differ signicantly from
exposure to diapers, hygiene products, cosmetics, sun blocks, that of adults. An allergen found in higher frequency in children
textiles with dyes and re retardant materials, medications, pets than in adults is lanolin/wool alcohols that can be found in
and pet products, school projects, sports, and so on. The inu- healing ointments, aftershave, baby and bath oil, hand sanitizers,
ence of fashion trends, hobbies, and lifestyle activity such as body and creams, reecting the frequency of use of the products
piercing, decorative skin paintings (eg, PPD-laced black henna containing this contactant. Thimerosal positive PT has been
tattoos), natural remedies, and cosmetics (eg, tea tree oil), or reported in both adults and children, with the main source of
products with fragrances and herbal ingredients have all been sensitization likely due to previous vaccination and may not be a
associated with ACD in this population. clinically relevant allergen. There are additional highly relevant
Perioral dermatitis in children is associated with lip licking, lip allergens in children that correlate with unique exposures such as
chewing, thumb sucking, or excessive drooling. Metals including (1) MCI/MI, a preservative found in infant products (wet wipes,
mercury, chromate, nickel, gold, cobalt, beryllium, and palladium liquid soaps, shampoos); (2) CAPB, a surfactant in cleansing
are important allergens in patients with dental implants, ortho- products (eg, No More Tears formulations); (3) disperse dyes in
dontic devices, or who play an instrument. ICD is the most diaper material and colored garments (school and athletic uni-
common cause of diaper dermatitis in infancy because of friction, forms); (4) carbamates and thiuram used in rubber (gloves,
occlusion, maceration, and increased exposure to water, moisture, garments, shoes, and toys); (5) dialkyl thioureas; and (6) p-tert-
urine, and feces. Allergic CD to rubber chemicals (mercapto- butyl formaldehyde resin found in rubber and neoprene (shin
benzothiazole, cyclohexyl thiophathalimide) or glues (p-tertiary- guards, protective pads, and wetsuits).
butylphenol-formaldehyde resin) has been reported to cause The same test concentrations used in adults can be used in
CD,228 a dermatitis that is predominantly on the outer buttocks children.229 However, it has been suggested that in very young
and on the hips in toddlers. This is frequently caused by the elastic children (<6 years of age), allergens such as formaldehyde,
bands that hold tightly on the thighs to prevent leaking. formaldehyde releasing preservatives, mercaptobenzothiazole, and
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S23
VOLUME 3, NUMBER 3S

TABLE VI. Substances that may be present in different types of implant or device and that potentially should be considered for diagnostic
patch testing
Implant or device
Orthopedic
Substances or alloy3 Dental Pre-implant Post-implant Intravascular Pacemaker and ICD Gynecological

Aluminum X X X - X -
Beryllium X - - - - -
Cadmium X - - - - -
Chromium X X X X X X
Cobalt X X X X X -
Copper X - - - - X
Gold X - - X - -
Indium X - - - - -
Iridium - - - - X X
Iron X X X X - -
Manganese X X X X - X
Mercury X - - - X -
Molybdenum X X X X X -
Nickel X X X X X X
Niobium X X X - - -
Palladium X - - - - -
Phosphorus X X X - - -
Platinum X - - - X X
Rhodium X - - - - -
Ruthenium X - - - - -
Silicon - X X - - -
Silver - - - - X X
Tantalum - X X - X -
Tin X - - - - X
Titanium X X X X X X
Tungsten - X - X - -
Vanadium X X X - X -
Zinc X - - - - X
Zirconium X X X - - -
Custom-made disk of relevant alloy X X X X X -
ICD, irritant contact dermatitis.
Used with permission from Contact Dermatitis 2011;66:4-19.

thiuram be diluted 50%, and potassium dichromate diluted 25% for if there is a relevant exposure history, for example, black
in petrolatum, to avoid irritant false-positive reactions.230,231 rubber mix, dialkyl thioureas, mercaptobenzothiazole, PPD, and
The German Contact Dermatitis Group (GCDG)232 rec- p-tert-butylphenol formaldehyde resin. In conclusion, PT can
ommends that children under 6 years should only be PT if there and should be performed in children and remains the gold
is a high degree of clinical suspicion and only to the suspected standard for the diagnosis of ACD with appropriate parental
allergens. Children over the age of 12 can be tested in the same informed consent.
manner as adults.
The ideal number of PT to be applied depends on the patient Occupational contact dermatitis. Summary Statement
and could be limited by the surface available for testing and the 39: In a patient who presents with dermatitis associated with
potential risk of active sensitization. Thus, Jacob et al.233 workplace exposures (ie, OCD), consider ICD as well as
recommend a basic North American Standard Series for children ACD. [Strength of Recommendation: Strong; C Evidence]
aged 6-12 years to include 20 selected allergens that are the most Contact dermatitis is one of the most common types of
prevalent in the pediatric population with the highest clinical occupational illness, with estimated annual costs exceeding $1
relevance and therefore would be the highest yield as a basic billion (http://www.cdc.gov/niosh/topics/skin). An occupational
series. These are bacitracin, budesonide, carba mix, cobalt health supplement (OHS) to the 2010 National Health Inter-
chloride, cocamidopropyl betaine, colophonium, Compositae view Survey (NHIS) noted that 10%, or approximately 15.2
mix/dandelion extract, disperse blue, ethylenediamine, formal- million US current or recent workers reported the presence of
dehyde, FM I, FM II, lanolin alcohol, MCI/MI, BOP, neomycin dermatitis. There was a higher prevalence rate in women (11.2%;
sulfate, nickel sulfate, potassium dichromate, quaternium-15, 95% CI 10.4-12.0) than in men (8.5%; 95% CI 7.8-9.3). The
and tixocortol-21-pivalate. Additional allergens can also be tested estimate of work-related dermatitis was 7.4% or 1.12 million.234
S24 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

Occupational CD is classically divided into ICD and ACD. In food processing workers with OCD, the prevailing factors
Although the mechanisms differ between the two, the clinical are exposure to food ingredients, even intact proteins, and hand
and histologic appearance may be similar. washing. A review of NACDG results for hairdressers and
Irritant CD represents approximately 80% of all cases of cosmetologists demonstrated that glyceryl thioglycolate in
OCD. Common irritant exposures include wet work, solvents permanent wave solutions, PPD in hair dyes, nickel sulfate, 2-
and alcohols, cutting oils, coolants, degreasers, soaps, detergents, hydroxyethyl methacrylate, and quaternium-15 are common
and other cleaning agents and disinfectants. The major chemical sources of allergens.239
groups associated with ACD include metals, rubber-related ma- Among health professionals, hand dermatitis may be due to
terials, epoxies, resins and acrylics, organic dyes, plants, foods, ICD, ACD, and IgE-mediated CU. With the advent of increased
medications, biocides, and germicides.235 barrier control recommended for health professionals, the rapidly
A workers skin may be exposed through direct contact with increased need for latex gloves resulted in a spike in the prevalence
contaminated surfaces, deposition of aerosols or vapors, skin im- of both immune-mediated and irritant skin reactions. IgE-medi-
mersion, or splashes. The hands are most commonly affected by ated responses include CU, rhinitis, asthma, and/or anaphylaxis,
OCD and followed by the wrists, arms, and face. OCD can present and sensitization can be conrmed by specic prick or in vitro tests.
at any stage in a workers career, including apprenticeship.236 The Health care workers may also develop ACD to rubber accelerants
common agents that cause ICD and ACD in OCD as reported by and other chemicals in gloves, which include bisphenol A in vinyl
the NACDG in the United States include carba mix, cobalt chlo- gloves. In one study of 3448 patients (1058 health care workers)
ride, epoxy resin, formaldehyde, glutaraldehyde, glyceryl thio- with occupational dermatitis due to suspected glove allergy, 13%
glycolate, mercaptobenzothiazole, nickel sulfate, potassium were sensitized to thiurams, 3.5% to dithiocarbamates, 3% to
dichromate, quaternium-15, and thiuram. In addition, The Health mercaptobenzothiazole and/or its derivatives, 0.4% to thioureas,
and Occupation Reporting System, the European Prevention and 3% to 1,3-diphenylguanidine.240 Patch testing to rubber
Initiative for Dermatological Malignancies, and the Occupational chemical mix or the suspected article itself is appropriate.
Physicians Reporting Activity in the UK reported chromes and/or In 132 farmers with OCD, metals, disinfectants, rubber, and
chromates, foods, latex, rubber chemicals, PPD, preservatives, pesticides were the most important allergens. Less commonly,
resins and acrylics, soaps and cleansers, wet work, cutting oils and they reacted to colophony, lanolin, and propolis (especially bee
coolants, petroleum products, solvents, and alcohols. keepers). Contact dermatitis lesions in farmers are frequently
Summary Statement 40: In patients with suspected occu- aggravated by irritant chemicals in fertilizers and pesticides.
pation-related CD, the examining physician should verify the A survey of Danish cleaners and/or housekeepers who had
diagnosis by conrming that the dermatitis was caused or OCD showed signicantly increased rates of sensitization to
aggravated by workplace exposures. [Strength of Recom- formaldehyde and rubber additives such as thiurams, zinc
mendation: Moderate; C Evidence] diethyldithiocarbamate and mercaptobenzothiazole compared
Accepted and validated criteria should be used to establish with controls.241
causation and aggravation of OCD. Mathias237 proposed 7 In the military, common causes of ACD include exposure to
criteria as a practical guideline for conrming this diagnosis: (1) plants and insects, formaldehyde resins, disperse dyes, and chro-
the clinical appearance that is consistent with CD; (2) potential mate-containing dyes in uniforms, methylchloroisothiazolinone/
culprit cutaneous irritants and/or allergens are present in the methylisothiazolinone in coolants and cutting oils, metal allergy to
workplace; (3) the anatomic distribution of dermatitis is embedded shrapnel, and phenoxyethanol, formaldehyde,
consistent with workplace skin exposure; (4) the temporal rela- neomycin, aluminum, and thimerosal in vaccines.242
tionship between exposure and onset of symptoms is consistent Summary Statement 41: Consider botanical-related ACD
with CD; (5) nonoccupational exposures are excluded as prob- in outdoor workers, or others exposed to plants, including
able causes of the dermatitis; (6) the dermatitis improves when orists, gardeners, landscapers, maintenance workers, and
absent from work exposure, and re-exposure results in exacer- park and wildlife ofcials. [Strength of Recommendation:
bation; and (7) PT performed according to established guidelines Moderate; C Evidence]
demonstrates positive and relevant reactions.237 Of these 7 The most common causes of plant dermatitis in outdoor
criteria, 4 must be present to conclude that the dermatitis is workers are plants within the genus Toxicodendron, still identied
OCD. The validity of the Mathias criteria for establishing as Rhus in the dermatological literature. These include poison
occupational causation and aggravation of CD was recently ivy, poison oak, and poison sumac. The allergenic substance,
conrmed in a 2- to 5-year prospective study.238 urushiol, derives its name from the Japanese word for the sap
Industries and jobs that pose a high risk for development of found in the Japanese lacquer tree. It contains a mixture of
OCD are as follows: catechols (1,2-dihydroxybenzenes) and resorcinols (1,3-dihy-
droxybenzenes). Urushiol avidly binds to skin, but it is readily
1. Food service and food processing (cooks and caterers) degraded in the presence of water. Therefore, soak exposed skin
2. Cosmetology (beauticians and hairdressers) with cool water as soon as contact is suspected. Interestingly, the
3. Health care (personnel) nonleaf portions of the plant can also induce dermatitis, even in
4. Agriculture, forestry, and shing the winter (http://telemedicine.org/botanica/bot6.htm). The
5. Cleaning diagnosis is made on the basis of the history. Patch testing to
6. Painting Toxicodendron is generally not recommended because it can
7. Mechanics, metal working, and vehicle assembly cause sensitization in an otherwise nonsensitized person and also
8. Electronics industry large bullous reactions.
9. Printing and/or lithography Alstroemeria (Peruvian lily) is the most frequent cause of hand
10. Construction. dermatitis in oral workers. Lily and tulip sensitivity is caused by
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S25
VOLUME 3, NUMBER 3S

sensitivity to alpha-methylene-gamma-butyrolactone or tulipalin some patients. On occasion, partnering with an occupational

A, which is derived from the glycoside tuliposide A. The aller- health professional may help with patient management.
genic chemical is found in several of the lily orae, including Summary Statement 43: In addition to avoidance of
Alstroemeria (Peruvian or Inca lily), Bomarea (restios or grasses exposure, the physician should prescribe appropriate adjunct
from South Africa), Erythronium (dog tooth violet, trout lily, medical treatment. [Strength of recommendation: Strong; B
adders tongue), and Tulipa. It is present in less amount in Evidence]
Dioscorea hispida (water yam), Fritillaria (snakes head, chess A number of professional organizations provide guidelines and
ower, frog-cup, guinea-hen ower, checkered lily), and Gagea consensus statements related to medical treatment. Several recent
(Yellow Star-of-Bethlehem), and in at least one species of onion, reviews provide guidelines for the medical management of hand
Allium triquetrum. The allergen is present in both the ower and dermatitis.255,256 Key components of medical management
the bulb. Because the allergen penetrates latex and vinyl gloves, include TCS with second line therapies including phototherapy,
nitrile protective gloves should be used by allergic individuals oral retinoids, and immunosuppression.
when handling tulips and Alstroemeria.243 Calcium oxalate TCS are widely accepted as the treatment of acute and
crystals in the plant sap may also cause an irritant dermatitis.244 chronic dermatitis.257 The selection of TCS for efcacy, po-
There are few standardized testing extracts available for plant tency, and acceptability is determined by many factors
allergens, although some companies do offer a limited plant series including the severity, the location, and the acuteness of the
that includes alpha-methylene-gamma-butyrolactone and a few dermatitis. TCS may be sufcient for localized lesions, but
other ower allergens. In the absence of commercially available acute extensive and severe dermatitis such as extensive Tox-
extracts, PT may be performed with caution by using small icodendron dermatitis may need systemic therapy. The clinician
amounts of the fresh plant or bulb, as severe bullous reactions should avoid the prolonged use of systemic steroids for man-
may result from their high allergy content.245,246 Because of the agement of chronic dermatitis. Ointments and potent uori-
potential for severe bullous reactions, it is recommended that an nated CS should be avoided on areas of thinner skin such as the
open test without occlusion be done. intertrigenous areas, eyelids and face, and in young children.
The use of TCS over prolonged periods of time should be
avoided and should not be a substitute for dening the etiology
Treatment of contact dermatitis. Summary Statement of the dermatitis. If symptoms worsen, the possibility of contact
42: Once the allergen or irritant has been identied, the sensitization to the CS itself, the vehicle, or other ingredients in
patient should be counseled on avoidance of contact with the the TCS should be considered.258-260
offending agent and informed of any cross-reactivity con- Several topical T-cell selective inhibitors have been used suc-
cerns. [Strength of Recommendation: Strong; B Evidence] cessfully in the treatment of AD, but their efcacy in ACD or
The identication and avoidance of contact with the offend- ICD has not been established. Topical tacrolimus has been
ing agent(s) is the key to successful treatment of ICD and ACD. shown to be effective in the murine model of nickel ACD.261
Recovery is possible if the agent is identied and avoided. However, there are no published randomized, double-blind
For cosmetic products, if PT identies specic allergens, the studies to verify these preliminary results. Pimecrolimus has been
patient should be informed of these allergens and counseled shown to inhibit the elicitation phase but has no demonstrable
regarding avoidance. However, typical allergen names are long, effect on the sensitization phase of ACD in the murine model.
difcult to spell, commonly have numerous complex synonyms, Several preliminary studies suggest that pimecrolimus may be
and are often intimidating for patients making compliance with effective in the treatment of ACD.262,263
allergen avoidance difcult. To improve compliance,247,248 there Other treatments including cyclosporin, azathioprine, and
are currently 2 computer-generated databases available in the psoralen plus UVA have been used for steroid-resistant ACD
United States. These databases list of products that are free of the such as chronic hand dermatitis.255,264-266 The risks and benets
suspected allergens. One database is the CAMP that is available of these treatment options need to be considered; informed
for members of the American Contact Dermatitis Society (www. consent before use is necessary.
contactderm.org) and the other is Mayo Clinics SkinSAFE
Database (www.SkinSAFEapp.com) that is available for physi-
cians for purchase, and patients of enrolled providers. Prevention. Summary Statement 44: To prevent CD, avoid
The dimethyl-glyoxime test (nickel spot test) can be used to exposure to irritants and allergens and use appropriate skin
detect nickel released from metal objects. It has a limit of protection. [Strength of Recommendation: Strong; B Evidence]
detection of 0.13 mcg/cm2.249 The sensitivity of the test has Primary prevention of ICD and ACD involves avoidance of
been estimated at 59%, and a specicity of 97%.250 The cobalt exposure to possible irritants and allergens and appropriate skin
spot test is based on disodium-1-nitroso-2-naphthol-3,6-disul- protection.
fonate251 and may serve to detect dermal exposure.252 There are Avoidance of exposure may be accomplished by several means.
wipe tests that can detect nickel, cobalt, and chromium on the Elimination of an irritant or an allergen from exposure may not
skin.253,254 Detection of these metals can aid in avoidance of always be possible. Nevertheless, removal of chromium from
exposure. cement in Europe is an example of successful elimination.236
If contact with the culprit allergen or irritant continues, the Substitution of a potential allergen with another agent in the
dermatitis may become chronic, more generalized, disabling, and workplace that is less allergenic may be effective.236 Training is
become a problem with continued employment and quality of life. an important component of avoiding exposure in the work-
There is some evidence that the use of conditioning creams may place.236,267 Rotation of job task may also reduce irritant expo-
improve the skin condition. However, even with removal from sure but may not eliminate the risk of sensitization. Examples of
exposure and avoidance of contact, the dermatitis may persist in methods of reducing exposure include using long handled
S26 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

cleaning tools (brush with a handle), vacuuming, or wet from the British reporting system EPIDERM found that 7% had
sweeping. been unemployed and 17% had taken time off work.278
Skin protection remains the primary goal of prevention of A Danish study found similar results with prolonged sick leave
occupational dermatitis. This should include the use of personal reported by 20% of patients.276 A recent study reported work
protective equipment such as gloves, goggles and/or face shields, status at 6 months postdiagnosis found 38% unemployed
uniforms, and equipment to protect the skin from the exposure. because of their skin disease.279 Another Toronto follow-up
The use of cotton liners under gloves can be useful.236 In some studyat least 2 years postdiagnosisfound that 78% were
instances, this may also involve the use of specialized skin creams working, but 57% had changed jobs and 35% had lost time of at
such as barrier creams containing quaternium-18 bentonite least 1 month.280 Two recent studies have also reported on job
(organoclay) to prevent Rhus dermatitis or creams containing change many years after the diagnosis of OCD. Meding et al, in a
chelators such as pentaacetic acid to prevent nickel, chrome, or 12-year follow-up, found that 82% had some change in their
copper dermatitis.268 In general, pre-work creams have not been work, with 44% changing jobs.281 In a Finish follow-up study at
demonstrated to be useful, but skin care to protect the barrier 7-14 years postdiagnosis, 54% had job modications, 34% had
function of the skin is important. This involves the use of changed jobs, 20% were re-trained, and 25% were not work-
moisturizers, particularly lipid-rich moisturizers.236,268 ing.277 Only 8% had no change in their work.
Screening, to detect disease at an early stage when the disease There are a small percentage of individuals with occupational
is still reversible, is used in the occupational setting. Although hand dermatitis who do poorly even with removal from expo-
screening for early detection appears to be feasible, there is little sure. In a recent Australian study,282 18% of those with OCD
information available on its effectiveness. dermatitis had persistent dermatitis.
Given the visual nature of dermatitis, screening for hand
dermatitis seems feasible and has been recommended in the REFERENCES
occupational setting.269 Other than a program in Germany 1. Velykoredko Y, Houle MC, Skotnicki S. Contact dermatitis mimickers: a
tertiary care centers experience. J Cutan Med Surg 2013;17:429-32 (III).
focused on dermatologists270 and several research studies focused 2. Rietschel RL. Clues to an accurate diagnosis of contact dermatitis. Dermatol
on the intervention,271,272 there are no reports of its general use Ther 2004;17:224-30 (IV).
in workplaces with a high risk of OCD. As such, there is no 3. Josefson A, Farm G, Meding B. Validity of self-reported nickel allergy.
evidence of the effectiveness of surveillance programs or partic- Contact Dermatitis 2010;62:289-93 (IIb).
ular methods for screening.236 4. Marks JG, Belsito DV, DeLeo VA, Fowler JF Jr, Fransway AF, Maibach HI,
et al. North American Contact Dermatitis Group patch test results for the
detection of delayed-type hypersensitivity to topical allergens. J Am Acad
Prognosis. Summary Statement 45: Education of the Dermatol 1998;38(Pt 1):911-8 (III).
workers with ACD or ICD should include prognosis and 5. Marks JG Jr, Belsito DV, DeLeo VA, Fowler JF Jr, Fransway AF, Maibach HI,
information that their disease may persist and need long- et al. North American Contact Dermatitis Group patch-test results, 1998 to
2000. Am J Contact Dermat 2003;14:59-62 (III).
term management even after treatment and workplace mod- 6. Pratt MD, Belsito DV, DeLeo VA, Fowler JF Jr, Fransway AF, Maibach HI,
ications. [Strength of Recommendation: Moderate; C et al. North American Contact Dermatitis Group patch-test results, 2001-2002
Evidence] study period. Dermatitis 2004;15:176-83 (III).
In a review of 15 studies reporting prognosis in OCD between 7. Britton JE, Wilkinson SM, English JS, Gawkrodger DJ, Ormerod AD,
Sansom JE, et al. The British standard series of contact dermatitis allergens:
1958 and 2002, the range of complete clearance of the dermatitis
validation in clinical practice and value for clinical governance. Br J Dermatol
was 18% to 72%.273 Two Australian studies from the 1980s 2003;148:259-64 (III).
documented ongoing problems in a signicant proportion of 8. Jain VK, Aggarwal K, Passi S, Gupta S. Role of contact allergens in pom-
affected workers. In one study, 55% had ongoing problems from pholyx. J Dermatol 2004;31:188-93 (III).
between 6 months and 8 years following diagnosis, and the other 9. Zelickson BD, McEvoy MT, Fransway AF. Patch testing in prurigo nodularis.
Contact Dermatitis 1989;20:321-5 (III).
study documented that 29% were unchanged or worse on 10. Clayton TH, Wilkinson SM, Rawcliffe C, Pollock B, Clark SM. Allergic
average of between 1 and 5 years postdiagnosis.274,275 A Toronto contact dermatitis in children: should pattern of dermatitis determine referral?
study that evaluated outcomes at a minimum of 2 years post- A retrospective study of 500 children tested between 1995 and 2004 in one
diagnosis found that 63% were clear of disease, 28% had mild U.K. centre. Br J Dermatol 2006;154:114-7 (III).
11. Bohm I, Brody M, Bauer R. Comparison of personal history with patch test
disease, 15% had moderate disease, and 5% had severe dis-
results in metal allergy. J Dermatol 1997;24:510-3 (III).
ease.108 Seventy-eight percent of the patients noted improve- 12. Zug KA, Rietschel RL, Warshaw EM, Belsito DV, Taylor JS, Maibach HI,
ment, 17% were unchanged, and 5% reported it to be worse et al. The value of patch testing patients with a scattered generalized distri-
than at diagnosis. Two recent studies provide prognostic infor- bution of dermatitis: retrospective cross-sectional analyses of North American
mation in workers with occupational hand dermatitis. A 1-year Contact Dermatitis Group data, 2001 to 2004. J Am Acad Dermatol 2008;59:
426-31 (III).
follow-up study found that 41% had improved, but 25% had 13. Lee TY, Lam TH. Patch testing of 490 patients in Hong Kong. Contact
persistent, aggravated, or severe disease.276 A longer term study Dermatitis 1996;35:23-6 (III).
with a follow-up between 7 and 14 years found that 40% had 14. Usmani N, Wilkinson SM. Allergic skin disease: investigation of both im-
not experienced any dermatitis in the past year.277 Atopic mediate- and delayed-type hypersensitivity is essential. Clin Exp Allergy 2007;
37:1541-6 (III).
dermatitis was associated with poorer outcomes, whereas contact
15. Agrup G. Sensitization induced by patch testing. Br J Dermatol 1968;80:631-4
allergy was not. The longer the duration of the hand dermatitis (III).
before diagnosis, the poorer the outcome. 16. Yoshifuku A, Kawai K, Saruwatari H, Higashi Y, Kanekura T. Active sensiti-
A number of studies have examined work outcomes in zation to beryllium by diagnostic patch tests. J Dermatol 2012;39:1084-5 (IV).
workers with OCD. These studies demonstrate that there is 17. Devos SA, Van Der Valk PG. Epicutaneous patch testing. Eur J Dermatol
2002;12:506-13 (IV).
signicant job disruption for workers with CD. Some studies 18. Rajagopalan R, Anderson R. Impact of patch testing on dermatology-specic
report work absence at the time of assessment and others report quality of life in patients with allergic contact dermatitis. Am J Contact Dermat
the results of a follow-up study. Status at the time of assessment 1997;8:215-21 (III).
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S27
VOLUME 3, NUMBER 3S

19. Mirabelli MC, Vizcaya D, Marti Margarit A, Anto JM, Arjona L, Barreiro E, 47. Klaschka U. Contact allergens for armpitsallergenic fragrances specied on
et al. Occupational risk factors for hand dermatitis among professional cleaners deodorants. Int J Hyg Environ Health 2012;215:584-91 (III).
in Spain. Contact Dermatitis 2012;66:188-96 (III). 48. Jorgensen PH, Jensen CD, Rastogi S, Andersen KE, Johansen JD. Experi-
20. Lazzarini R, Duarte IA, Sumita JM, Minnicelli R. Allergic contact dermatitis mental elicitation with hydroxyisohexyl-3-cyclohexene carboxaldehyde-
among construction workers detected in a clinic that did not specialize in containing deodorants. Contact Dermatitis 2007;56:146-50 (IIa).
occupational dermatitis. An Bras Dermatol 2012;87:567-71 (III). 49. Svedman C, Bruze M, Johansen JD, Andersen KE, Goossens A, Frosch PJ,
21. Lan CC, Tu HP, Lee CH, Wu CS, Ko YC, Yu HS, et al. Hand dermatitis et al. Deodorants: an experimental provocation study with hydroxycitronellal.
among university hospital nursing staff with or without atopic eczema: Contact Dermatitis 2003;48:217-23 (IIa).
assessment of risk factors. Contact Dermatitis 2011;64:73-9 (III). 50. Sheu M, Simpson EL, Law SV, Storrs FJ. Allergic contact dermatitis from a
22. Keegel T, Saunders H, LaMontagne AD, Nixon R. Are material safety data natural deodorant: a report of 4 cases associated with lichen acid mix allergy.
sheets (MSDS) useful in the diagnosis and management of occupational J Am Acad Dermatol 2006;55:332-7 (III).
contact dermatitis? Contact Dermatitis 2007;57:331-6. 51. Bruze M, Johansen JD, Andersen KE, Frosch P, Goossens A, Lepoittevin JP,
23. Pedersen LK, Johansen JD, Held E, Agner T. Augmentation of skin response et al. Deodorants: an experimental provocation study with isoeugenol. Contact
by exposure to a combination of allergens and irritantsa review. Contact Dermatitis 2005;52:260-7.
Dermatitis 2004;50:265-73 (III). 52. Bruze M, Johansen JD, Andersen KE, Frosch P, Lepoittevin JP, Rastogi S,
24. Belsito DV, Fransway AF, Fowler JF Jr, Sherertz EF, Maibach HI, Mark JG Jr, et al. Deodorants: an experimental provocation study with cinnamic aldehyde.
et al. Allergic contact dermatitis to detergents: a multicenter study to assess J Am Acad Dermatol 2003;48:194-200 (IIb).
prevalence. J Am Acad Dermatol 2002;46:200-6. 53. Gall H, Kempf E. Contact allergy due to the topical antiperspirant prop-
25. Proksch E, Brasch J. Abnormal epidermal barrier in the pathogenesis of antheline bromide (authors transl). Derm Beruf Umwelt 1982;30:55-6. 7 (III).
contact dermatitis. Clin Dermatol 2012;30:335-44 (IV). 54. Przybilla B, Schwab U, Holzle E, Ring J. Contact sensitization to an
26. Warshaw EM, Belsito DV, Taylor JS, Sasseville D, Dekoven JG, Zirwas MJ, antiperspirant with the active ingredient propantheline bromide. Hautarzt 1983;
et al. North American Contact Dermatitis Group Patch Test Results: 2009 to 34:459-62.
2010. Dermatitis 2013;24:50-9 (III). 55. Giusti F, Massone F, Bertoni L, Pellacani G, Seidenari S. Contact sensitization
27. Toledo F, Garcia-Bravo B, Fernandez-Redondo V, De la Cuadra J, Gimenez- to disperse dyes in children. Pediatr Dermatol 2003;20:393-7 (III).
Arnau AM, Borrego L, et al. Patch testing in children with hand eczema. A 56. Wentworth AB, Richardson DM, Davis MD. Patch testing with textile
5-year multicentre study in Spain. Contact Dermatitis 2011;65:213-9. allergens: the mayo clinic experience. Dermatitis 2012;23:269-74 (III).
28. Feser A, Plaza T, Vogelgsang L, Mahler V. Periorbital dermatitisa recalci- 57. Ryberg K, Isaksson M, Gruvberger B, Hindsen M, Zimerson E, Bruze M.
trant disease: causes and differential diagnoses. Br J Dermatol 2008;159: Contact allergy to textile dyes in southern Sweden. Contact Dermatitis 2006;
858-63 (III). 54:313-21 (III).
29. Gordon LA. Compositae dermatitis. Aust J Dermatol 1999;40:123-8 (IV). 58. Winnicki M, Shear NH. A systematic approach to systemic contact dermatitis
30. Temesvari E, Ponyai G, Nemeth I, Hidvegi B, Sas A, Karpati S. Periocular and symmetric drug-related intertriginous and exural exanthema (SDRIFE): a
dermatitis: a report of 401 patients. J Eur Acad Dermatol Venereol 2009;23: closer look at these conditions and an approach to intertriginous eruptions. Am
124-8. J Clin Dermatol 2011;12:171-80 (IV).
31. Novitskaya ES, Dean SJ, Craig JP, Alexandroff AB. Current dilemmas and 59. Warshaw EM, Furda LM, Maibach HI, Rietschel RL, Fowler JF Jr,
controversies in allergic contact dermatitis to ophthalmic medications. Clin Belsito DV, et al. Anogenital dermatitis in patients referred for patch testing:
Dermatol 2011;29:295-9 (IV). retrospective analysis of cross-sectional data from the North American Contact
32. Landeck L, Schalock PC, Baden LA, Gonzalez E. Periorbital contact sensiti- Dermatitis Group, 1994-2004. ArchDermatol 2008;144:749-55.
zation. Am J Ophthalmol 2010;150:366-370 e2 (III). 60. Bauer A, Geier J, Elsner P. Allergic contact dermatitis in patients with ano-
33. Guin JD. Eyelid dermatitis: a report of 215 patients. Contact Dermatitis 2004; genital complaints. J Reproduct Med 2000;45:649-54 (III).
50:87-90 (III). 61. Chang MW, Nakrani R. Six children with allergic contact dermatitis to
34. Zug KA, Kornik R, Belsito DV, DeLeo VA, Fowler JF Jr, Maibach HI, et al. methylisothiazolinone in wet wipes (baby wipes). Pediatrics 2014;133:e434-8
Patch-testing North American lip dermatitis patients: data from the (III).
North American Contact Dermatitis Group, 2001 to 2004. Dermatitis 2008;19: 62. Theler B, Bucher C, French LE, Ballmer Weber B, Hofbauer GF. Clinical
202-8 (III). expression of nickel contact dermatitis primed by diagnostic patch test.
35. Lim SW, Goh CL. Epidemiology of eczematous cheilitis at a tertiary derma- Dermatology 2009;219:73-6 (IIb).
tological referral centre in Singapore. Contact Dermatitis 2000;43:322-6 (III). 63. Corazza M, Mantovani L, Montanari A, Virgili A. Allergic contact dermatitis
36. Francalanci S, Sertoli A, Giorgini S, Pigatto P, Santucci B, Valsecchi R. from transdermal estradiol and systemic contact dermatitis from oral estradiol.
Multicentre study of allergic contact cheilitis from toothpastes. Contact A case report. J Reproduct Med 2002;47:507-9 (III).
Dermatitis 2000;43:216-22 (III). 64. Isaksson M, Bruze M. Allergic contact dermatitis in response to budesonide
37. Tran A, Pratt M, DeKoven J. Acute allergic contact dermatitis of the lips from reactivated by inhalation of the allergen. J Am Acad Dermatol 2002;46:880-5
peppermint oil in a lip balm. Dermatitis 2010;21:111-5 (III). (III).
38. Kirshen C, Pratt M. Dental allergic contact dermatitis: an interesting case series 65. Landeck L, Uter W, John SM. Patch test characteristics of patients referred for
and review of the literature. Dermatitis 2012;23:222-6 (III). suspected contact allergy of the feet-retrospective 10-year cross-sectional study
39. Torgerson RR, Davis MD, Bruce AJ, Farmer SA, Rogers RS 3rd. Contact of the IVDK data. Contact Dermatitis 2012;66:271-8.
allergy in oral disease. J Am Acad Dermatol 2007;57:315-21 (III). 66. Warshaw EM, Schram SE, Belsito DV, DeLeo VA, Fowler JF Jr, Maibach HI,
40. Carlsen BC, Menne T, Johansen JD. 20 Years of standard patch testing in an et al. Shoe allergens: retrospective analysis of cross-sectional data from the
eczema population with focus on patients with multiple contact allergies. North American contact dermatitis group, 2001-2004. Dermatitis 2007;18:
Contact Dermatitis 2007;57:76-83 (III). 191-202 (III).
41. Dotterud LK. The prevalence of allergic contact sensitization in a general 67. Warshaw EM, Cook JW, Belsito DV, DeLeo VA, Fowler JF Jr, Maibach HI,
population in Tromso, Norway. Int J Circumpolar Health 2007;66:328-34 (III). et al. Positive patch-test reactions to mixed dialkyl thioureas: cross-sectional
42. Warshaw EM, Buchholz HJ, Belsito DV, Maibach HI, Fowler JF Jr, data from the North American Contact Dermatitis Group, 1994 to 2004.
Rietschel RL, et al. Allergic patch test reactions associated with cosmetics: Dermatitis 2008;19:190-201 (III).
retrospective analysis of cross-sectional data from the North American Contact 68. Darling MI, Horn HM, McCormack SK, Schoeld OM. Sole dermatitis in
Dermatitis Group, 2001-2004. J Am Acad Dermatol 2009;60:23-38 (III). children: patch testing revisited. Pediatric Dermatol 2012;29:254-7 (III).
43. Yazar K, Boman A, Liden C. p-Phenylenediamine and other hair dye sensi- 69. Smart V, Alavi A, Coutts P, Fierheller M, Coelho S, Linn Holness D, et al.
tizers in Spain. Contact Dermatitis 2012;66:27-32 (III). Contact allergens in persons with leg ulcers: a Canadian study in contact
44. Zirwas M, Moennich J. Shampoos. Dermatitis 2009;20:106-10. sensitization. Int J Low Extrem Wounds 2008;7:120-5 (III).
45. Hillen U, Grabbe S, Uter W. Patch test results in patients with scalp dermatitis: 70. Barbaud A, Collet E, Le Coz CJ, Meaume S, Gillois P. Contact allergy in
analysis of data of the Information Network of Departments of Dermatology. chronic leg ulcers: results of a multicentre study carried out in 423 patients and
Contact Dermatitis 2007;56:87-93 (III). proposal for an updated series of patch tests. Contact Dermatitis 2009;60:
46. Johansen JD, Hald M, Andersen BL, Laurberg G, Danielsen A, Avnstorp C, 279-87 (III).
et al. Classication of hand eczema: clinical and aetiological types. Based on 71. Carlsen BC, Andersen KE, Menne T, Johansen JD. Sites of dermatitis in a
the guideline of the Danish Contact Dermatitis Group. Contact Dermatitis patch test population: hand dermatitis is associated with polysensitization. Br J
2011;65:13-21. Dermatol 2009;161:808-13 (IIa).
S28 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

72. Renner R, Simon JC, Treudler R. Contact sensitization to modern wound 98. Hillen U, Jappe U, Frosch PJ, Becker D, Brasch J, Lilie M, et al. Late reactions
dressings in 70 patients with chronic leg ulcers. Dermatitis 2013;24:60-3 (IIb). to the patch-test preparations para-phenylenediamine and epoxy resin: a pro-
73. Thyssen JP, Linneberg A, Engkilde K, Menne T, Johansen JD. Contact spective multicentre investigation of the German Contact Dermatitis Research
sensitization to common haptens is associated with atopic dermatitis: new Group. Br J Dermatol 2006;154:665-70 (IIb).
insight. Br J Dermatol 2012;166:1255-61 (III). 99. Aalto-Korte K, Alanko K, Kuuliala O, Jolanki R. Late reactions in patch tests:
74. Zug KA, McGinley-Smith D, Warshaw EM, Taylor JS, Rietschel RL, a 4-year review from a clinic of occupational dermatology. Contact Dermatitis
Maibach HI, et al. Contact allergy in children referred for patch testing: North 2007;56:81-6 (III).
American Contact Dermatitis Group data, 2001-2004. Arch Dermatol 2008; 100. Flannigan SA, Smolensky MH, Harrist R, Machinski G, McGovern JP. Time
144:1329-36 (III). considerations in scoring contact irritant patch test sites. Contact Dermatitis
75. Thyssen JP, Linneberg A, Ross-Hansen K, Carlsen BC, Meldgaard M, 1983;9:519-20 (IIb).
Szecsi PB, et al. Filaggrin mutations are strongly associated with 101. Davis MD, Scalf LA, Yiannias JA, Cheng JF, El-Azhary RA, Rohlinger AL,
contact sensitization in individuals with dermatitis. Contact Dermatitis 2013; et al. Changing trends and allergens in the patch test standard series: a mayo
68:273-6 (III). clinic 5-year retrospective review, January 1, 2001, through December 31,
76. Malajian D, Belsito DV. Cutaneous delayed-type hypersensitivity in patients 2005. Arch Dermatol 2008;144:67-72.
with atopic dermatitis. J Am Acad Dermatol 2013;69:232-7. 102. Dickel H, Taylor JS, Evey P, Merk HF. Delayed readings of a standard
77. Jacob SE, Brod B, Crawford GH. Clinically relevant patch test reactions in screening patch test tray: frequency of lost, found, and persistent re-
childrena United States based study. Pediatric Dermatol 2008;25:520-7 (III). actions. Am J Contact Dermatitis 2000;11:213-7.
78. Anveden I, Lindberg M, Andersen KE, Bruze M, Isaksson M, Liden C, et al. 103. Carlson S, Gipson K, Nedorost S. Relevance of doubtful (equivocal) late
Oral prednisone suppresses allergic but not irritant patch test reactions in in- patch-test readings. Dermatitis 2010;21:102-8 (III).
dividuals hypersensitive to nickel. Contact Dermatitis 2004;50:298-303 (Ib). 104. Duarte I, Lazzarini R, Bedrikow R. Excited skin syndrome: study of 39 pa-
79. Rosmarin D, Gottlieb AB, Asarch A, Scheinman PL. Patch-testing while on tients. Am J Contact Dermat 2002;13:59-65 (IIb).
systemic immunosuppressants. Dermatitis 2009;20:265-70 (III). 105. Lazzarini R, Duarte I, de Farias DC, Santos CA, Tsai AI. Frequency and main
80. Wee JS, White JM, McFadden JP, White IR. Patch testing in patients treated sites of allergic contact dermatitis caused by nail varnish. Dermatitis 2008;19:
with systemic immunosuppression and cytokine inhibitors. Contact Dermatitis 319-22.
2010;62:165-9 (III). 106. Cockayne SE, Gawkrodger DJ. Angry back syndrome is often due to marginal
81. Green C. The effect of topically applied corticosteroid on irritant and allergic irritants: a study of 17 cases seen over 4 years. Contact Dermatitis 2000;43:
patch test reactions. Contact Dermatitis 1996;35:331-3 (IIb). 280-2.
82. Prens EP, Benne K, Geursen-Reitsma AM, van Dijk G, Benner R, van Joost T. 107. White JM. Patch testing: what allergists should know. Clin Exp Allergy 2012;
Effects of topically applied glucocorticosteroids on patch test responses and 42:180-5 (IV).
recruitment of inammatory cells in allergic contact dermatitis. Agents Actions 108. Nethercott JR, Holness DL. Disease outcome in workers with occupational
1989;26:125-7 (IIb). skin disease. J Am Acad Dermatol 1994;30:569-74 (III).
83. Aldridge RD, Sewell HF, King G, Thomson AW. Topical cyclosporin A in 109. Fransway AF, Zug KA, Belsito DV, Deleo VA, Fowler JF Jr, Maibach HI,
nickel contact hypersensitivity: results of a preliminary clinical and immuno- et al. North American Contact Dermatitis Group patch test results for 2007-
histochemical investigation. Clin Exp Immunol 1986;66:582-9 (IIb). 2008. Dermatitis 2013;24:10-21 (III).
84. Alomar A, Puig L, Gallardo CM, Valenzuela N. Topical tacrolimus 0.1% 110. van der Valk PG, Devos SA, Coenraads PJ. Evidence-based diagnosis in patch
ointment (protopic) reverses nickel contact dermatitis elicited by allergen testing. Contact Dermatitis 2003;48:121-5 (IV).
challenge to a similar degree to mometasone furoate 0.1% with greater sup- 111. De Groot A. Test Concentrations and Vehicles for 4350 Chemicals. 3rd ed.
pression of late erythema. Contact Dermatitis 2003;49:185-8 (Ib). Wapserveen, The Netherlands: A.C. DeGroot Publishing; 2008 (IV).
85. Damian DL, Halliday GM. Measurement of ultraviolet radiation-induced 112. Mendelow AY, Forsyth A, Florence AT, Baillie AJ. Patch testing for nickel
suppression of recall contact and delayed-type hypersensitivity in humans. allergy. The inuence of the vehicle on the response rate to topical nickel
Methods 2002;28:34-45 (IV). sulphate. Contact Dermatitis 1985;13:29-33 (IIb).
86. Damian DL, Halliday GM, Barnetson RS. Broad-spectrum sunscreens provide 113. Tanglertsampan C, Maibach HI. The role of vehicles in diagnostic patch
greater protection against ultraviolet-radiation-induced suppression of contact testing. A reappraisal. Contact Dermatitis 1993;29:169-74 (III).
hypersensitivity to a recall antigen in humans. J Invest Dermatol 1997;109: 114. Batchelor RJ, Wilkinson SM. Photopatch testinga retrospective review using
146-51 (IIa). the 1 day and 2 day irradiation protocols. Contact Dermatitis 2006;54:75-8
87. Chen XJ, Chen LL, Shi X, Xie LX, Leng H, Ji J, et al. The effect of deslor- (III).
atadine on patch test reactions in Chinese patients. Asian Pac J Allergy 115. Lachapelle JM, Maibach HI. Patch Testing and Prick Testing. A Practical
Immunol 2012;30:209-13 (IIb). Guide. 2nd ed. Berlin, Heidelberg, Springer Verlag: 2009 (IV).
88. Zug KA, Warshaw EM, Fowler JF Jr, Maibach HI, Belsito DL, Pratt MD, et al. 116. Pacheco K, Barker L, Maier L, Erb S, Sills M, Knight V. Development of a
Patch-test results of the North American Contact Dermatitis Group 2005-2006. validated blood test for nickel sensitization. J Allergy Clin Immunol 2013;132:
Dermatitis 2009;20:149-60 (III). 767-9 (IIb).
89. Ale SI, Maibach HI. Reproducibility of patch test results: a concurrent right- 117. Spiewak R, Moed H, von Blomberg BM, Bruynzeel DP, Scheper RJ,
versus-left study using TRUE Test. Contact Dermatitis 2004;50:304-12 (IIb). Gibbs S, et al. Allergic contact dermatitis to nickel: modied in vitro test
90. Goh CL. Comparative study of TRUE Test and Finn Chamber patch test protocols for better detection of allergen-specic response. Contact Derma-
techniques in Singapore. Contact Dermatitis 1992;27:84-9. 1992. titis 2007;56:63-9 (IIb).
91. Wilkinson JD, Bruynzeel DP, Ducombs G, Frosch PJ, Gunnarsson Y, 118. Lindemann M, Rietschel F, Zabel M, Grosse-Wilde H. Detection of chromium
Hannuksela M, et al. European multicenter study of TRUE Test, Panel 2. allergy by cellular in vitro methods. Clin Exp Allergy 2008;38:1468-75 (IIb).
Contact Dermatitis 1990;22:218-25 (III). 119. Moed H, von Blomberg M, Bruynzeel DP, Scheper R, Gibbs S, Rustemeyer T.
92. Wilkinson DS, Fregert S, Magnusson B, Bandmann HJ, Calnan CD, Improved detection of allergen-specic T-cell responses in allergic contact
Cronin E, et al. Terminology of contact dermatitis. Acta Derm Venereol dermatitis through the addition of cytokine cocktails. Exp Dermatol 2005;14:
1970;50:287-92 (IV). 634-40 (IIb).
93. Kalimo K, Lammintausta K. 24 and 48 h allergen exposure in patch testing. 120. Kreiss K, Newman LS, Mroz MM, Campbell PA. Screening blood test iden-
Comparative study with 11 common contact allergens and NiCl2. Contact ties subclinical beryllium disease. J Occup Med 1989;31:603-8 (IIb).
Dermatitis 1984;10:25-9 (III). 121. Fischer LA, Johansen JD, Menne T. Nickel allergy: relationship between patch
94. Davis MD, Bhate K, Rohlinger AL, Farmer SA, Richardson DM, Weaver AL. test and repeated open application test thresholds. Br J Dermatol 2007;157:
Delayed patch test reading after 5 days: the Mayo Clinic experience. J Am 723-9 (IIb).
Acad Dermatol 2008;59:225-33 (III). 122. Zaghi D, Maibach HI. Quantitative relationships between patch test reactivity
95. Jonker MJ, Bruynzeel DP. The outcome of an additional patch-test reading on and use test reactivity: an overview. Cutan Ocular Toxicol 2008;27:241-8 (III).
days 6 or 7. Contact Dermatitis 2000;42:330-5. 123. Kerschenlohr K, Darsow U, Burgdorf WH, Ring J, Wollenberg A. Lessons
96. Geier J, Gefeller O, Wiechmann K, Fuchs T. Patch test reactions at D4, D5 and from atopy patch testing in atopic dermatitis. Curr Allergy Asthma Reports
D6. Contact Dermatitis 1999;40:119-26 (III). 2004;4:285-9 (IV).
97. Gawkrodger DJ, Paul L. Late patch test reactions: delayed immune response 124. Darsow U, Vieluf D, Ring J. The atopy patch test: an increased rate of reac-
appears to be more common than active sensitization. Contact Dermatitis 2008; tivity in patients who have an air-exposed pattern of atopic eczema. Br J
59:185-7 (III). Dermatol 1996;135:182-6 (IIb).
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S29
VOLUME 3, NUMBER 3S

125. Towers GH, Mitchell JC. The current status of the weed Parthenium hyster- American Contact Dermatitis Group Data, 1994-2004. J Am Acad Dermatol
ophorus L. as a cause of allergic contact dermatitis. Contact Dermatitis 1983;9: 2007;57:301-14.
465-9 (IV). 153. Bruze M, Dahlquist I, Fregert S, Gruvberger B, Persson K. Contact allergy to
126. Sharma VK, Sethuraman G. Parthenium dermatitis. Dermatitis 2007;18: the active ingredients of Kathon CG. Contact Dermatitis 1987;16:183-8 (IIb).
183-90 (IV). 154. Administration DFFaD. Frequency of use of cosmetic ingredients. 2007. http://
127. Yokozeki H, Satoh T, Katayama I, Nishioka K. Airborne contact dermatitis www.fda.gov/cosmetics/registrationprogram/default.htm. Accessed March 31,
due to Japanese cedar pollen. Contact Dermatitis 2007;56:224-8 (III). 2015. (III).
128. Schumacher MJ, Silvis NG. Airborne contact dermatitis from Ambrosia del- 155. Castanedo-Tardana MP, Zug KA. Methylisothiazolinone. Dermatitis 2013;24:
toidea (triangle-leaf bursage). Contact Dermatitis 2003;48:212-6 (III). 2-6 (IV).
129. Munoz FJ, Delgado J, Palma JL, Gimenez MJ, Monteseirin FJ, Conde J. 156. Lundov MD, Thyssen JP, Zachariae C, Johansen JD. Prevalence and cause of
Airborne contact urticaria due to mulberry (Morus alba) pollen. Contact methylisothiazolinone contact allergy. Contact Dermatitis 2010;63:164-7 (III).
Dermatitis 1995;32:61 (III). 157. Fisher AA. Paraben dermatitis due to a new medicated bandage: the paraben
130. Uter W, Schnuch A, Geier J, Pfahlberg A, Gefeller O. Association between paradox. Contact Dermatitis 1979;5:273-4 (IV).
occupation and contact allergy to the fragrance mix: a multifactorial analysis of 158. Coutts I, Shaw S, Orton D. Patch testing with pure tea tree oil12 months
national surveillance data. Occup Environ Med 2001;58:392-8. experience. Br J Dermatol 2002;147:67-74.
131. Nethercott JR, Nield G, Holness DL. A review of 79 cases of eyelid dermatitis. 159. Walgrave SE, Warshaw EM, Glesne LA. Allergic contact dermatitis from
J Am Acad Dermatol 1989;21(Pt 1):223-30 (IIa). propolis. Dermatitis 2005;16:209-15 (IV).
132. Nedorost S, Wagman A. Positive patch-test reactions to gold: patients 160. Orton DI, Wilkinson JD. Cosmetic allergy: incidence, diagnosis, and man-
perception of relevance and the role of titanium dioxide in cosmetics. agement. Am J Clin Dermatol 2004;5:327-37 (IV).
Dermatitis 2005;16:67-70 (III). 161. Fowler JF Jr, Zug KM, Taylor JS, Storrs FJ, Sherertz EA, Sasseville DA, et al.
133. Johansen JD, Frosch PJ, Svedman C, Andersen KE, Bruze M, Pirker C, et al. Allergy to cocamidopropyl betaine and amidoamine in North America.
Hydroxyisohexyl 3-cyclohexene carboxaldehyde- known as Lyral: quantitative Dermatitis 2004;15:5-6 (IIa).
aspects and risk assessment of an important fragrance allergen. Contact 162. Kimber I, Quirke S, Cumberbatch M, Ashby J, Paton D, Aldridge RD, et al.
Dermatitis 2003;48:310-6 (Ib). Lymphocyte transformation and thiuram sensitization. Contact Dermatitis
134. Larsen W, Nakayama H, Lindberg M, Fischer T, Elsner P, Burrows D, et al. 1991;24:164-71.
Fragrance contact dermatitis: a worldwide multicenter investigation (Part I). 163. Fowler JF, Fowler LM, Hunter JE. Allergy to cocamidopropyl betaine may be
Am J Contact Dermat 1996;7:77-83 (IIb). due to amidoamine: a patch test and product use test study. Contact Dermatitis
135. Api AM. Sensitization methodology and primary prevention of the research 1997;37:276-81 (IIa).
institute for fragrance materials. Dermatology 2002;205:84-7 (III). 164. Zapolanski T, Jacob SE. para-Phenylenediamine. Dermatitis 2008;19:E20-1
136. Naldi L. The epidemiology of fragrance allergy: questions and needs. (IV).
Dermatology 2002;205:89-97 (III). 165. Krasteva M, Cristaudo A, Hall B, Orton D, Rudzki E, Santucci B, et al.
137. Rastogi SC, Menne T, Johansen JD. The composition of ne fragrances is Contact sensitivity to hair dyes can be detected by the consumer open test. Eur
changing. Contact Dermatitis 2003;48:130-2 (IV). J Dermatol 2002;12:322-6 (IIb).
138. Scheinman PL. The foul side of fragrance-free products: what every clinician 166. Scheman A, Cha C, Bhinder M. Alternative hair-dye products for persons
should know about managing patients with fragrance allergy. J Am Acad allergic to para-phenylenediamine. Dermatitis 2011;22:189-92 (IIb).
Dermatol 1999;41:1020-4 (IV). 167. Schnuch A, Lessmann H, Frosch PJ, Uter W. para-Phenylenediamine: the
139. Johansen JD. Fragrance contact allergy: a clinical review. Am J Clin Dermatol prole of an important allergen. Results of the IVDK. Br J Dermatol 2008;159:
2003;4:789-98 (IV). 379-86 (III).
140. Heydorn S, Menne T, Andersen KE, Bruze M, Svedman C, White IR, et al. 168. Ho SG, Basketter DA, Jefferies D, Rycroft RJ, White IR, McFadden JP.
Citral a fragrance allergen and irritant. Contact Dermatitis 2003;49:32-6. Analysis of para-phenylenediamine allergic patients in relation to strength of
141. Gimenez-Arnau A, Gimenez-Arnau E, Serra-Baldrich E, Lepoittevin JP, patch test reaction. Br J Dermatol 2005;153:364-7 (IIb).
Camarasa JG. Principles and methodology for identication of fragrance al- 169. Storrs FJ. Permanent wave contact dermatitis: contact allergy to glyceryl
lergens in consumer products. Contact Dermatitis 2002;47:345-52 (IIb). monothioglycolate. J Am Acad Dermatol 1984;11:74-85 (III).
142. Wohrl S, Hemmer W, Focke M, Gotz M, Jarisch R. The signicance of 170. Stechschulte SA, Avashia N, Jacob SE. Tosylamide formaldehyde resin.
fragrance mix, balsam of Peru, colophony and propolis as screening tools in Dermatitis 2008;19:E18-9.
the detection of fragrance allergy. Br J Dermatol 2001;145:268-73 (IIb). 171. Freeman S, Lee MS, Gudmundsen K. Adverse contact reactions to sculptured
143. Ting PT, Silver S. Allergic contact dermatitis to propolis. J Drugs Dermatol acrylic nails: 4 case reports and a literature review. Contact Dermatitis 1995;
2004;3:685-6 (IV). 33:381-5 (III).
144. Wenk KS, Ehrlich A. Fragrance series testing in eyelid dermatitis. Dermatitis 172. Madnani NA, Khan KJ. Nail cosmetics. Indian J Dermatol. Venereol Leprol
2012;23:22-6 (IIb). 2012;78:309-17 (IV).
145. Schllnast R, Krnke B, Aberer W. Anal and palmar contact dermatitis caused 173. Deleo VA. Photocontact dermatitis. Dermatol Ther 2004;17:279-88 (IV).
by iodopropynyl butylcarbamate in moist sanitary wipes. Hautarzt 2003;54: 174. Scheuer E, Warshaw E. Sunscreen allergy: a review of epidemiology, clinical
970-4 (III). characteristics, and responsible allergens. Dermatitis 2006;17:3-11 (IV).
146. Badreshia S, Marks JG Jr. Iodopropynyl butylcarbamate. Am J Contact Dermat 175. Scheman A. Adverse reactions to cosmetic ingredients. Dermatol Clin 2000;
2002;13:77-9 (IV). 18:685-98 (IV).
147. Skinner SL, Marks JG. Allergic contact dermatitis to preservatives in topical 176. Schauder S, Ippen H. Contact and photocontact sensitivity to sunscreens.
medicaments. Am J Contact Dermatitis 1998;9:199-201 (III). Review of a 15-year experience and of the literature. Contact Dermatitis 1997;
148. Wilkinson JD, Shaw S, Andersen KE, Brandao FM, Bruynzeel DP, Bruze M, 37:221-32 (IV).
et al. Monitoring levels of preservative sensitivity in Europe. A 10-year 177. Prystowsky SD, Allen AM, Smith RW, Nonomura JH, Odom RB, Akers WA.
overview (1991-2000). Contact Dermatitis 2002;46:207-10 (III). Allergic contact hypersensitivity to nickel, neomycin, ethylenediamine, and
149. De Groot A, White IR, Flyvholm MA, Lensen G, Coenraads PJ. Formalde- benzocaine. Relationships between age, sex, history of exposure, and reactivity
hyde-releasers in cosmetics: relationship to formaldehyde contact allergy. Part to standard patch tests and use tests in a general population. Arch Dermatol
2. Patch test relationship to formaldehyde contact allergy, experimental 1979;115:959-62 (III).
provocation tests, amount of formaldehyde released, and assessment of risk to 178. Malhotra V, Kaur I, Saraswat A, Kumar B. Frequency of patch-test positivity
consumers allergic to formaldehyde. Contact Dermatitis 2010;62:18-31 (III). in patients with psoriasis: a prospective controlled study. Acta Derm Venereol
150. De Groot AC, Flyvholm MA, Lensen G, Menne T, Coenraads PJ. Formal- 2002;82:432-5 (IIb).
dehyde-releasers: relationship to formaldehyde contact allergy. Contact allergy 179. Antevil JL, Muldoon MP, Battaglia M, Green R. Intraoperative
to formaldehyde and inventory of formaldehyde-releasers. Contact Dermatitis anaphylactic shock associated with bacitracin irrigation during revision
2009;61:63-85 (III). total knee arthroplasty. A case report. J Bone Joint Surg Am 2003;85-A:
151. Diepgen TL, Weisshaar E. Contact dermatitis: epidemiology and frequent 339-42 (IV).
sensitizers to cosmetics. J Eur Acad Dermatol Venereol 2007;21(Suppl 2): 180. Smack DP, Harrington AC, Dunn C, Howard RS, Szkutnik AJ, Krivda SJ,
9-13 (III). et al. Infection and allergy incidence in ambulatory surgery patients using
152. Warshaw EM, Ahmed RL, Belsito DV, DeLeo VA, Fowler JF Jr, Maibach HI, white petrolatum vs bacitracin ointment. A randomized controlled trial. JAMA
et al. Contact dermatitis of the hands: cross-sectional analyses of North 1996;276:972-7 (Ib).
S30 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

181. Shackelford KE, Belsito DV. The etiology of allergic-appearing foot derma- 210. Thyssen JP, Menne T, Schalock PC, Taylor JS, Maibach HI. Pragmatic
titis: a 5-year retrospective study. J Am Acad Dermat 2002;47:715-21 (III). approach to the clinical work-up of patients with putative allergic disease to
182. Rani Z, Hussain I, Haroon TS. Common allergens in shoe dermatitis: our metallic orthopaedic implants before and after surgery. Br J Dermatol 2011;
experience in Lahore, Pakistan. Int J Dermatol 2003;42:605-7 (IV). 164:473-8 (IV).
183. Zmudzinska M, Czarnecka-Operacz M, Silny W. Contact allergy to gluco- 211. Niki Y, Matsumoto H, Otani T, Yatabe T, Kondo M, Yoshimine F, et al.
corticosteroids in patients with chronic venous leg ulcers, atopic dermatitis and Screening for symptomatic metal sensitivity: a prospective study of 92 patients
contact allergy. Acta Dermatovenerol Croat 2008;16:72-8 (IIa). undergoing total knee arthroplasty. Biomaterials 2005;26:1019-26 (III).
184. Baeck M, Goossens A. Immediate and delayed allergic hypersensitivity to 212. Andrews ID, Scheinman P. Systemic hypersensitivity reaction (without cuta-
corticosteroids: practical guidelines. Contact Dermatitis 2012;66:38-45 (IIb). neous manifestations) to an implantable cardioverter-debrillator. Dermatitis
185. Bennett ML, Fountain JM, McCarty MA, Sherertz EF. Contact allergy to 2011;22:161-4 (III).
corticosteroids in patients using inhaled or intranasal corticosteroids for 213. Kang J, Simpson CS, Campbell D, Borici-Mazi R, Redfearn DP, Michael KA,
allergic rhinitis or asthma. Am J Contact Dermat 2001;12:193-6 (III). et al. Cardiac rhythm device contact dermatitis. Ann Noninvasive Electro-
186. Isaksson M. Corticosteroids. Dermatol Ther 2004;17:314-20 (IV). cardiol 2013;18:79-83 (III).
187. McFadden J. Contact allergic reactions in patients with atopic eczema. Acta 214. Jetty P, Jayaram S, Veinot J, Pratt M. Supercial femoral artery nitinol stent in
Derm Venereol Suppl 2005;215:28-32. a patient with nickel allergy. J Vasc Surg 2013;58:1388-90 (III).
188. Ferguson AD, Emerson RM, English JS. Cross-reactivity patterns to budeso- 215. Khamaysi Z, Bergman R, Weltfriend S. Positive patch test reactions to aller-
nide. Contact Dermatitis 2002;47:337-40 (III). gens of the dental series and the relation to the clinical presentations. Contact
189. Lepoittevin JP, Drieghe J, Dooms-Goossens A. Studies in patients with Dermatitis 2006;55:216-8 (III).
corticosteroid contact allergy. Understanding cross-reactivity among different 216. Purello DAmbrosio F, Ricciardi L, Isola S, Gangemi S, Cilia M, Levanti C,
steroids. Arch Dermatol 1995;131:31-7 (III). et al. Systemic contact dermatitis to copper-containing IUD. Allergy 1996;51:
190. Coopman S, Degreef H, Dooms-Goossens A. Identication of cross-reaction 658-9 (III).
patterns in allergic contact dermatitis from topical corticosteroids. Br J Der- 217. Carlsson A, Moller H. Implantation of orthopaedic devices in patients with
matol 1989;121:27-34 (IIb). metal allergy. Acta Derm Venereol 1989;69:62-6.
191. Bjarnason B, Flosadottir E, Fischer T. Assessment of budesonide patch tests. 218. Gawkrodger DJ. Nickel sensitivity and the implantation of orthopaedic pros-
Contact Dermatitis 1999;41:211-7 (IIa). theses. Contact Dermatitis 1993;28:257-9 (III).
192. Boffa MJ, Wilkinson SM, Beck MH. Screening for corticosteroid contact 219. Cousen PJ, Gawkrodger DJ. Metal allergy and second-generation metal-
hypersensitivity. Contact Dermatitis 1995;33:149-51 (IIa). on-metal arthroplasties. Contact Dermatitis 2012;66:55-62 (IV).
193. Jacob SE, Zapolanski T. Systemic contact dermatitis. Dermatitis 2008;19: 220. Thyssen JP, Engkilde K, Menne T, Johansen JD, Hansen PR, Gislason GH. No
9-15 (IV). association between metal allergy and cardiac in-stent restenosis in patients with
194. Wilkinson SM. Corticosteroid cross-reactions: an alternative view. Contact dermatitis-results from a linkage study. Contact Dermatitis 2011;64:138-41 (III).
Dermatitis 2000;42:59-63 (IV). 221. Basko-Plluska JL, Thyssen JP, Schalock PC. Cutaneous and systemic hyper-
195. Romano A, Viola M, Gaeta F, Rumi G, Maggioletti M. Patch testing in sensitivity reactions to metallic implants. Dermatitis 2011;22:65-79 (IV).
non-immediate drug eruptions. Allergy Asthma Clin Immunol 2008;4: 222. Bircher A, Friederich NF, Seelig W, Scherer K. Allergic complications from
66-74 (IV). orthopaedic joint implants: the role of delayed hypersensitivity to benzoyl
196. Barbaud A. Skin testing in delayed reactions to drugs. Immunol Allergy Clin peroxide in bone cement. Contact Dermatitis 2012;66:20-6 (III).
North Am 2009;29:517-35. 223. Haughton AM, Belsito DV. Acrylate allergy induced by acrylic nails resulting
197. Barbaud A, Reichert-Penetrat S, Trechot P, Jacquin-Petit MA, Ehlinger A, in prosthesis failure. J Am Acad Dermatol 2008;59(Suppl):S123-4 (III).
Noirez V, et al. The use of skin testing in the investigation of cutaneous 224. Lee PW, Elsaie ML, Jacob SE. Allergic contact dermatitis in children: com-
adverse drug reactions. Br J Dermatol 1998;139:49-58 (IIa). mon allergens and treatment: a review. Curr Opin Pediatr 2009;21:491-8 (IV).
198. Cham PM, Warshaw EM. Patch testing for evaluating drug reactions due to 225. Lewis VJ, Statham BN, Chowdhury MM. Allergic contact dermatitis in 191
systemic antibiotics. Dermatitis 2007;18:63-77 (IV). consecutively patch tested children. Contact Dermatitis 2004;51:155-6 (IIb).
199. Bruynzeel DP, de Groot AC, Weyland JW. Contact dermatitis to lauryl 226. Seidenari S, Giusti F, Pepe P, Mantovani L. Contact sensitization in 1094
pyridinium chloride and benzoxonium chloride. Contact Dermatitis 1987;17: children undergoing patch testing over a 7-year period. Pediatric Dermatol
41-2 (IV). 2005;22:1-5 (III).
200. Lammintausta K, Kortekangas-Savolainen O. The usefulness of skin tests to 227. Kutting B, Brehler R, Traupe H. Allergic contact dermatitis in children: stra-
prove drug hypersensitivity. Br J Dermatol 2005;152:968-74 (IIa). tegies of prevention and risk management. Eur J Dermatol 2004;14:80-5 (IV).
201. Barbaud A. Drug patch testing in systemic cutaneous drug allergy. Toxicology 228. Belhadjali H, Giordano-Labadie F, Rance F, Bazex J. Lucky Luke contact
2005;209:209-16 (IV). dermatitis from diapers: a new allergen? Contact Dermatitis 2001;44:248 (IV).
202. Barbaud A, Trechot P, Reichert-Penetrat S, Granel F, Schmutz JL. The use- 229. Weston WL, Weston JA, Kinoshita J, Kloepfer S, Carreon L, Toth S, et al.
fulness of patch testing on the previously most severely affected site in a Prevalence of positive epicutaneous tests among infants, children, and ado-
cutaneous adverse drug reaction to tetrazepam. Contact Dermatitis 2001;44: lescents. Pediatrics 1986;78:1070-4 (IIa).
259-60 (IV). 230. Fisher AA. Allergic contact dermatitis in early infancy. Cutis 1994;54:300-2 (IV).
203. Brockow K, Romano A, Blanca M, Ring J, Pichler W, Demoly P. General 231. Carder KR. Hypersensitivity reactions in neonates and infants. Dermatol Ther
considerations for skin test procedures in the diagnosis of drug hypersensi- 2005;18:160-75 (IV).
tivity. Allergy 2002;57:45-51. 232. Worm M, Aberer W, Agathos M, Becker D, Brasch J, Fuchs T, et al. Patch
204. Atanaskova Mesinkovska N, Tellez A, Molina L, Honari G, Sood A, testing in childrenrecommendations of the German Contact Dermatitis
Barsoum W, et al. The effect of patch testing on surgical practices and out- Research Group (DKG). J Dtsch Dermatol Ges 2007;5:107-9 (IV).
comes in orthopedic patients with metal implants. Arch Dermatol 2012;148: 233. Jacob SE, Admani S, Herro EM. Invited commentary: recommendation for a North
687-93 (IIb). American pediatric patch test series. Curr Allergy Asthma Rep 2014;14:444 (IV).
205. Schalock PC, Menne T, Johansen JD, Taylor JS, Maibach HI, Liden C, 234. Luckhaupt SE, Dahlhamer JM, Ward BW, Sussell AL, Sweeney MH, Sestito JP,
et al. Hypersensitivity reactions to metallic implantsdiagnostic algorithm et al. Prevalence of dermatitis in the working population, United States, 2010
and suggested patch test series for clinical use. Contact Dermatitis 2011;66: National Health Interview Survey. Am J Indus Med 2013;56:625-34 (IIb).
4-19 (IV). 235. Holness DL. Recent advances in occupational dermatitis. Curr Opin Allergy
206. Reed KB, Davis MD, Nakamura K, Hanson L, Richardson DM. Retrospective Clin Immunol 2013;13:145-50.
evaluation of patch testing before or after metal device implantation. Arch 236. Nicholson PJ, Llewellyn D, English JS. Guidelines Development Group. Ev-
Dermatol 2008;144:999-1007 (III). idence-based guidelines for the prevention, identication and management of
207. Krecisz B, Kiec-Swierczynska M, Chomiczewska-Skora D. Allergy to ortho- occupational contact dermatitis and urticaria. Contact Dermatitis 2010;63:
pedic metal implantsa prospective study. Int J Occup Med Environ Health 177-86 (IIa).
2012;25:463-9 (III). 237. Mathias CG. Contact dermatitis and workers compensation: criteria for
208. Thomas P. Patch testing and hypersensitivity reactions to metallic implants: establishing occupational causation and aggravation. J Am Acad Dermatol
still many open questions. Dermatitis 2013;24:106-7 (IV). 1989;20(Pt 1):842-8 (IV).
209. Granchi D, Cenni E, Giunti A, Baldini N. Metal hypersensitivity testing in 238. Ingber A, Merims S. The validity of the Mathias criteria for establishing
patients undergoing joint replacement: a systematic review. J Bone Joint Surg occupational causation and aggravation of contact dermatitis. Contact
Br 2012;94:1126-34 (Ia). Dermatitis 2004;51:9-12 (III).
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S31
VOLUME 3, NUMBER 3S

239. Warshaw EM, Raju SI, Fowler JF Jr, Maibach HI, Belsito DV, Zug KA, et al. 262. Meingassner JG, Fahrngruber H, Bavandi A. Pimecrolimus inhibits the elici-
Positive patch test reactions in older individuals: retrospective analysis from tation phase but does not suppress the sensitization phase in murine contact
the North American Contact Dermatitis Group, 1994-2008. J Am Acad Der- hypersensitivity, in contrast to tacrolimus and cyclosporine A. J Invest Der-
matol 2012;66:229-40. matol 2003;121:77-80 (IIb).
240. Geier J, Lessmann H, Mahler V, Pohrt U, Uter W, Schnuch A. Occupational 263. Amrol D, Keitel D, Hagaman D, Murray J. Topical pimecrolimus in the
contact allergy caused by rubber glovesnothing has changed. Contact treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol
Dermatitis 2012;67:149-56 (IV). 2003;91:563-6 (IIa).
241. Liskowsky J, Geier J, Bauer A. Contact allergy in the cleaning industry: 264. Granlund H, Erkko P, Reitamo S. Comparison of the inuence of cyclosporine
analysis of contact allergy surveillance data of the Information Network of and topical betamethasone-17,21-dipropionate treatment on quality of life in
Departments of Dermatology. Contact Dermatitis 2011;65:159-66 (III). chronic hand eczema. Acta Dermato-Venereol 1997;77:54-8 (Ib).
242. Dever TT, Walters M, Jacob S. Contact dermatitis in military personnel. 265. Murphy GM, Maurice PD, Norris PG, Morris RW, Hawk JL. Azathioprine
Dermatitis 2011;22:313-9 (III). treatment in chronic actinic dermatitis: a double-blind controlled trial with
243. Guin JD, Franks H. Fingertip dermatitis in a retail orist. Cutis 2001;67: monitoring of exposure to ultraviolet radiation. Br J Dermatol 1989;121:
328-30 (III). 639-46 (Ib).
244. Mascarenhas R, Robalo-Cordeiro M, Fernandes B, Oliveira HS, Goncalo M, 266. Rosen K, Mobacken H, Swanbeck G. Chronic eczematous dermatitis of the
Figueiredo A. Allergic and irritant occupational contact dermatitis from Al- hands: a comparison of PUVA and UVB treatment. Acta Dermato-Venereol
stroemeria. Contact Dermatitis 2001;44:196-7 (III). 1987;67:48-54 (Ib).
245. Gette MT, Marks JE Jr. Tulip ngers. Arch Dermatol 1990;126:203-5 (III). 267. van Gils RF, Boot CR, van Gils PF, Bruynzeel D, Coenraads PJ, van
246. Bruynzeel DP. Bulb dermatitis. Dermatological problems in the ower bulb Mechelen W, et al. Effectiveness of prevention programmes for hand
industries. Contact Dermatitis 1997;37:70-7 (IV). dermatitis: a systematic review of the literature. Contact Dermatitis 2011;64:
247. El-Azhary RA, Yiannias JA. A new patient education approach in contact 63-72 (Ib).
allergic dermatitis: the Contact Allergen Replacement Database (CARD). Int J 268. Saary J, Qureshi R, Palda V, DeKoven J, Pratt M, Skotnicki-Grant S, et al.
Dermatol 2004;43:278-80 (IV). A systematic review of contact dermatitis treatment and prevention. J Am
248. Yiannias JA, Miller R, Kist JM. Creation, history, and future of the Contact Acad Dermatol 2005;53:845 (Ib).
Allergen Replacement Database (CARD). Dermatitis 2009;20:322-6 (IV). 269. Emmett EA. Dermatological screening. J Occup Med 1986;28:1045-50 (IV).
249. Julander A, Skare L, Vahter M, Liden C. Nickel deposited on the skin-visu- 270. Dickel H, Kuss O, John SM, Blome O, Hagemann KH, Schwanitz HJ. Early
alization by DMG test. Contact Dermatitis 2011;64:151-7. secondary prevention of occupational skin disease in Germany: the derma-
250. Thyssen JP, Skare L, Lundgren L, Menne T, Johansen JD, Maibach HI, et al. tologists procedure in perspective. Int Arch Occup Environ Health 2004;77:
Sensitivity and specicity of the nickel spot (dimethylglyoxime) test. Contact 142-9 (III).
Dermatitis 2010;62:279-88 (IIa). 271. Apfelbacher CJ, Soder S, Diepgen TL, Weisshaar E. The impact of mea-
251. Thyssen JP, Menne T, Johansen JD, Liden C, Julander A, Moller P, et al. sures for secondary individual prevention of work-related skin diseases in
A spot test for detection of cobalt releaseearly experience and ndings. health care workers: 1-year follow-up study. Contact Dermatitis 2009;60:
Contact Dermatitis 2010;63:63-9 (IIb). 144-9 (III).
252. Midander K, Julander A, Skare L, Thyssen JP, Liden C. The cobalt spot test 272. Wulfhorst B, Bock M, Gediga G, Skudlik C, Allmers H, John SM. Sustain-
further insights into its performance and use. Contact Dermatitis 2013;69: ability of an interdisciplinary secondary prevention program for hairdressers.
280-7 (IIb). Int Arch Occup Environ Health 2010;83:165-71 (III).
253. Liden C, Skare L, Lind B, Nise G, Vahter M. Assessment of skin exposure to 273. Cahill J, Nixon R. Allergic contact dermatitis to methylprednisolone aceponate
nickel, chromium and cobalt by acid wipe sampling and ICP-MS. Contact in a topical corticosteroid. Aust J Dermatol 2004;45:192-3.
Dermatitis 2006;54:233-8 (IIb). 274. Wall LM, Gebauer KA. A follow-up study of occupational skin disease in
254. Liden C, Skare L, Nise G, Vahter M. Deposition of nickel, chromium, and Western Australia. Contact Dermatitis 1991;24:241-3 (III).
cobalt on the skin in some occupationsassessment by acid wipe sampling. 275. Rosen RH, Freeman S. Prognosis of occupational contact dermatitis in New
Contact Dermatitis 2008;58:347-54 (IIb). South Wales, Australia. Contact Dermatitis 1993;29:88-93 (III).
255. Bourke J, Coulson I, English J. British Association of Dermatologists Therapy 276. Cvetkovski RS, Zachariae R, Jensen H, Olsen J, Johansen JD, Agner T.
Guidelines and Audit Subcommittee. Guidelines for the management of con- Prognosis of occupational hand eczema: a follow-up study. Arch Dermatol
tact dermatitis: an update. Br J Dermatol 2009;160:946-54 (IV). 2006;142:305-11 (III).
256. Diepgen TL, Elsner P, Schliemann S, Fartasch M, Kollner A, Skudlik C, et al. 277. Malkonen T, Alanko K, Jolanki R, Luukkonen R, Aalto-Korte K, Lauerma A,
Guideline on the management of hand eczema ICD-10 Code: L20, L23, L24, et al. Long-term follow-up study of occupational hand eczema. Br J Dermatol
L25, L30. J Dtsch Dermatol Ges 2009;7(Suppl 3):S1-16 (IV). 2010;163:999-1006 (III).
257. Veien NK, Olholm Larsen P, Thestrup-Pedersen K, Schou G. Long-term, 278. Adisesh A, Meyer JD, Cherry NM. Prognosis and work absence due to
intermittent treatment of chronic hand eczema with mometasone furoate. Br J occupational contact dermatitis. Contact Dermatitis 2002;46:273-9.
Dermatol 1999;140:882-6 (Ib). 279. Holness DL. Workers with occupational contact dermatitis: work outcomes
258. Dooms-Goossens A, Pauwels M, Bourda A, Degreef H, Kinget R. Patch testing and return to work process in the rst six months following diagnosis.
with corticosteroids in xerogel formulations. Contact Dermatitis 1992;26:206-7. J Allergy 2011;2011:170693.
259. Dooms-Goossens A, Morren M. Results of routine patch testing with corti- 280. Holness DL, Nethercott JR. Work outcome in workers with occupational skin
costeroid series in 2073 patients. Contact Dermatitis 1992;26:182-91. disease. Am J Indus Med 1995;27:807-15.
260. Davis MD, el-Azhary RA, Farmer SA. Results of patch testing to a cortico- 281. Meding B, Lantto R, Lindahl G, Wrangsjo K, Bengtsson B. Occupational
steroid series: a retrospective review of 1188 patients during 6 years at Mayo skin disease in Swedena 12-year follow-up. Contact Dermatitis 2005;53:
Clinic. J Am Acad Dermatol 2007;56:921-7 (III). 308-13.
261. Belsito D, Wilson DC, Warshaw E, Fowler J, Ehrlich A, Anderson B, et al. 282. Lau MY, Matheson MC, Burgess JA, Dharmage SC, Nixon R. Disease
A prospective randomized clinical trial of 0.1% tacrolimus ointment in a model severity and quality of life in a follow-up study of patients with occupational
of chronic allergic contact dermatitis. J Am Acad Dermatol 2006;55:40-6 (IIb). contact dermatitis. Contact Dermatitis 2011;65:138-45.
S32 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
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APPENDIX A. MEMBERS OF THE JOINT TASK development of practice parameters; selects the workgroup chair(s);
FORCE CONTACT DERMATITIS PARAMETER and reviews drafts of the parameters for accuracy, practicality, clarity,
WORKGROUP, REVIEWERS OF THE CONTACT and broad utility of the recommendations for clinical practice.
DERMATITIS PARAMETER, AND MEMBERS OF Joann Blessing-Moore, MD
THE JOINT TASK FORCE ON PRACTICE Adjunct Professor of Medicine and Pediatrics
PARAMETERS Stanford University Medical Center
Department of Immunology
CONTACT DERMATITIS WORK GROUP Palo Alto, California
The Joint Task Force has made a concerted effort to acknowledge
all contributors to this parameter. If any contributors have been David A. Khan, MD
excluded inadvertently, the Task Force will ensure that appropriate Associate Professor of Internal Medicine
recognition of such contributions is made subsequently. University of Texas Southwestern Medical Center
Dallas, Texas
WORKGROUP CHAIR AND CHIEF CO-EDITOR
David M. Lang, MD
Luz Fonacier, MD Head, Allergy/Immunology Section
Professor of Medicine Respiratory Institute
State University of New York at Stony Brook Director, Allergy and Immunology Fellowship Training Program
Head of Allergy & Training Program Director Cleveland Clinic Foundation
Winthrop University Hospital Cleveland, Ohio
Mineola, New York
Richard A. Nicklas, MD
Clinical Professor of Medicine
JOINT TASK FORCE LIAISON AND CHIEF CO-EDITOR
George Washington Medical Center
David Bernstein, MD Washington, DC
Professor of Clinical Medicine and Environmental Health John Oppenheimer, MD
Division of Immunology, Allergy and Rheumatology Department of Internal Medicine
University of Cincinnati College of Medicine New Jersey Medical School
Cincinnati, Ohio Pulmonary and Allergy Associates
OTHER WORK GROUP MEMBERS: Morristown, New Jersey

Karin Pacheco, MD Jay M. Portnoy, MD

Associate Professor Chief, Section of Allergy, Asthma & Immunology
Division of Environmental & Occupational Health Sciences The Childrens Mercy Hospital
Department of Medicine Professor of Pediatrics
National Jewish Health and University of Missouri-Kansas City School of Medicine
University of Colorado School of Public Health Kansas City, Missouri
Denver, Colorado Christopher C. Randolph
D. Linn Holness, MD Professor
Professor Pediatrics/Allergy/Immunology
Dalla Lana School of Public Health and Department of Medicine Yale Afliated Hospitals
University of Toronto Center for Allergy, Asthma, & Immunology
Toronto, Canada Waterbury, Connecticut
Diane E. Schuller, MD
REVIEWERS
Emeritus, Professor of Pediatrics
Marcella Aquino, MDMineola, New York Emeritus Chief of Allergy and Immunology
Leonard Bielory, MDSpringeld, New Jersey Pennsylvania State University, Milton S. Hershey Medical College
Earnest Charlesworth, MDSan Angelo, Texas Hershey, Pennsylvania
Sharon Jacob, MDLoma Linda, California Sheldon L. Spector, MD
Michael Keiley, MDBoise, Idaho Clinical Professor of Medicine
Maeve OConnor, MDCharlotte, North Carolina UCLA School of Medicine
Jacob Thyssen, MDGentofte, Denmark Los Angeles, California

JOINT TASK FORCE ON PRACTICE PARAMETERS Stephen A. Tilles, MD

Clinical Assistant Professor of Medicine
MEMBERS
University of Washington School of Medicine
The Joint Task Force on Practice Parameters is a 13-member task Redmond, Washington
force consisting of 6 representatives assigned by the American Dana Wallace MD
Academy of Allergy, Asthma & Immunology, 6 by the American Assistant Clinical Professor of Medicine
College of Allergy, Asthma & Immunology, and 1 by the Joint Nova Southeastern University College of Osteopathic Medicine
Council of Allergy and Immunology. This task force oversees the Davie, Florida
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S33
VOLUME 3, NUMBER 3S

APPENDIX B. CLASSIFICATION OF Category of Evidence

RECOMMENDATIONS AND EVIDENCE
Recommendation Rating Scale Ia Evidence from meta-analysis of randomized controlled
trials
Statement Definition Implication Ib Evidence from at least one randomized controlled trial
IIa Evidence from at least one controlled study without
Strong A strong recommendation means Clinicians should
randomization
recommen- the benets of the follow a strong
dation recommended approach clearly recommendation
IIb Evidence from at least one other type of quasi-experi-
(StrRec) exceed the harms (or that the unless a clear and mental study
harms clearly exceed the compelling III Evidence from nonexperimental descriptive studies, such
benets in the case of a strong rationale for an as comparative studies
negative recommendation) and alternative IV Evidence from expert committee reports or opinions or
that the quality of the approach is clinical experience of respected authorities or both
supporting evidence is present.
excellent (Grade A or B)*. In Strength of Recommendation*
some clearly identied
circumstances, strong A Directly based on category I evidence
recommendations may be B Directly based on category II evidence or extrapolated
made based on lesser evidence
recommendation from category I evidence
when high-quality evidence is
impossible to obtain and the
C Directly based on category III evidence or extrapolated
anticipated benets strongly recommendation from category I or II evidence
outweigh the harms. D Directly based on category IV evidence or extrapolated
Moderate A recommendation means the Clinicians should recommendation from category I, II, or III evidence
(Mod) benets exceed the harms (or also generally LB Laboratory based
that the harms exceed the follow a NR Not rated
benets in the case of a recommendation
negative recommendation), but but should remain
the quality of evidence is not as alert to new APPENDIX C. ALLERGENS ASSOCIATED WITH
strong (Grade B or C)*. In information and
some clearly identied sensitive to
SYSTEMIC CONTACT DERMATITIS
circumstances, patient
recommendations may be preferences. Contact sensitizer Systemic reaction to
made based on lesser evidence
Glucocorticoids Oral corticosteroids
when high-quality evidence is
impossible to obtain and the Benadryl cream Oral diphenhydramine
anticipated benets outweigh Neomycin Oral neomycin
the harms. Penicillin Oral penicillin
Weak (Weak) A weak recommendation means Clinicians should be Sulfonamide Para-amino sulfonamide hypoglycemics
that either the quality of exible in their (tolbutamide, chlorpropamide)
evidence that exists is suspect decision making Thiuram Antabuse
(Grade D)* or that well-done regarding Colophony, balsam of Spices: clove, nutmeg, cinnamon, cayenne
studies (Grade A, B, or C)* appropriate Peru, fragrance mix pepper
show little clear advantage to practice, although
Ethylenediamine Aminophylline
one approach vs another. they may set
Piperazine and ethanolamine (Atarax,
bounds on
Antivert)
alternatives;
patient preference Nickel Nickel in tap water, utensils, and food
should have a
substantial
inuencing role.
No recommen- No recommendation means there Clinicians should APPENDIX D. SPECIAL OCCUPATIONAL PATCH
dation is both a lack of pertinent feel little
(NoRec) evidence (Grade D)* and an constraint in their
TEST ALLERGEN PANELS
unclear balance between decision making  Bakery
benets and harms. and be alert to
 Dental screeninghealth care providers
new published
evidence that
 Dental screeningpatients
claries the  Hairdressing
balance of benet  Machinistsoil & cooling uids and/or metalworking
vs harm; patient  Photographic chemicals
preference should
have a substantial
inuencing role.
*Refer to the next column.
S34 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

APPENDIX E. ALLERGEN PANELS BASED ON APPENDIX H. TRUE TEST PANEL ALLERGENS

SPECIFIC EXPOSURES
Panel 1.2
 Cosmetics Nickel sulfate
 Epoxy series Wool alcohols
 Eyelid dermatitis Neomycin sulfate
 Footwear and/or shoes Potassium dichromate
 Fragrance and/or perfumes Caine mix
 Isocyanates Fragrance mix
 Methacrylate series: adhesives, dental, nails, and others Colophony
 Photoallergens Paraben mix
 Photochemicals and/or photopatch Negative control
 Plastics and glues Balsam of Peru
 Rubber additives and/or chemicals Ethylenediamine dihydrochloride
 Sunscreens Cobalt dichloride
 Textile colors and nish
Panel 2.2
APPENDIX F. MEDICATIONS, TREATMENTS, AND p-tert-Butylphenol formaldehyde resin
FOOD PANELS Epoxy resin
Carba mix
 Antibiotics and/or antimycotics Black rubber mix
 Corticosteroids Cl Me isothiazolinone (MCI/MI)
 Local anesthetics Quaternium-15
 Medicinal substances Methyldibromo glutaronitrile
 Antimicrobials and/or preservatives p-Phenylenediamine
 External agents and/or emulsiers Formaldehyde
 Food additives Mercapto mix
 Leg ulcer Thimerosal
 Metal compounds and implants Thiuram mix
 Plants and/or compounds of natural origin
Panel 3.2
APPENDIX G. SOURCE OF PATCH TEST Diazolidinyl urea
ALLERGENS Quinoline mix
Tixocortol-21-pivalate
Sources of Patch Test Allergens Gold sodium thiosulfate
Imidazolidinyl urea
AllergEAZE by Smart Practice Canada Budesonide
SmartPractice Canada
Hydrocortizone-17-butyrate
2175 29th Street NE, Unit 90
Calgary, AB T1Y 7H8
Mercaptobenzothiazole
Phone: 866-903-2671 Bacitracin
Fax: 866-903-2672 Parthenolide
E-mail: [email protected] Disperse blue 106
Dormer.com: http://www.dormer.com/Allergens/ReimCan.aspx 2-Bromo-2-nitropropane-1,3-diol (Bronopol)
91 Keleld, Suite 5
Rexdale, Ontario M9W 5A3
Phone: (416) 242 6167
Fax: (416) 242 9487 or 1-877-436-7637
True Test (Smart Practice): http://www.truetest.com/
Allerderma SmartPractice afliate
3400 E. McDowell Rd.
Phoenix, AZ 85008-7899
Customer Service: 1-800-878-3837
E-mail: [email protected]
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S35
VOLUME 3, NUMBER 3S

APPENDIX I. EXAMPLE OF A PATCH TEST FORM

Patch # Contact Allergen 1st Read 2nd Read 3rd Read Interpretation Relevance

DATE
1 2,5-diazolidinylurea (Germall II) 1.0% pet
2 bisphenol A epoxy resin 1.0% pet
3 2-bromo-2-nitropropane-1,3-diol (Bronopol) 0.5% pet
4 2-hydroxy-4-methoxy-benzophenone 10.0% pet
5 2-mercaptobenzothiazole 1.0% pet
6 4-chloro-3,5-xylenol (PCMX) 1.0% pet
7 4-phenylenediamine base 1.0% pet
8 4-tert-butylphenol formaldehyde resin 1.0% pet
9 methychloroisothiazolinone/methylisothiazolinone 0.1% water
10 amidoamine (stearamidopropyl dimethylamine) 0.1% water
11 bacitracin 20.0% pet
12 balsam of Peru 25.0% pet
13 benzocaine 5.0% pet
14 bisphenol F 1.0% pet
15 black rubber mix 0.6% pet
16 budesonide 0.1% pet
17 budesonide 0.01% pet
18 carba mix 3.0% pet
19 cinnamic aldehyde 1.0% pet
20 clobetasol-17-propionate 1.0% pet
21 cobalt (II) chloride hexahydrate 1.0% pet
22 cocamidopropyl betaine 1.0% water
23 coconut diethanolamide (cocamide DEA) 0.5% pet
24 colophony 20% pet
25 petrolatum
26 dibucaine (cinchocaine-HCl) 2.5% pet
27 dimethylol dihydroxyethyleneurea 4.5% water
28 disperse blue 106 1.0% pet
29 dl alpha tocopherol acetate 100%
30 DMDM hydantoin 1.0% pet
31 ethyl acrylate 0.1% pet
32 ethylenediamine dihydrochloride 1.0% pet
33 ethyleneurea, melamine formaldehyde mix 5.0% pet
34 formaldehyde 1.0% water
35 fragrance mix 8.0% pet
(Continued)
S36 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

APPENDIX I. (Continued)
Patch # Contact Allergen 1st Read 2nd Read 3rd Read Interpretation Relevance

36 glutaraldehyde 0.3% pet

37 glyceryl monothioglycolate 1.0% pet
38 Hydrocortisone 1.0% pet
39 imidazolidinyl urea (Germall 115) 2% pet
40 iodopropynyl butyl carbamates 0.5% pet
41 iodopropynyl butyl carbamates 0.1% pet
42 jasmine abs 2.0% pet
43 llidocaine-HCl 15.0% pet
44 mercapto mix A 1.0% pet
45 methyl methacrylate 2.0% pet
46 methyldibromo glutaronitrile phenoxyethanol(MDGN/PE) 2.0% pet
47 neomycin sulphate 20.0% pet
48 nickel sulfate hexahydrate 2.5% pet
49 paraben mix 12% pet
50 potassium dichromate 0.25% pet
51 propylene glycol 5% pet
52 quaternium 15 2.0% pet
53 sesquiterpenelactone mix 0.1% pet
54 tea tree oil, oxidized 5% pet
55 thiourea 1.0% pet
56 thiuram mix 1.0% pet
57 tixocortol-21-pivalate 1.0% pet
58 tosylamideformaldehyde resin 1.0% pet
59 Triamcinoloneacetonide 1.0% pet
60 wool alcohols (lanolin) 100%
61 ylang ylang oil 2.0% pet
62 benzyl alcohol 1.0% pet
63 desoximetasone 1.0% pet
64 fragrance mix II 14.0% pet
65 propolis 10.0% pet
66 (2-hydroxyethyl)-methacrylate 2.0% pet

Patch # Personal products

Physician Signature Date

PATCH TEST MORPHOLOGY CODES

() Negative reaction
(?) Doubtful reaction with faint erythema only
(1) Weak positive reaction with non vesicular erythema, inltration, possible papules
(2) Strong positive reaction with vesicular erythema, inltration and papules
(3) Extreme positive reaction with intense erythema and inltration coalescing vesicles, bullous reaction
(IR) Irritant reaction

PATCH TEST INTERPRETATION CODES

N Negative
A Allergic
U Unknown
I Irritant

RELEVANCE
Denite: if a use test with the putative item containing the suspected allergen is positive or positive patch to object/product
Probable: if the substance identied by patch testing can be veried as present in the known skin contactants of the patient.
Possible :if the patient is exposed to circumstances in which skin contact with materials known to contain the putative allergen will likely occur
Past
Unknown
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S37
VOLUME 3, NUMBER 3S

APPENDIX J. STRUCTURAL GROUPS OF CORTICOSTEROIDS AND POTENCY CLASSIFICATION WITH

EXAMPLES OF COMMERCIALLY AVAILABLE PREPARATIONS

A: Hydrocortisone
Hydrocortisone & C: BTM D2: MPL aceponate
tixocortol pivalate: B: TCL acetonide nonesterified D1: BTM-dipropionate labile esters w/o C16
has C17 or C21 short Acetonides: has C16 C17 Betamethasone: has C16 methyl group & methyl nor B ring
Steroid group chain ester cis-ketal or -diol additions has C16 methyl group halogenated B ring halogen substitution

Prevalence 2.7% 1.5% <0.2% 0.8% 0.8%

Class 7: Least HC
Potent [Hytone C/L (1%/
2.5%)]
[Cortaid, C/O/Sp]
[Egocort C 1%]
HC Acetate
[Cortisone, Lanacort,
Wellcortin, Gynecort,
Lanacort]
Class 6: Low Desonide Aclometasone
[DesOwen (0.05%) C/L] dipropionate
FLU acetonide [Aclovate C/O (0.05%)]
[Capex Sh, Dermasmooth
F/S/ oil (0.01%)]
TCL acetonide
[Aristocort A C, Kenalog L
(0.025%)]
Class 5: Lower Desonide Fluticasone HC-17-valerate
Mid [Tridesilon, DesOwen O propionate [Westcort C (0.2%)]
(0.05%)] [Cutivate C (0.05%)] Prednicarbate
FLU acetonide [DermAtop C (0.1%)]
[Synalar, Synemol C
(0.025%)]
Flurandrenolide
[Cordran C/L/Tape
(0.05%)]
Class 4: Mid FLU acetonide Desoximetasone Mometasone Furorate HC 17-butyrate
[Synalar, Synemol [Topicort LP C/O [Elocon C/L (0.1%)] [Locoid C/L/O (0.1%)]
(0.01%-0.2%)] (0.05%)] HC-17-valerate
Flurandrenolide [Westcort O (0.2%)]
[CordranO (0.05%)]
TCL acetonide
[Kenalog, Aristocort A O
(0.1%)]
Class 3: Upper TCL acetonide Halometasone BTM 17 valerate
Mid [Kenalog, Aristocort C [Halometasone (0.05%)] [Luxiq F (0.12%)]
(0.5%)] [Valisone O (0.1%)]
Triamcinolone Diacetate BTM dipropionate
[Amcort, Aristocort C/O [Diprosone C (0.05%)]
(0.025%-0.1%)] Clobetasone 17
butyrate
[Eumovate C (0.05%)]
Fluticasone
propionate
[Cutivate O (0.005%)]
Mometasone Furorate
[Elocon O (0.1%)]
(Continued)
S38 FONACIER ET AL J ALLERGY CLIN IMMUNOL PRACT
MAY/JUNE 2015

APPENDIX J. (Continued)
A: Hydrocortisone
Hydrocortisone & C: BTM D2: MPL aceponate
tixocortol pivalate: B: TCL acetonide nonesterified D1: BTM-dipropionate labile esters w/o C16
has C17 or C21 short Acetonides: has C16 C17 Betamethasone: has C16 methyl group & methyl nor B ring
Steroid group chain ester cis-ketal or -diol additions has C16 methyl group halogenated B ring halogen substitution

Class 2: High Amcinonide Desoximetasone BTM 17 valerate

[Cyclocort O/L/C (0.05%- [Topicort C/O (0.25%)] [Betnovate C/O (0.1%)]
0.1%)] [Topicort G (0.05%)] BTM dipropionate
Fluocinonide Clocortolone [Diprolene AF C
[Lidex C/G/O/S (0.05%)] [Cloderm C ( 0.1%)] (0.05%)]
Halcinonide [Diprosone O (0.05%)]
[Halog C/O/S (0.05%-
0.1%)]
Class 1: Super Fluocinonide BTM dipropionate
[Vanos C (0.1%)] [Diprolene O/G/L
(0.05%)]
Clobetasol propionate
[Clobex L/spray/sh,
Dermovate C/O,
Olux F, Temovate C/
O/S/G (0.05%)]
[Olux F (0.05%)]
Diorasone Diacetate
[ApexiCon, Psorcon C/
O, Florone O
(0.05%)]
Halobetasol
[Ultravate C/O
(0.05%)]
Oral/Systemic Cortisone acetate Budesonide BTM sodium phosphate BTM Oral/IM BTM HC Oral/IV
Preparation HC-21-acetate TCM Injectable Suspension dipropionate
MPL acetate [Atolone Tablets (I)] [Celestone]
[Medrol] TCM benetonide Dexamethasone acetate
intra-articular, TCM diacetate Dexamethasone-sodium
intralesional, TCM hexacetonide phosphate Injection
intrasynovial [Decadron]
Prednisone Paramethasone acetate
[Cortan, Deltasone,
Meticorten, Orasone]
Prednisoloneacetate
[Prediapred, Prelone
syrup]
Cloprednol
Fludrocortisone
Acetate
[Florinef]
HC sodium
[Solucortef]
Cross Reactions Cross reacts with D2 Budesonide specically Cross reacts with Class
cross-reacts with D2 A & Budesonide
Patch Test Tixocortol 21-pivalate Budesonide Clobetasole-17- HC-17-butyrate
Substance TCL acetonide propionate

(Continued)
J ALLERGY CLIN IMMUNOL PRACT FONACIER ET AL S39
VOLUME 3, NUMBER 3S

APPENDIX J. (Continued)
A: Hydrocortisone
Hydrocortisone & C: BTM D2: MPL aceponate
tixocortol pivalate: B: TCL acetonide nonesterified D1: BTM-dipropionate labile esters w/o C16
has C17 or C21 short Acetonides: has C16 C17 Betamethasone: has C16 methyl group & methyl nor B ring
Steroid group chain ester cis-ketal or -diol additions has C16 methyl group halogenated B ring halogen substitution

International and Cloprednol Flucoronide procinonide Diuocortolone HC aceponate

other [Syntestan (Germany)] [Topilar] (pivalate, valerate) [Efcort]
noncutaneous Dichlorisone Acetate Budesonide [Naricort C [Nerisone C C/O] MPL aceponate
preparations [Dermaren (Spain)] 0.025%] Flumethasone (Vet use) [Advantan C/O]
Fluprednisolone [Pulmicort INH, Rhinocort Fluocortin butyl
acetate NS Butacort, Entocort] [Vaspit (Spain)]
[Medinost (Georgia)] Fluocinonide Fluocortolone
[Prednisolon STADA [Aerobid INH] (hexanoate, pivalate,
(Germany)] Flunisolide caproate)
Meprednisone [Aerospan] [Ultralan] [Ultraproct]
[Cortipyren [Nasalide NS] Fluprednidene acetate
(Argentina)] Triamcinalone acetonide [Decoderm]
[Deltisona B [Azmacort INH]
(Argentina)]
[Meprednisona All Pro,
(Argentina)]
Tixocortol
[Pivalone]
[Thiovalone]
Fluorometholone
[FML Oph O]
Medrysone
[HMS 1.0%]
[LIQUIFILM Oph Su]
Prednisolone acetate
[Pred Forte,
Blephamide Oph]
HC, hydrocortisone; MPL, methylprednisolone; BTM, betamethasone; FLU, uocinolone; TCL, triamcinolone; CLO, clobetasol; C, cream; O, ointment; L, lotion; F, foam;
G, gel; S, solution; Su, suspension; Sp, spray; Sh, shampoo; Inh, inhaler; Oph, ophthalmic; NS, nasal spray.
In parenthesis are examples of products available. For this manuscript the allergenicity is classied as Groups A, B, C, D1, and D2 and the potency is from Class 1-7; 1 being the
most potent and 7 being the weakest class. The classication of potency may vary depending on factors such as the vehicle and reference source.