Journal Reading Kulit - Nixal Kurniawan (En)

Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 18

Current Dermatology Reports (2022) 11:41–51

https://doi.org/10.1007/s13671-021-00351-4

CONTACT DERMATITIS (BRANDON ADLER AND VINCENT DELEO, SECTION EDITORS)

Irritant Contact Dermatitis — a Review


Kajal Patel1 · Rosemary Nixon1

Accepted: 3 December 2021 / Published online: 7 April 2022


© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022

Abstract
Purpose of Review Irritant contact dermatitis is the most common form of contact dermatitis and the most common occu-
pational skin disease. This review provides a comprehensive summary of the endogenous and exogenous factors that play
a role in the pathogenesis of irritant contact dermatitis.
Recent Findings In conjunction with avoidance of irritants, barrier protection, and regular application of moisturizers,
management now emphasizes the importance of primary prevention through educational initiatives in high-risk
workplaces. Summary The diagnosis of irritant contact dermatitis is often difficult, as there is no confirmatory test, and it
is often a default diagnosis after allergic contact dermatitis has been excluded. Early recognition, prevention, and treatment
are vital in management, especially in the occupational setting.

Keywords Irritant contact dermatitis · Skin irritation · Occupational · Hand · Allergy · Patch testing

Introduction
The purpose of this review is to provide a
Irritant contact dermatitis (ICD) is an inflammatory cutane- comprehensive update with regard to the pathogenesis, risk
ous condition caused by skin barrier disruption, in combi- factors, clinical features, and management of ICD.
nation with the activation of innate immune responses.
ICD results from skin barrier damage from external agents
or environmental factors. ICD commonly affects the hands Contributing Factors in the Development
and can affect people of all ages and sex. ICD is more of ICD
prevalent than allergic contact dermatitis (ACD) [1] and is
the most common presentation of occupational skin disease Both exogenous and endogenous factors play a vital role in
(OSD). At a tertiary referral occupational dermatology the pathogenesis of ICD [5].
clinic in Australia, ICD was diagnosed in 71% of patients
with OSD [2••]. However, in the general patch testing
population, the most common diagnosis is ACD with a Exogenous
default diagnosis of an endogenous dermatitis, so ICD is
less commonly diag- nosed [3]. High-risk occupations for Skin Irritants
ICD include healthcare workers, food service workers,
metal workers, hairdressers, and construction workers [4]. The most common skin irritant is wet work [6] followed by
soaps, detergents, solvents, and oils [7]. Wet work has been
This article is part of the Topical Collection on Contact Dermatitis defined as:

1. Exposure of skin to liquid for > 2 h per day


2. Use of occlusive gloves for > 2 h per day or change of
 Kajal Patel Carlton 3053, Australia
[email protected]
Rosemary Nixon
[email protected]
1
Occupational Dermatology Research and Education
Centre, Skin Health Institute, Level 1/80 Drummond Street,

13
2 Current Dermatology Reports (2022) 11:41–51
gloves > 20 times per day
3. Frequent hand washing > 20 times per day or use of
hand disinfectants > 20 times per day [8]

Exposure to wet work can occur both at work as


well as at home. High-risk occupations involving wet
work include cleaners, butchers, cooks, beauticians,
and health care

13
Current Dermatology Reports (2022) 11:41–51

workers [9•]. The only regulations regarding exposure to Susceptibility of the skin to irritants decreases with age. It
wet work are found in Germany, the Technical Standards is postulated that differences in microcirculatory efficiency,
for Hazardous Substances (TRGS) 401[10], a guideline for
employers, providing information on occupational
hazardous skin exposure and prevention of OSD.
Since the start of the COVID-19 pandemic, the use of
soaps and alcohol-based hand sanitizers (ABHS) and the
frequency of handwashing have increased significantly
[11] resulting in a higher incidence of ICD [12, 13].
The potency of a chemical irritant and its ability to
pene- trate the skin are denoted by its properties including
molecu- lar size, ionization state, and fat solubility.
Different irritants target different structures in the
epidermis. For example, sodium lauryl sulfate targets
lipid synthesis [14] whereas acetone targets the
proliferation of basal keratinocytes [15]. Factors such as
concentration, volume, and duration of irri- tant exposure
will all contribute to an irritant’s ability to pen- etrate the
skin. Increasing the volume and duration of exposure will
enhance the ability of an irritant to penetrate the skin [16].
Increasing intervals between exposures will usually reduce
the chance of irritation. Recurrent irritant exposure may
result in an additive effect, with repeated exposures initially
inducing an increase, then a reduction in trans-epidermal
water loss (TEWL)
[17] , indicating functional adaptation or skin hardening.

Physical, Mechanical, and Environmental Factors

The role of physical, mechanical, and environmental factors


in the development of ICD is often ignored. Mechanical
factors include occlusion, friction, pressure, and vibration.
The use of gloves or clothing can create an occlusive,
humid environ- ment, which increases irritation caused by
heat and sweating. Environmental factors include heat,
cold, humidity, and UV irradiation. Exposure of skin to
heat often results in sweating. The retention of sweat can
contribute to skin irri- tation, as sweat is more irritating
than water [18]. Heat, espe-
cially in combination with occlusion, can precipitate ICD.
Exposure to low ambient humidity and cold
temperatures are contributing factors to reduced water
content in the stra- tum corneum (SC) and as a result
increase the permeability of irritants in the skin. Cold
temperatures have also been associated with reducing the
plasticity of the horny layer with subsequent cracking of
the SC; however, a study has shown that exposure to cold
averted the development of ICD [19].

Endogenous

Age

13
4 Current Dermatology Reports (2022) 11:41–51
percutaneous penetration, SC turnover time, and loss of
cor- neocyte cohesion [20] associated with increasing age
cause a slower and less intense response to irritants. This
is reflected in the decrease of TEWL in aged skin [21].

Sex

ICD is more common in women [22], likely as a result of


greater exposure to irritants rather than biological
factors. A study from Denmark showed women had 78%
higher odds of engaging in occupations involving wet
work [9•]. It is not clear whether women have a greater
susceptibility to irritants, given that experimental studies
show no dif- ference of irritant reactivity between sexes
[21]. However, one study produced differing results [23]
demonstrating an increased skin reactivity in males
compared to females. Further studies are required to
determine the difference in risk of developing ICD
between sexes.

Race

There is a paucity of evidence to demonstrate a significant


difference between black or Asian and Caucasian skin.
Studies using bioengineering techniques showed no
differ- ence in irritant susceptibility between black and
Caucasian skin [24] despite conflicting results from
previous studies that relied on visual scoring [25]. A study
showed Asian skin was significantly more susceptible to
ICD when com- pared to Caucasian skin both in
subjective and objective skin measurements [26].

Atopy

Atopy is a recognized risk factor for ICD involving the


hands [27]. Mucosal atopy is less predictive of irritant
reactivity, compared to prior atopic dermatitis (AD) [28].
Individuals with a history of AD are thought to
have a higher risk for the development of ICD, relating to
impairment of the epidermal barrier, higher TEWL, and
increased skin permeability to allergens and irritants,
com- pared to those with clinically normal skin [29].

Genetic Factors

Filaggrin is a protein which plays a role in skin barrier


function and SC hydration. Filaggrin loss-of-function
mutations are associated with increased expression of
interleukin (IL)-1, a cytokine which is key to the
initia- tion of the inflammatory response in ICD [30].
A study has shown an increased risk of the
development of ICD in individuals with filaggrin loss-
of-function mutations;

13
Current Dermatology Reports (2022) 11:41–51 43

however, it was observed that the association was depend- the secretion of further chemokines including CXCL 8, CCL
ent on the presence of atopy [31]. Atopy, in combination 20,
with filaggrin loss-of-function mutation carrier status, has
shown to contribute to the severity of ICD affecting the
hands [32].
Single nucleotide polymorphisms (SNPs) within the
major histocompatibility complex (MHC) class I, II, and
III are significantly associated with skin response to
irritants [33, 34]. MHC SNPs have been demonstrated to
contribute to chemical irritancy thresholds, with different
MHC vari- ants being associated with different chemical
irritants. At present, the exact mechanism is unknown.
A link has been recognized between a tumor necro-
sis factor (TNF)-α gene polymorphism and susceptibility
to ICD. At the position P308 within the promoter region
of the TNF-α gene, a G to A transition polymorphism has
been detected. A study of genotypes showed an association
between the A allele and a low irritant threshold [35],
which has also been significantly linked to contact
sensitization to allergens such as p-phenylenediamine
(PPD) [36] and chro- mium [37]. Another G to A transition
polymorphism at the position of P238 has been identified.
A study found a poten- tial protective effect of the A allele
with carriers being less susceptible to developing ICD [38].
This has been specu- lated to result from increased
transcriptional repression of TNF α [39, 40].
These advancements represent a novel potential
approach in the detection of ICD susceptibility.

Pathogenesis

Previously, the pathogenesis of ICD was thought to be a


non- immunological reaction; however, it is now
recognized that the immune system plays a vital role in
causing ICD [41].
Irritation occurs by either damaging epidermal cells
[42], disruption of the epidermal barrier, or a combination
of both [43]. Disruption of the epithelial barrier allows for
increased permeability of irritants [44]. Keratinocytes act
as “signal transducers” responsible for instigating cutaneous
inflamma- tion via the conversion of exogenous stimuli into
the secretion of cytokines, adhesion molecules, and
chemotactic factors [45]. Upon damage to the keratinocyte,
upregulation of pri- mary cytokines IL-1α, IL-1β, and
TNF-α occurs [46] which triggers the proliferation of
keratinocytes and formation of lipids [47] playing a role in
restoring the epidermal barrier. Additional cytokines IL-6,
IL-8, and GM-SCF are subse- quently secreted, activating
Langerhans cells, dermal den- dritic cells, and endothelial
cells [44] which further recruits inflammatory cells to the
site of chemical trauma [48].
ICAM1, an adhesion molecule, is upregulated on
endothelial cells and fibroblasts in the skin and results in

13
44 Current Dermatology Reports (2022) 11:41–51
and IFN gamma [49]. CCL21, a chemokine which enables
naïve T lymphocyte migration, is upregulated in ICD [46,
50]. T lymphocytes recruited to irritated skin often
express the CLA antigen [51], which plays an important
role in transendothelial T lymphocyte migration.
Irritants can also trigger pattern recognition receptors
such as toll-like receptors (TLRs) and NOD-like
receptors, which result in activation of the innate immune
response via inflammasome and NFĸB pathways [44, 52].
There is growing evidence that oxidative stress with
the formation of reactive oxygen species plays a role in
the pathogenesis of ICD [53]. It has been postulated that
tar- geting oxidative stress could be beneficial in the
treatment of ICD, with clinical studies demonstrating the
therapeutic benefits of antioxidants [54].

Clinical Types

Acute Irritant Contact Dermatitis

Acute ICD occurs when the skin is exposed to a potent


irri- tant often in a single exposure, such as concentrated
acids, strong alkalis, and solvents such acrylonitrile. In
severe cases, this may present as burns, such as from
kneeling in wet concrete.
The irritant reaction quickly reaches a peak and then
begins to heal, usually described as a “decrescendo
phenom- enon” [55]. Symptoms reported include burning,
stinging, and soreness of affected skin. The clinical signs
of ICD are variable and include erythema, edema, bullae,
and necrosis [56]. While ACD may present with similar
clinical signs, it is characterized by a “crescendo
phenomenon” where signs worsen, despite removal of the
offending allergen [55].
Complete healing can take weeks in acute ICD,
generally with a good prognosis [57].

Delayed Acute Irritant Contact Dermatitis

Delayed acute ICD represents the most common form of


ICD. Chemicals such as benzalkonium chloride, anthralin,
calcipotriol, and tretinoin may cause a delayed inflamma-
tory response, not visible until 8–24 h after primary expo-
sure [58]. This may lead to misdiagnosis as ACD. Clinical
symptoms are similar to acute ICD with the skin
becoming sensitive to touch and water [59].

Irritant Reaction

Irritant reaction is a subclinical type of ICD that typically


affects individuals exposed to wet work. Clinical features
are monomorphic, characterized by erythema, scaling,
vesicles,
13
Current Dermatology Reports (2022) 11:41–51 45

pustules, and erosions [59]. It often begins on fingers under


occlusive jewelry such as rings and spreads to involve the Traumatic ICD
hands and forearms.
This condition may spontaneously resolve with Traumatic ICD occurs after acute trauma to the skin such
cessation of exposure, or can also progress to cumulative as burns, lacerations, or exposure to a potent irritant. The
ICD [60]. hands are the most commonly involved; however, there are
reported cases of nail involvement [67]. Usually, there is
delayed healing of the original trauma followed by the
Subjective/Sensorial Irritation
devel- opment of eczematous lesions [64]. It is usually a
chronic condition and may be resistant to treatment.
Subjective or sensorial irritation is characterized as sensory
discomfort in the form of stinging, burning, or a sensation
Pustular and Acneiform Dermatitis
of itch, in the absence of clinical or histological evidence
of skin irritation. Neural pathways are believed to be
Exposure to oils, naphthalene, chlorinated aromatic hydro-
respon- sible [61]. Irritants identified include propylene
carbons, and fluorinated compounds may result in pustular
glycol, hydroxy acids, ethanol, lactic acid, azelaic acids,
and acneiform dermatitis. Patients most affected are those
benzoic acid, benzoyl peroxide, mequinol, and tretinoin.
with seborrheic dermatitis, prior acne vulgaris, and atopy.
The prognosis is variable.
Non-Erythematous Irritation
Asteatotic Irritant Dermatitis
Non-erythematous ICD refers to early skin irritation with-
out clinical signs of inflammation. Associated SC barrier Asteatotic irritant dermatitis, also referred to as “exsicca-
changes can be demonstrated using assays that are usually tion eczematid,” “winter eczema,” and “eczema craquelé,”
available only in research settings [62]. Symptoms are is seen primarily during winter in cool climates. This
com- parable to subjective irritation. Prognosis is variable. variant is common amongst the elderly with dry skin on the
lower legs, especially in low-humidity environments.
Cumulative (Chronic) ICD Individuals report intense pruritus, dry skin, and scaling.
Reduction in natural moisturizing factors and lipids in the
Cumulative ICD is a result of multiple subthreshold insults SC is thought to contribute. Intense pruritus is usually
to the skin, if the interval between skin exposures is too relieved by the use of moisturizing creams, and topical
short to allow complete recovery of the skin barrier corticosteroid ointments are helpful [68].
function [63]. It develops slowly and is linked to exposures
to weak irritants [64]. Airborne Dermatitis
Clinical features include erythema, vesicles, and dry-
ness with progression to lichenification, hyperkeratosis, Airborne ICD results from exposure to irritants such as fib-
and chapping. Clinical features develop when the dam- ers, floating dusts, solvents, and sprays [69] dispersed and
age goes beyond the elicitation threshold. The threshold is carried in the air before coming into contact with exposed
dependent on the individual and may decrease as the skin [64]. Most cases are reported in occupational settings
disease progresses. [70].
Given that exposure to weak irritants often occurs both
at home and in the workplace, cumulative ICD may result
from exposure to multiple irritants, rather than a single Diagnosis
agent. The impact of combined multiple irritants produces
an increased skin inflammatory response; however, the ICD is a diagnosis of exclusion, as there is no routine diag-
extent of interac- tive effect is unpredictable [65]. nostic test. The diagnosis is established from the history,
clinical examination, and by excluding ACD with negative
Frictional Dermatitis patch testing. A thorough history regarding occupational
and domestic exposures is crucial, and relevant information
Frictional dermatitis results from repeated frictional includes the frequency, intensity, and duration of exposure
trauma, specifically shearing forces acting horizontally to to skin irritants, as well as the affected skin area(s) [44].
the skin sur- face [66]. It is characterized by hyperkeratosis, The pattern and distribution of dermatitis plays a key
acanthosis, and lichenification. Frictional ICD is role in the diagnosis. ICD always starts at the site of skin
recognized to contribute to ACD by enhancing percutaneous contact with the irritant and generally does not spread.
penetration of allergens [66]. Common

13
46 Current Dermatology Reports (2022) 11:41–51

sites include the hands, face, and perineal areas, well as glove permeation time will determine the necessary
particularly in infants and adults experiencing type of glove material [80]. For example, neoprene gloves
incontinence.
Patch testing is recommended to exclude the differential
diagnosis of ACD, which may be clinically
indistinguishable from ICD. Even if the results are
negative, patch testing has been shown to have a positive
impact on quality of life [71]. Bioengineering techniques,
such as the measurement of TEWL, provide a non-
invasive method to measure skin irri- tation in ICD;
however, these are not always available in a
clinical setting.
The role of skin biopsy remains limited in the diagnosis
of ICD, given that histopathological changes vary between
irritants and relates to their mode of action and concentra-
tion [72]. Histological findings in chronic ICD are gener-
ally similar to those of ACD. Reflectance-mode confocal
microscopy (RCM) is a non-invasive novel technique
which can be used to differentiate between acute ICD and
ACD in experimental settings, with superficial epidermal
changes (SC disruption, parakeratosis, and separation of
individ- ual corneocytes) being more prominent in ICD
compared to ACD [73, 74]. RCM is postulated to be more
sensitive and specific than clinical examination during
patch testing and could potentially play a role in
distinguishing between doubtful-positive and negative
reactions [75]. RCM allows repeated observation of the
affected area in real time, which is non-invasive compared
to conventional histology [76].

Prevention

Approaches to preventing exposure to irritants in the work-


place involve standard occupational hygiene principles
including elimination and/or substitution of the irritant,
isolation, and engineering controls including changing the
way a job is performed, administrative controls, and finally
use of personal protective equipment (PPE) [77].
Recent studies have highlighted the importance of pre-
employment screening tools in the workplace in early iden-
tification of hand dermatitis [78].
The use of PPE is recommended in the prevention of
ICD. The choice of PPE is guided by the nature of the
irritants, the areas of skin exposed, the chemical and
physical properties of PPE, and its functionality in relation
to the occupation [79].
Gloves are a frequently used form of PPE, given that
ICD usually affects the hands. Selection of appropriate
gloves for the management of ICD may be challenging,
given that the protective capabilities of gloves are
dependent on many variables.
Gloves should be selected based on the specific task and
associated chemical exposures. The nature of the irritant as

13
Current Dermatology Reports (2022) 11:41–51 47
have been shown to be the most protective against application has been shown to exacerbate some skin
acrylate monomers compared with polythene polymer conditions [101]. Nevertheless, BC can raise awareness of
gloves [81]. Occasionally, components of protective the possibility of skin problems in the workplace.
gloves can cause sensitization and ACD; common culprits
include thiurams and carbamates found in both latex and
nitrile gloves, but are absent from those made of polyvinyl
chloride [82].
Glove thickness plays a major role in chemical permea-
tion. However, thin gloves provide greater user comfort
and dexterity than thicker gloves made from the same
material [83].
Even when a suitable glove has been chosen, if the
user does not don or remove the glove appropriately,
skin con- tamination can occur. Incorrect glove sizing can
increase the rate of glove perforation [84]. It is important
that gloves are changed regularly, as sweating may
exacerbate existing der- matitis [85]. Additionally, there
is evidence that occlusion from gloves may impair the
function of the skin barrier [86]. Training in glove choice
and use has been shown to reduce user error and
allergen exposure [87, 88]; however, studies have shown
that workplace glove education remains
limited [89, 90].
Given that half of the cases of occupational contact
der- matitis (OCD) have been observed to appear within
the first 2 years of employment [91], there is a role for
educational strategies to promote awareness of potential
irritants, appro- priate use of PPE, and recognition of the
early signs of OCD, specifically ICD. Interdigital
dermatitis, also referred to as the “sentinel” sign, is
regarded as an early stage of hand ICD in occupations
involving wet work [92]. The impact of work-related
educational programs has been shown to be effective in
Danish healthcare workers [93], student nurses [94], and
hairdressers [95].
A soap-free cleanser is preferable, as synthetic deter-
gents are less irritating to the skin because of the neutral
or slightly acidic pH [96]. The relatively high-free fatty
acid content of soap free cleansers also provides a
moisturizing effect, preventing hand irritation and
dryness. The use of ABHS including moisturizers
avoiding common allergens is recommended as an
alternative to detergents [97].
Barrier creams (BCs) are designed to prevent
penetration of irritants into the skin. They are thought to
play a role in the prevention of ICD but are only
recommended for low grade irritants [98]. A recent
Cochrane review found that use of barrier creams alone
may have a slight protective effect, but the evidence was
deemed low quality and not clinically significant [99••].
Application methods can impact the effi- cacy of barrier
creams, with studies highlighting that BCs are often
poorly applied during real-world use, especially on the
dorsa of the hands and at significantly lower doses than
required to prevent irritation [100]. Inappropriate
13
48 Current Dermatology Reports (2022) 11:41–51

Inflammasome-targeted therapies such as topical disul- There may be a role for topical corticosteroids in chronic
firam have been shown to be effective in inhibiting ICD in hyperkeratotic irritant dermatitis [56], but prolonged use can
a recent study on human subjects [102]. This is thought to result in epidermal atrophy and therefore increase irritant
be a result of the reduction in the inflammatory cytokine sensitivity. However,
IL-18. This advancement provides a novel approach in the
prevention of ICD.

Management

The primary treatment in ICD is avoidance, skin protection


from the offending irritant(s) both in the workplace and at
home [103], and use of topical therapy, particularly
moisturizing creams.
Moisturizers are commonly used to improve dry skin
symptoms and maintain healthy skin [104]. There is
increas- ing evidence of their role in the treatment of ICD
by prevent- ing the absorption of exogenous substances
and improving skin barrier recovery [105]. It is thought
that using moistur- izers increases skin hydration and that
their lipid compo- nents modify endogenous epidermal
lipids, with high lipid content moisturizers significantly
preventing ICD when compared to formulations with lower
lipid content [104]. Patients should be advised to apply
moisturizers frequently, particularly before and after
shifts, and after handwash- ing [106]. Evidence has also
shown the protective role that moisturizers play in the long
and short term, in the primary prevention of occupational
ICD [99••, 107].
Strontium salts have been shown to be effective in
treating sensory irritation and are thought to act by
selectively block- ing the activation of cutaneous type C
nociceptors [108]. However, this treatment is not
commonly used worldwide.
Cool compresses are a primary treatment of acute ICD
by providing an environment which reduces the
inflammation and surface temperature changes associated
with acute ICD [109, 110].
Complications of ICD include bacterial superinfections.
These are usually treated aggressively with antibiotics to
prevent the development of cellulitis.
Although histamine is not involved in the mechanism of
ICD, in clinical practice, oral antihistamines are often pre-
scribed for symptomatic relief. Studies on mice have
shown the potential role of topical antihistamines in ICD
by reduc- ing inflammation and enhancing barrier function
[111]. How- ever, to date, there have been no randomized
clinical trials demonstrating the efficacy of antihistamines
in ICD [111].
Despite the frequent use of topical corticosteroids in
ICD, their use remains controversial. In humans, studies of
clini- cal efficacy are inconsistent [112] with some
suggesting that they may reduce barrier function associated
with inhibition of lipid synthesis in the epidermis [113].

13
Current Dermatology Reports (2022) 11:41–51 49
systemic corticosteroids may be required during severe
acute phases of ICD [114].
The Osnabrueck tertiary intervention program (TIP) is
a multidisciplinary approach intended to treat severe
recalci- trant OSD, comprising a 3-week inpatient phase
followed by a 3 week no-exposure outpatient phase.
Therapy aims to be free of corticosteroids in order to
promote long-term stabi- lization of the epidermal barrier.
TIP intervention has been shown to significantly reduce
the use of corticosteroids [115, 116, 117••]. Management
also includes intensive patient education, health-
psychological intervention, and specialized employment
consultants [118]. Follow-up studies have shown a
significant reduction in hand eczema severity and days of
absence from work as well as improvement in quality of
life both in short-term [115] and long-term follow up [116,
117••]. Topical calcineurin inhibitors (TCIs) are topical
immu- nomodulators that provide a safe alternative to
corticoster- oids. An association of topical TCIs with
skin cancer has been suggested, but there is no strong
evidence [119], while there may be an association with
risk of lymphoma [120]. TCIs have been shown to be
favorable in the treatment of ICD [121, 122]. Other
systemic treatments include alitreti- noin, which has been
shown to be an effective treatment in study of patients
with chronic hand eczema, 43.2% of whom
were diagnosed with ICD [123].
Oral immunomodulators may be required in the
treatment of chronic ICD if other first- or second-line
treatments fail. Cyclosporine is reported to be beneficial
in the treatment of chronic hand eczema [114] but is used
with caution given its associated side effects.
Limited evidence has highlighted the use of dupilumab,
a monoclonal antibody treatment approved for the
treatment of atopic dermatitis, to be effective in the
treatment of chronic recalcitrant hyperkeratotic ICD [124]
and non-atopic hyper- keratotic hand eczema [125].
Further studies are required to determine the use of
dupilumab as a potential therapeutic agent in ICD.
Phototherapy has proven to be beneficial in the
treatment of cumulative ICD, where repeated low levels
of UV expo- sure upregulate skin barrier function by
reducing epidermal proliferation [126]. Grenz–ray therapy
is an alternative which may induce an extended response
by suppressing Langerhans cells [127, 128].

Prognosis

Severe ICD is associated with a poor prognosis despite


advancements in prevention and treatment strategies. A
worse prognosis is linked to history of atopy, female sex,
and delayed diagnosis [44]. Prognosis can be improved
with early detection, patch testing to clarify the diagnosis,
and exclude ACD and educational interventions to
increase knowledge of ICD in affected individuals [129].

13
50 Current Dermatology Reports (2022) 11:41–51

Conclusion 4. Zhai H, Maibach H. Skin occlusion and irritant and allergic


con- tact dermatitis: an overview. Contact Dermatitis.
ICD is a complex disease influenced by endogenous and 2001:201–6.
exogenous factors. ICD remains a diagnosis of exclusion, 5. Marks J, Elsner P, Deleo V. Allergic and irritant contact der-
matitis. Contact and Occupational Dermatology. St Louis:
and currently, there is no diagnostic test available. For Mosby; 2002. p. 3–12.
many clinicians, the diagnosis may be difficult, especially 6. Dickel H, Kuss O, Schmidt A, Kretz J, Deipgen T. Importance
if patch testing is not available. Delays in diagnosing ICD of irritanct dermatitis in occupational skin disease. Am J Clin
are associ- ated with a poorer prognosis. Advancements Dermatol. 2002;3:283–9.
7. Slodwnik D, Lee A, Nixon R. Irritant Contact Dermatitis: a
into RCM as a diagnostic approach appear to be promising. review. Australas J Dermatol. 2008;49:1–11.
The mainstay of treatment in ICD remains avoidance of 8. Menne T, Johansen J, Sommerlund M, Veien N. Hand eczema
skin irritants and the use of PPE, with moisturizers to guidelines based on the Danish guidelines for the diagnosis and
maintain skin barrier function. In cases of occupationally treatment of hand eczema. Contact Dermatitis. 2011;65(1):3–12.
9.• Lund T, Flachs E, Sorenson J, Ebbenhoj N, Bonde J, Agner T.
acquired ICD, the role of health promotion and A job-exposure matrix addressing hand exposure to wet work.
preventative strategies has been shown to be beneficial, but Int Arch Occup Environ Health. 2019;92:959–66. Established
are often poorly implemented in workplaces. Further framework to assess the extent of wet work exposure in dif-
ferent occupations.
studies are required to more fully evalu- ate predisposing
10. Federal Institue for Occupational Safety and Health. Technical
factors, as well as informing clinicians of therapeutic rules for hazardous substances: risks resulting from skin contact
approaches to better manage ICD. - identification, assessment, measures (TRGS 401). 2008.
11. Reinholz M, Kendziora B, Frey S, Oppel EM, Rueff F,
Abbreviations ACD: Allergic contact dermatitis; ICD: Irritant contact Clanner- Engelshofen BM, et al. Increased prevalence of
dermatitis; CLA: Cutaneous lymphocyte association; OSD: Occupa- irritant hand eczema in health care workers in a
tional skin disease; PPE: Personal protective equipment; SC: Stratum dermatological clinic due to increased hygiene measures
corneum; TEWL: Trans epidermal water loss; TNF: Tumor necrosis during the SARS-CoV-2 pan- demic. Eur J Dermatol.
factor 2021;31(3):392–5. https://doi.org/10. 1684/ejd.2021.4046.
12. Borch L, Thorsteinsson K, Warner TC, Mikkelsen CS, Bjerring
P, Lundbye-Christensen S, et al. COVID-19 reopening causes
high risk of irritant contact dermatitis in children. Dan Med J.
2020;67(9).
Compliance with Ethical Standards 13. Cristaudo A, Pigliacelli F, Pacifico A, Damiani G, Iacovelli
P, Morrone A. Teledermatology and hygiene practices during
Conflict of Interest Kajal Patel and Rosemary Nixon declare no con- the COVID-19 pandemic. Contact Dermatitis. 2020;83(6):536.
flicts of interest. https://doi.org/10.1111/cod.13683.
14. Fartasch M, Schnetz E, Diepgen T. Characterisation of
Human and Animal Rights and Informed Consent This article does not detergent induced barrier alterations - effect of barrier creas on
contain any studies with human or animal subjects performed by any irritation. J Investig Dermatol Symp Proc. 1998;3:121–7.
of the authors. 15. Grubauer G, Elias P, Feingold K. Transepidermal water loss:
the signal for recovery of barrier and function. J Lipid Res.
1989;30:323–33.
16. Aramaki J, Loffler C, Kawana S, Effendy I, Happle R, Loffler
H. Irritant patch testing with sodium lauryl sulphate: interrela-
tion between concentration and exposure times. Br J Dermatol.
References 2001;145:704–8.
17. Heinemann C, Paschold C, Fluhr J, Wigger-Alberti W,
Papers of particular interest, published recently, Schliemann-Willer S, Farwanah H, et al. Induction of a hard-
ening phenomenon by repeated application of SLS. Analy-
have been highlighted as: sis of lipid changes in the stratum corneum. Acta Dermato-
• Of importance Venereologica. 2005;85:290–5.
•• Of major importance 18. Hu C. Sweat-related dermatoses:old concept and new scenario.
Dermatologica. 1991;182:73–6.
1. Novak-Bilic G, Vucic M, Japundzic I, Mestrovic-Stefekov J, 19. Fluhr J, Bornkessel A, Akengin A, Fuchs S, Norgauer J, Kleesz
Stanic-Duktaj S, Lugovic-Mihic L. Irritant and allergic con- P, et al. Sequential application of cold and sodium lauryl sul-
tact dermatitis - skin lesion characteristics. Acta Clin Croat. phate decreases irritation and barrier disruption in vivo in
2018;57(4):713–20. https://doi.org/10.20471/acc.2018.57.04.13. humans. Br J Dermatol. 2005;152(4).
2.•• Cahill JL, Williams JD, Matheson MC, Palmer AM, Burgess 20. Zhai H, Meier-Davis S, Cayme B, Shudo J, Maibach H. Irri-
JA, Dharmage SC et al. Occupational skin disease in Victoria, tant contact dermatitis: effect of age. Cutan Ocul Toxicol.
Aus- tralia. Australas J Dermatol. 2016;57(2):108-14. 2012;31(2):138–43.
https://doi.org/ 10.1111/ajd.12375. Large retrospective review 21. Cua A, Wilhelm K, Maibach H. Cutaneous SLS irritation
evaluating risk factors of patients presenting with potential: age and regional variability. Br J Dermatol.
occupational skin disease. 1990;123:607–13.
3. DeKoven JG, DeKoven BM, Warshaw EM, Mathias CGT, 22. Meding B. Differences between the sexes with regard to work-
Taylor JS, Sasseville D et al. Occupational contact dermatitis: related skin disease. Contact Dermatitis. 2000;43(2):65–71.
retro- spective analysis of North American Contact Dermatitis 23. Robinson M. Population differences in acute skin irritation
Group Data, 2001 to 2016. J Am Acad Dermatol. 2021. responses. Race,sex,age,sensitive skin,and repeat subject com-
https://doi.org/ 10.1016/j.jaad.2021.03.042. parisons. Contact Dermatitits. 2002;46:86–93.
13
Current Dermatology Reports (2022) 11:41–51 51

24. Berardesca E, Maibach H. Racial difference in sodium lauryl Brinkman BM, Langermans JA, et al. TNF-alpha promoter
sulphate induced cutaneous irritation: black and white. Contact polymorphisms,
Dermatitis. 1988;18:65–70.
25. Anderson K, Maibach H. Black and white human skin differ-
ences. J Am Acad Dermatol. 1976;1:276–82.
26. Lee E, Kim S, Lee J, Cho SA, Shin K. Ethnic differences in
objective and subjective skin irritation response: an
international study. Skin Res Technol. 2014;20(3):265–9.
https://doi.org/10. 1111/srt.12111.
27. Meding B, Wrangsjo K, Jarvholm B. Fifteen-year follow-up of
hand eczema: predictive factors. J Invest Dermatol.
2005;124(5):893–7. https://doi.org/10.1111/j.0022-
202X.2005.23723.x.
28. Conti A, Di Nardo A, Seidenary S. No alteration of biophysi-
cal parameteres in the skin of subjects with respiratory atopy.
Dermatology. 1996;192:317–20.
29. Gittler J, Kreuger J, Guttman-Yassky E. Atopic dermatits
results in intrinsic barrier and immune abnormalities:
implications for contact dermatitis. J Allergy Clin Immunol.
2012;131:300–13.
30. Kezic S, O’regan G, Lutter R, Jakasa I, Koster E, Saunders S,
et al. Filaggrin loss-of-function mutations are associated with
enhanced expression of IL-1 cytokines in the stratum corneum
of patients with atopic dermatitis and in a murine model of
filaggrin deficiency. J Allergy Clin Immunol. 2012;129:1031–
9.
31. de Jongh C, Khrenova L, Verberk M, Calkoen F, van Dijk F,
Voss H, et al. Loss-of-function polymorphisms in the filaggrin
gene are associated with an increased susceptibility to chronic
irritant contact dermatitis: a case-control study. Br J Dermatol.
2008;159:621–7.
32. Landeck L, Visser M, Skudlik C, Brans R, Kezic S, John S.
Clinical course of occupational irritant contact dermatitis of the
hands in relation to the filaggrin genotype status and atopy. Br
J Dermatol. 2012;167:1302–9.
33. Yucesoy B, Talzhanov Y, Barmada MM, Johnson VJ, Kashon
ML, Baron E, et al. Genetic basis of irritant susceptibility in
health care workers. J Occup Environ Med. 2016;58(8):753–9.
https://doi.org/10.1097/JOM.0000000000000784.
34. Yucesoy B, Talzhanov Y, Michael Barmada M, Johnson VJ,
Kashon ML, Baron E, et al. Association of MHC region SNPs
with irritant susceptibility in healthcare workers. J Immunotox-
icol. 2016;13(5):738–44. https://doi.org/10.3109/1547691X.
2016.1173135.
35. de Jongh CM, John SM, Bruynzeel DP, Calkoen F, van Dijk
FJ, Khrenova L, et al. Cytokine gene polymorphisms and
suscepti- bility to chronic irritant contact dermatitis. Contact
Dermatitis. 2008;58(5):269–77. https://doi.org/10.1111/j.1600-
0536.2008. 01317.x.
36. Babic Z, Kezic S, Macan J. Individual susceptibility to contact
sensitization: the role of TNFalpha 308G>A polymorphism
and atopy. Eur J Dermatol. 2019;29(1):75–80. https://doi.org/
10.1684/ejd.2018.3485.
37. Wang BJ, Shiao JS, Chen CJ, Lee YC, Guo YL. Tumour
necrotizing factor-alpha promoter and GST-T1 genotype
predict skin allergy to chromate in cement workers in Taiwan.
Contact Dermatitis. 2007;57(5):309–15.
https://doi.org/10.1111/j.1600- 0536.2007.01242.x.
38. Landeck L, Visser M, Kezic S, John SM. Impact of tumour
necrosis factor-alpha polymorphisms on irritant contact derma-
titis. Contact Dermatitis. 2012;66(4):221–7. https://doi.org/10.
1111/j.1600-0536.2011.02045.x.
39. Hohler T, Kruger A, Gerken G, Schneider PM, zum
Buschenefelde MKH, Rittner C. A tumor necrosis factor-alpha
(TNF-alpha) pro- moter polymorphism is associated with
chronic hepatitis B infec- tion. Clin Exp Immunol.
1998;111(3):579–82. https://doi.org/10. 1046/j.1365-
2249.1998.00534.x.
40. Huizinga TW, Westendorp RG, Bollen EL, Keijsers V,
13
52 Current Dermatology Reports (2022) 11:41–51
production and susceptibility to multiple sclerosis in different
groups of patients. J Neuroimmunol. 1997;72(2):149–53.
https:// doi.org/10.1016/s0165-5728(96)00182-8.
41. Levin C, Maibach H. Irritant contact dermatitis: is there an
immunological component? Internation
Immunopharmacology. 2002;2:183–9.
42. Angelova-Fischer I. Irritants and skin barrier function. Curr
Probl Dermatol. 2016;49:80–9.
43. Welss T, Basketter DA, Schroder KR. In vitro skin irritation:
facts and future. State of the art review of mechanisms and
models. Toxicol In Vitro. 2004;18(3):231–43. https://doi.org/
10.1016/j.tiv.2003.09.009.
44. Bains S, Nash P, Fonacier L. Irritant contact dermatitis. Clin
Rev Allergy Immunol. 2019;56:99–109.
45. Gittler JK, Krueger JG, Guttman-Yassky E. Atopic derma-
titis results in intrinsic barrier and immune abnormalities:
implications for contact dermatitis. J Allergy Clin Immunol.
2013;131(2):300–13.
https://doi.org/10.1016/j.jaci.2012.06.048.
46. Spiekstra SW, Toebak MJ, Sampat-Sardjoepersad S, van Beek
PJ, Boorsma DM, Stoof TJ, et al. Induction of cytokine
(interleukin- 1alpha and tumor necrosis factor-alpha) and
chemokine (CCL20, CCL27, and CXCL8) alarm signals after
allergen and irritant exposure. Exp Dermatol.
2005;14(2):109–16. https://doi.org/10. 1111/j.0906-
6705.2005.00226.x.
47. Feingold K, Schmuth M, Elias P. The regulation of
permeability barrier homeostasis. J Investig Dermatol.
2007;127(7):1547–76.
48. Corsini E, Galli C. Epidermal cytokines in experimental
contact dermatitis. Toxicology. 2000;142(3):203–11.
49. Lee H, Stieger M, Yawalkar N, Kakeda M. Cytokines and
chemokines in irritant contact dermatitis. Mediators of
Inflam- mation. 2013.
50. Eberhand Y, Ortiz S, Ruiz L, A, Kuznitzky R, Serra H. Up-
regulation of the chemokine CCL21 in the skin of subjects
exposed to irritants. BMC Immunology. 2004;26:7.
51. Soler D, Humphreys TL, Spinola SM, Campbell JJ. CCR4
versus CCR10 in human cutaneous TH lymphocyte traffick-
ing. Blood. 2003;101(5):1677–82. https://doi.org/10.1182/
blood-2002-07-2348.
52. Ale I, Maibach H. Irritant contact dermatitis. Rev Environ
Health. 2014;29:195–206.
53. Nakai K, Yoneda K, Kubota Y. Oxidative stress in
allergica and irritant dermatitis: from basic reseach to clinical
man- agement. Recent Pat Inflammation Allergy Drug
Discovery. 2012;6(3):202–9.
54. Wagemaker TAL, Maia Campos P, Shimizu K, Kyotani D,
Yoshida D. Antioxidant-based topical formulations
influence on the inflammatory response of Japanese skin: a
clinical study using non-invasive techniques. Eur J Pharm
Biopharm. 2017;117:195–202.
https://doi.org/10.1016/j.ejpb.2017.03. 025.
55. Weltfriend S, Ramon N, Maibach H. Irritant dermatitis.
Derma- totoxicology. Boca Raton: CRC Press; 2004. p. 181–
228.
56. Antonov D, Schliemann S, Elsner P. Contact dermatitis due to
Irritation. In: 3, editor. Kanerva's Occupational Dermatology.
Switzerland: Springer Nature; 2020. p. 119–37.
57. Elsner P. Irritant dermatitis in the workplace. Dermatol Clin.
1994;12(3):461–7.
58. Malten K, den Arend J, Wiggers R. Delayed irritation: hexan-
ediol diacrylate and butanediol diacrylate. Contact Dermatitis.
1979;5(3):178–84.
59. Frosch P, John S. Clinical aspects of irritant contact
dermatitis. Contact dermatitis. Berlin: Springer; 2006. p. 255–
94.
60. Wigger-Alberti W, Elsner P, Wahlberg J, Maibach H. Irritant
dermatitis (irritation). Handbook of Occupational
Dermatology. New York: Springer; 2000. p. 99–110.
13
Current Dermatology Reports (2022) 11:41–51 53

61. Lee E, An S, Lee T, Kim H. Development of a novel method


for quantitative evaluation of sensory skin irritation inhibitors. guidelines for the management of contact dermatitis 2017. Br
Skin Research and Technology. 2009;15(4):464–9. J Dermatol. 2017;176(2):317–29. https://doi.org/10.1111/bjd.
62. Charbonnier VJ, Morrison B, Paye M, Maibach M. Subclini- 15239.
cal, non erythematous irritation with an open assay model 81. Andersson T, Bruze M, Gruvberger B, Bjorkner B. In vivo
(washing): sodium lauryl sulfate (SLES). Food Chem Toxicol. testing of the protection provided by non-latex gloves against
2001;39:279–86. a 2-hydroxyethyl methacrylate-containing acetone-based den-
63. Malten K. Thoughts on irritant contact dermatitis. Contact Der- tin-bonding product. Acta Derm Venereol. 2000;80(6):435–7.
matitis. 1981;7(5):238–47. https://doi.org/10.1080/000155500300012891.
64. Chew A-L, Maibach H. Ten genotypes of irritant contact 82. Kersh AE, Helms S, de la Feld S. Glove-related allergic
derma- titis. Irritant dermatitis. Berlin: Springer; 2006. p. 5–9. contact dermatitis. Dermatitis. 2018;29(1):13–21.
65. Pedersen LK, Johansen JD, Held E, Agner T. Augmentation of https://doi.org/10. 1097/DER.0000000000000335.
skin response by exposure to a combination of allergens and 83. Ramadan MZ. The effects of industrial protective gloves and
irri- tants - a review. Contact Dermatitis. 2004;50(5):265–73. hand skin temperatures on hand grip strength and discomfort
https:// doi.org/10.1111/j.0105-1873.2004.00342.x. rating. Int J Environ Res Public Health. 2017;14(12).
66. McMullen E, Gawkrodger DJ. Physical friction is under-rec- https://doi. org/10.3390/ijerph14121506.
ognized as an irritant that can cause or contribute to contact 84. Zare A, Choobineh A, Jahangiri M, Seif M, Dehghani F. Does
dermatitis. Br J Dermatol. 2006;154(1):154–6. https://doi.org/ size affect the rate of perforation? A cross-sectional study of
10.1111/j.1365-2133.2005.06957.x. medical gloves. Ann Work Expo Health. 2021. https://doi.org/
67. Darr-Foit S, Tittelnbach J, Elsner P. Postraumatic irritant 10.1093/annweh/wxab007.
contact dermatitis - an underdiagnosed entity? Deutsch 85. Bourke K, Coulson I, English J. Guidelines for the man-
Dermatolgische Gesellschaft. 2014;12(4). agement of contact dermatitis: an update. Br J Dermatol.
68. Diepgen TL, Andersen KE, Brandao FM, Bruze M, Bruynzeel 2009;160:946–54.
DP, Frosch P, et al. Hand eczema classification: a cross- 86. Antonov D, Kleesz P, Elsner P, Schliemann S. Impact of glove
sectional, multicentre study of the aetiology and morphology of occlusion on cumulative skin irritation with or without hand
hand eczema. Br J Dermatol. 2009;160(2):353–8. cleanser-comparison in an experimental repeated irritation
https://doi.org/10. 1111/j.1365-2133.2008.08907.x. model. Contact Dermatitis. 2013;68(5):293–9. https://doi.org/
69. Lachapelle J. Enviromental airborne contact dermatoses. 10.1111/cod.12028.
Reviews on Enviromental Health. 2014;29:2210231. 87. Oreskov KW, Sosted H, Johansen JD. Glove use among hair-
70. Santos R, Goossens A. An update on airborne contact dressers: difficulties in the correct use of gloves among hair-
dermatitis. Contact Dermatitis. 2007:353–60. dressers and the effect of education. Contact Dermatitis.
71. Woo P, Hay I, Ormerod A. An audit of the value of patch 2015;72(6):362–6. https://doi.org/10.1111/cod.12336.
testing and its effect on quality of life. Contact Dermatitis. 88. Geens T, Aerts E, Borguet M, Haufroid V, Godderis L. Expo-
2003;48:244–7. sure of hairdressers to aromatic diamines: an interventional
72. Weedon D. Weedon's skin pathology. Churchill Livingstone; study confirming the protective effect of adequate glove use.
2009. Occup Environ Med. 2016;73(4):221–8.
73. Swindells K, Burnett N, Rius-Diaz F, Gonzalez E, Mihm MC, https://doi.org/10.1136/ oemed-2014-102708.
Gonzalez S. Reflectance confocal microscopy may 89. Keegel TG, MacFarlane E, Nixon R, Lamontagne A. Provision
differentiate acute allergic and irritant contact dermatitis in of control measures for exposure of the hands to wet-working
vivo. J Am Acad Dermatol. 2004;50(2):220–8. conditions in Australian workplaces. Int J Occup Environ Health.
https://doi.org/10.1016/j.jaad. 2003.08.005. 2012;18(4):312–9. https://doi.org/10.1179/2049396712Y.
74. Astner S, Gonzalez S, Gonzalez E. Noninvasive evaluation of 0000000010.
allergic and irritant contact dermatitis by in vivo reflectance 90. Rowley K, Ajami D, Gervais D, Mooney L, Belote A, Kudla I,
con- focal microscopy. Dermatitis. 2006;17(4):182–91. et al. Glove use and glove education in workers with hand der-
https://doi. org/10.2310/6620.2006.05052. matitis. Dermatitis. 2016;27(1):30–2. https://doi.org/10.1097/
75. Maarouf M, Costello CM, Gonzalez S, Angulo I, Curiel- DER.0000000000000155.
Lewandrowski CN, Shi VY. In vivo reflectance confocal 91. Dickel H, Kuss O, Schmidt A, Diepgen T. Occupational skin
microscopy: emerging role in noninvasive diagnosis and dis- eases in Northern Bavaria between 1990 and 1999: a
monitoring of eczematous dermatoses. Actas Dermosifiliogr. population- based study. Br J Dermatol. 2008;145(3):453–62.
2019;110(8):626–36. https://doi.org/10.1016/j.ad.2018.08.008. 92. Schwanitz HJ, Uter W. Interdigital dermatitis: sentinel skin
76. Suarez-Perez J, Bosch R, Gonzalez S, Gonzalez E. dam- age in hairdressers. Br J Dermatol. 2000;142(5):1011–2.
Pathogenesis and diagnosis of contact dermatitis: application https:// doi.org/10.1046/j.1365-2133.2000.03487.x.
of reflectance confocal microscopy. World Journal of 93. Clemmensen KK, Randboll I, Ryborg MF, Ebbehoj NE, Agner
Dermatology. 2014;2. T. Evidence-based training as primary prevention of hand
77. The National Institute for Occupational Safety and Health eczema in a population of hospital cleaning workers. Contact
(NIOSH). Hierachy of Controls. https://www.cdc.gov/niosh/ Dermatitis. 2015;72(1):47–54.
topics/hierarchy/. Accessed April 2021. https://doi.org/10.1111/cod.12304.
78. Nichol K, Copes R, Spielmann S, Kersey K, Eriksson J, 94. Held E, Wolff C, Gyntelberg F, Agner T. Prevention of work-
Holness DL. Workplace screening for hand dermatitis: a pilot related skin problems in student auxiliary nurses: an
study. Occup Med (Lond). 2016;66(1):46–9. intervention study. Contact Dermatitis. 2001;44(5):297–303.
https://doi.org/10.1093/occmed/ kqv126. https://doi.org/ 10.1034/j.1600-0536.2001.440509.x.
79. Garrigoua A, Laurent C, Berthet A, Colosiod C, Jase N, 95. Bregnhoj A, Menne T, Johansen JD, Sosted H. Prevention of
Daubas- Letourneux V, JacksonFilhog JM, Jouzelh J-N, Samuel hand eczema among Danish hairdressing apprentices: an inter-
O, Baldia I, Lebailly P, Galey L, Goutille F, Judona N. Critical vention study. Occup Environ Med. 2012;69(5):310–6. https://
review of the role of PPE in the prevention of risks related to doi.org/10.1136/oemed-2011-100294.
agricultural pesticide use. Safety Science. 2020;123. 96. Abtahi-Naeini B. Frequent handwashing amidst the COVID-19
80. Johnston GA, Exton LS, Mohd Mustapa MF, Slack JA, outbreak: prevention of hand irritant contact dermatitis and
Coulson IH, English JS, et al. British Association of other
Dermatologists’
13
54 Current Dermatology Reports (2022) 11:41–51

considerations. Health Sci Rep. 2020;3(2): e163. https://doi.org/10.1097/DER.0000000000000574.


https://doi.org/ 10.1002/hsr2.163.
97. Rundle CW, Presley CL, Militello M, Barber C, Powell DL,
Jacob SE, et al. Hand hygiene during COVID-19: Recommen-
dations from the American Contact Dermatitis Society. J Am
Acad Dermatol. 2020;83(6):1730–7. https://doi.org/10.1016/j.
jaad.2020.07.057.
98. Mostosi C, Simonart T. Effectiveness of barrier creams against
irritant contact dermatitis. Dermatology. 2016;232(3):353–62.
https://doi.org/10.1159/000444219.
99.•• Bauer A, Ronsch H, Elsner P, Dittmar D, Bennett C,
Schuttelaar MLA, et al. Interventions for preventing
occupational irritant hand dermatitis. Cochrane Database Syst
Rev. 2018;4:CD004414.
https://doi.org/10.1002/14651858.CD004414.pub3. Large sys-
tematic review of interventions in preventing occupational
irritant hand dermatitis. It showed the protective role of
moisturizers and educational strategies in preventing hand
dermatitis.
100. Schliemann S, Petri M, Elsner P. Preventing irritant contact
der- matitis with protective creams: influence of the application
dose. Contact Dermatitis. 2014;70(1):19–26.
https://doi.org/10.1111/ cod.12104.
101. Alvarez MS, Brown LH, Brancaccio RR. Are barrier creams
actually effective? Curr Allergy Asthma Rep. 2001;1(4):337–
41. https://doi.org/10.1007/s11882-001-0045-z.
102. Bonnekoh H, Vera C, Abad-Perez A, Radetzki S, Neuenschwander
M, Specker E, et al. Topical inflammasome inhibition with
disulfiram prevents irritant contact dermatitis. Clin Transl Allergy.
2021;11(5): e12045. https://doi.org/10.1002/clt2.12045.
103. Diepgen T, Anderson K, Brandao F, Bruze M, Bruynzeel D,
Goncalo M, et al. Hand eczema classification:a cross-sectional
multicentre study of the aetiology and morphology of hand
eczema. Br J Dermatol. 2009;160(2):353–8.
104. Held E, Agner T. Effect of moisturizers on skin susceptibility
to irritants. Acta Derm Venereol. 2001;81(2):104–7.
https://doi. org/10.1080/00015550152384227.
105. Purnamawati S, Indrastuti N, Danarti R, Saefudin T. The role of
mois- turizers in addressing various kinds of dermatitis: a review.
Clin Med Res. 2017;15(3–4):75–87.
https://doi.org/10.3121/cmr.2017.1363.
106. Hines J, Wilkinson SM, John SM, Diepgen TL, English J,
Rustemeyer T, et al. The three moments of skin cream application:
an evidence- based proposal for use of skin creams in the
prevention of irritant contact dermatitis in the workplace. J Eur
Acad Dermatol Venereol. 2017;31(1):53–64.
https://doi.org/10.1111/jdv.13851.
107. Saary J, Qureshi R, Palda V, DeKoven J, Pratt M, Skotnicki-
Grant S, et al. A systematic review of contact dermatitis treat-
ment and prevention. J Am Acad Dermatol. 2005;53(5):845.
https://doi.org/10.1016/j.jaad.2005.04.075.
108. Zhai H, Hannon W, Hahn GS, Pelosi A, Harper RA, Maibach
HI. Strontium nitrate suppresses chemically-induced sensory
irrita- tion in humans. Contact Dermatitis. 2000;42(2):98–100.
https:// doi.org/10.1034/j.1600-0536.2000.042002098.x.
109. Levin C, Maibach H. Do cool water or physiological saline
com- presses enhance resolution of experimentally-induced
irritant contact dermatitis? Contact Dermatitis. 2001;45:146–
50.
110. Yoshizawa Y, Tanojo H, Kim S, Maibach H. Sea water or its
components alter experimental irritant contact dermatitis in
man. Skin Res Technol. 2001;7:36–9.
111. Lin T, Man M, Santiago J, Park K, Roelandt T, Oda Y, et al.
Topical antihistamines display potent anti-inflammatory activ-
ity linked in part to enhanced permeability barrier function. J
Investig Dermatol. 2013;133:469–78.
112. Azizi N, Maibach HI. Are topical corticoids efficacious in
acute irritant dermatitis: the evidence. Dermatitis.
2020;31(4):244–6.
13
Current Dermatology Reports (2022) 11:41–51 55
113. Kao J, JW F, Man MQ F, AJ Hachem, JP, Crumrine D, Ahn Occu- pational Enviromental Medicine. 2004;61:722–6.
S, BE B, et al. Short-term glucocorticoid treatment
compromises both permeability barrier homeostasis and
stratum corneum intergrity: inhibition of epidermal lipid
synthesis accounts for functional abnormalities. J Investig
Dermatol. 2003;120:456–64.
114. Elsner P, Agner T. Hand eczema: a “neglected” disease. J Eur
Acad Dermatol Venereol. 2020;34(Suppl 1):3. https://doi.org/
10.1111/jdv.16081.
115. Skudlik C, Weisshaar E, Scheidt R, Elsner P, Wulfhorst B,
Schonfeld M, et al. First results from the multicentre study
reha- bilitation of occupational skin diseases–optimization and
quality assurance of inpatient management (ROQ). Contact
Dermatitis. 2012;66(3):140–7. https://doi.org/10.1111/j.1600-
0536.2011. 01991.x.
116. Weisshaar E, Skudlik C, Scheidt R, Matterne U, Wulfhorst B,
Schonfeld M, et al. Multicentre study ’rehabilitation of occu-
pational skin diseases -optimization and quality assurance of
inpatient management (ROQ)’-results from 12-month follow-
up. Contact Dermatitis. 2013;68(3):169–74. https://doi.org/10.
1111/j.1600-0536.2012.02170.x.
117.••Brans R, Skudlik C, Weisshaar E, Scheidt R, Ofenloch R,
Elsner P et al. Multicentre cohort study 'Rehabilitation of
Occupational Skin Diseases - Optimization and Quality
Assurance of Inpatient Management (ROQ)': results from a 3-
year follow-up. Contact Dermatitis. 2016;75(4):205–12.
https://doi.org/10.1111/cod. 12614. Long term follow up
multicentre cohort study assess- ing the impact of tertiary
prevention in severe hand eczema demonstrated significant
reduction in severity of hand eczema and use of topical
corticosteroids and improvement in quality of life scores.
118. Skudlik C, Wulfhorst B, Gediga G, Bock M, Allmers H, John
SM. Tertiary individual prevention of occupational skin dis-
eases: a decade’s experience with recalcitrant occupational
der- matitis. Int Arch Occup Environ Health.
2008;81(8):1059–64. https://doi.org/10.1007/s00420-008-
0300-x.
119. Asgari MM, Tsai AL, Avalos L, Sokil M, Quesenberry
CP Jr. Association between topical calcineurin inhibitor use
and keratinocyte carcinoma risk among adults with atopic
derma- titis. JAMA Dermatol. 2020;156(10):1066–73.
https://doi.org/ 10.1001/jamadermatol.2020.2240.
120. Lam M, Zhu JW, Tadrous M, Drucker AM. Association
between topical calcineurin inhibitor use and risk of cancer,
including lymphoma, keratinocyte carcinoma, and melanoma:
a systematic review and meta-analysis. JAMA Dermatol.
2021;157(5):549–
58. https://doi.org/10.1001/jamadermatol.2021.0345.
121. Engel K, Reuter J, Seiler CSM, J, Jakob T, Schempp C. Anti
inflammatory effect4 of pimecrolimus in the sodium laurly
sul- phate test. J Eur Acad Dermatol Venereol.
2007;22(4):447–50.
122. Grassberger.M, Steinhoff M, Schneider D, Luger T.
Pimecroli- mus - anti-inflammatory drug targeting the skin.
Exp Dermatol. 2004;13(12):721–30.
123. Ferrucci S, Persichini P, Gola M, Scandagli I, Pigatto P,
Legori A, et al. DECISA Project (DErmatology Clinics in
Italy: Sur- vey on Alitretinoin): a real-life retrospective cohort
multicenter study on 438 subjects with chronic hand eczema.
Dermatol Ther. 2021;34(3): e14911.
https://doi.org/10.1111/dth.14911.
124. Zhu GA, Honari G, Ko JM, Chiou AS, Chen JK. Dupilumab
for occupational irritant hand dermatitis in a nonatopic
individual: a case report. JAAD Case Rep. 2020;6(4):296–8.
https://doi.org/ 10.1016/j.jdcr.2020.02.010.
125. Loman L, Diercks GFH, Schuttelaar MLA. Three cases of
non- atopic hyperkeratotic hand eczema treated with dupilumab.
Contact Dermatitis. 2021;84(2):124–7.
https://doi.org/10.1111/cod.13693.
126. English J. Current concepts of irritant contact dermatitis.
13
56 Current Dermatology Reports (2022) 11:41–51

127. Simpson BM, Foster SK, Chapman CN, Simpson EL. The
effec- tiveness of grenz ray therapy for chronic dermatoses of 129. Cahill J, Keegel T, Nixon R. The prognosis of occupational
the hands and feet. Dermatitis. 2014;25(4):205–8. contact dermatitis in. Contact Dermatitis. 2004;2004:219–56.
https://doi.org/10.1097/ DER.0000000000000050.
128. Fenton L, Dawe RS. Six years’ experience of grenz ray therapy Publisher's Note Springer Nature remains neutral with regard to
for the treatment of inflammatory skin conditions. Clin Exp jurisdictional claims in published maps and institutional affiliations.
Dermatol. 2016;41(8):864–70.
https://doi.org/10.1111/ced.12960.

13

You might also like