Dermatitis

Cheah Hwei Yan 1002057843

Looi Hoong Seng 1001954366
Ong Wan Ling
1002059801
 Table of contents

01 Atopic Dermatitis

02 Seborrhoeic Dermatitis

03 Irritant & Allergic Contact Dermatitis

Atopic
Dermatitis
CHEAH HWEI YAN 1002057843 01
 Atopic Dermatitis
⧫ Atopic eczema
○ Atopy refers to the tendency to asthma, eczema and hay fever.
⧫ Most common inflammatory skin disease → approximately 230 million people affected
⧫ Lifetime prevalence is >15% especially in wealthier countries
⧫ Typically affects people with an ‘atopic tendency’ clustering with hay fever, asthma, and
food allergies.
⧫ Usually starts in infancy, affecting up to 20% of children
⧫ Approximately 80% of children affected develop it before the age of 6 years.
⧫ Prevalence in young adults up to 26 years of age is 5–15%.
 Pathophysiology
Current theories identify that atopic dermatitis is primarily a disease of the immune system,
with cytokines being critical components to the disease.
- IL-4 and IL-13 (Th2 pathway cytokines) and IL-22 (the Th22 axis cytokine) cause
barrier defects and inflammation that result in the clinical features of eczema.

Inherited abnormalities in skin barrier: Filaggrin mutation

● Filaggrin: filament-associated proteins which bind to keratin fibres in the epidermal
cells.
● Loss of filaggrin results in:
○ Corneocyte deformation (flattening of surface skin cells) → disrupts the
organisation of the extracellular lipid (fat) — the lamellar bilayers.
○ A reduction in natural moisturising factors, which include metabolites of pro-
filaggrin.
○ An increase in skin pH which encourages serine protease activity — these are
enzymes which digest lipid-processing enzymes and the proteins that hold
epidermal cells together. Serine proteases also generate active cytokines like IL-1a
and Il-1beta and promote skin inflammation.
 Pathophysiology
The immune system
● In healthy individuals, balance exists between important subsets of T cells (eg, Th1, Th2, Th17, Th22).
● The primary immune dysfunction hypothesis invokes an imbalance in the T cell subsets, with Th2 cells
predominating;
○ results in the production of type 2 cytokines such as interleukin (IL)–4, IL-5, and IL-13, causing an increase in
IgE from plasma cells
● Th2 associated cytokines contribute to the loss of skin barrier function:
○ Water is lost
○ Irritants may penetrate (soap, detergent, solvents, dirt etc.)
○ Allergens may penetrate it (pollens, dust-mite antigens, microbes).
● Specialised immune cells of the epidermis (Langerhans cells) have an increased response to these antigens in atopic
dermatitis and interact with dermal T cells to produce an even greater Th2 response further exacerbating the barrier
defect.
○ Ceramide (a fatty acid) is reduced
○ Filaggrin is reduced
○ Antimicrobial peptides are reduced
○ Bacteria colonise and infect the skin
○ Infections are more difficult to control
 Etiology
➔ Genetics
➔ Infection
◆ S. Aureus
◆ Herpes simplex virus
◆ Molluscum contagiosum and viral warts
◆ Malassezia and candida
➔ Hygiene
➔ Climate
◆ Cold, damp climates may cause eczema to become more resistant to treatment
➔ Allergens
➔ Stress
 Clinical Presentation
❖ Characterised by remission and relapse with acute flares
on a background of chronic dermatitis.

Primary findings:
- Xerosis (dry skin)
- Lichenification (thickening of the skin and an increase in
skin markings)
- Eczematous lesions (skin inflammation)
- Acute dermatitis is red (erythematous), weeping/crusted
(exudative) and may have blisters (vesicles or bullae).

Eczematous changes and its morphology are seen in different

locations, depending on the age of the patient (ie, infant, child,
or adult).
 Clinical Presentation
Infantile
⧫ initially present as infantile seborrhoeic dermatitis
○ Involves scalp, and the armpit and groin creases
○ skin often feels dry and rough
○ With time → face, especially the cheeks, and flexures
become involved.
⧫ Young infants cannot scratch and will often rub affected areas
○ eg: the back of the head, causing temporary hair loss.
⧫ Backs of the hands can be affected due to sucking.
⧫ The napkin area is typically spared due to the moisture
retention of nappies
○ irritant contact napkin dermatitis can still develop.
 Clinical Presentation
Childhood Manifestations seen particularly in
Distribution changes as child grow school-age children and
⧫ Crawling → the extensor aspects of the elbows and adolescents:
wrists, knees and ankles are affected. ➔ Pityriasis alba,
⧫ Walking → flexural aspects, particularly involving the ➔ pompholyx
antecubital and popliteal fossae (elbow and knee ➔ discoid eczema
creases). ➔ pityriasis amiantacea
⧫ Dribble and food → mouth and chin. ➔ lip licker’s dermatitis
⧫ Scratching and chronic rubbing → the skin become ➔ atopic dirty neck
lichenified (thickened and dry), and around the eyes can
lead to eye damage.
 Clinical Presentation

Pruritic atopic dermatitis Pompholyx

Eyelid atopic eczema
Pityriasis amiantacea

Atopic cheilitis
Pityriasis alba
Atopic dirty neck Discoid eczema
 Clinical Presentation
Adult
⧫ May continue in the school-age flexural pattern or become diffuse.
⧫ Chronic rubbing → Madarosis, nodular prurigo, and lichenification
⧫ Discoid and papular patterns can develop.
⧫ Atopic dermatitis in childhood with subsequent complete resolution
○ may recur on the hands due to occupational and domestic duties
⧫ May develop for the first time in adulthood, as ‘adult onset’ atopic
dermatitis. (uncommon)
⧫ In women and some men, involvement of the nipples and areolae can
be problematic
 Diagnosis
❖ Usually diagnosed clinically
 Management
Investigations
- No biomarker for atopic dermatitis hence lab investigations are seldom necessary

Treatment
1. Moisturization
- Frequent baths with the addition of emulsifying oils (1 capful added to lukewarm
bath water) for 5-10 minutes hydrate the skin.
- Advise patients to apply an emollient (moisturizer) such as petrolatum or Aquaphor
all over the body while wet, to seal in moisture and allow water to be absorbed
through the stratum corneum
1. Topical steroids (mainstay of treatment!)
- Ointment bases are preferred
1. Topical calcineurin inhibitors
- Pimecrolimus and tacrolimus are suitable for treating atopic dermatitis in sensitive
sites such as the eyelids, skin folds, and genital areas.
1. Phototherapy
 Management
Treatment
5. Systemic treatment
- Antihistamines
- Systemic steroids
- Immunosuppressive or anti-inflammatory agent such as:
- Methotrexate
- Azathioprine
- Ciclosporin
- Mycophenolate mofetil.
 Outcome

⧫ Children who developed atopic dermatitis before the age of 2 years had a lower risk of
persistent disease than those who developed atopic dermatitis later in childhood or
adolescence.
⧫ Atopic dermatitis is typically worst between the ages of two and four years, and often
improves or even clears after this.
⧫ May be aggravated or reappear in adult life due to exposure to irritants or allergens
related to caregiving, domestic duties, or certain occupations.
 02
Seborrhoeic
Dermatitis
 Introduction

❖ Common chronic dermatosis with papulosquamous morphology (redness & scaling) in areas rich
in sebaceous glands
➢ Face
➢ Scalp
➢ Presternal area
➢ Body folds
❖ Epidemiology
➢ Age of onset
■ Infantile seborrhoeic dermatitis : occur w/i first 3 months, self-limiting, spontaneous
resolve w/i 1 yr
■ Adult seborrhoeic dermatitis : puberty - 50s, relapsing and remitting
➢ M>F
➢ 2-5% of population
 Etiology
❖ Multifactorial origin Proposed pathogenesis
❖ Exact mechanism remains unknown
i. Disruption of skin microbiota
1. Abnormal inflammatory reaction to skin ii. Impaired immune reaction to Malassezia
normal flora (Malassezia spp.) spp., diminished T cell response and
a. The effectiveness of ketoconazole and activation of complement
selenium as treatment iii. Increased unsaturated fatty acid on skin
b. Isolation from SD lesion surface
2. Hereditary tendency iv. Disruption of cutaneous neurotransmitter
3. Associated psoriasis v. Abnormal shedding of keratinocytes
4. Parkinson disease/Immunosuppression vi. Epidermal barrier disturbances associated
(HIV/AIDS)/facial paralysis with genetic factors
5. Nutritional deficiency
a. Zinc
b. Niacin
c. Pyridoxine
 Clinical Manifestation
❖ Gradual onset
❖ Worsen in winter/dry and cold environment
❖ Sunlight exposure cause flare in few patients, but also promote improvement in others

Infantile seborrhoeic dermatitis

1. Redness
2. Greasy scales
3. Scalp, face, ear, neck, diaper area, skin folds
4. Not itchy
 Clinical Manifestation
Adult seborrhoeic dermatitis
1. Redness (orange-red)
2. Greasy/white dry scaly patches
3. Itchy, exacerbate by perspiration
4. Scalp, eyebrows, eyelashes, beard, forehead, nasolabial folds, glabella, ears, central chest,
axillae, groin, anogenital area, submammary area
5. Men : worse in hair bearing areas of face
 Diagnosis
❖ By history and physical findings : red scaly plaques
❖ Skin biopsy : rarely required to confirm diagnosis/to rule our other conditions mimicking SD

Differential Diagnosis
Mild psoriasis vulgaris Distinguish by the distribution of lesion
Sometimes indistinguishable

Impetigo Differentiate by smears for bacteria

Dermatophytosis, pityriasis versicolour, Rule out by KOH

intertriginous candidiasis

Subacute lupus erythematosus Rule out by biopsy

Secondary syphilis (seborrhoeic papules) Rule out by dark field microscopy and syphilis
serology
 Seborrhoeic Dermatitis vs Atopic Dermatitis in Infants

Infantile Seborrhoeic Dermatitis Atopic Dermatitis in Infants

Earlier onset (first 3 months) Later onset (2 - 6 months)

Limited to areas with highly active Can occur anywhere
sebaceous glands
Absence of itching, irritability and insomnia Lesions are itchy and inflamed, interfering
sleep
Lesions appear to be oily and waxy Lesions appear to be dry and dull
 Histopathology
❖ Dermatopathology is nonspecific

1. Surface and infundibular epidermis

a. Perivascular infiltration of lymphocytes
b. Acanthosis
c. Focal spongiosis
d. Focal parakeratosis
e. Malassezia may/may not present in stratum corneum

2. When progress to chronic SD

a. Spongiosis → psoriasiform hyperplasia
b. Development of lichenoid lymphocytic infiltration Spongiosis with an area of overlying scale crust situated over a
hair follicle

3. Severe SD
a. Keratinocyte necrosis
b. Focal interface destruction
c. Leukocytoclasis
 Course & Prognosis

❖ Improves in summer and flares in falls

❖ Recurrences and remissions are common
❖ Alopecia in severe cases involving the scalp
❖ Infantile and adolescents SD disappear with time

★ May progress to seborrhoeic erythroderma (generalized exfoliative dermatitis)

○ Seborrhoeic erythroderma + diarrhoea + failure to thrive in infants → Leiner disease
○ Associated with variety of immunodeficiency disorders
■ Defective yeast opsonization
■ C3 deficiency
■ Severe combined immunodeficiency, hypogammaglobulinemia and
hyperimmunoglobulinemia
 Treatment

❖ Cradle cap
➢ Resolve w/o treatment
1. Shampoo once a day with baby shampoo and gently remove scaly skin with a soft
brush (eg, a soft toothbrush) or fine-tooth comb after shampooing
2. Apply a small amount of an emollient (white petroleum jelly, vegetable oil, mineral
oil, baby oil) to the scalp (overnight, if necessary) to loosen the scaly patches,
followed by gentle scalp massage with a soft brush (to lift the scale), then shampoo
with a non-medicated baby shampoo.
3. If persist, mild topical corticosteroid/antifungal shampoo
 Treatment
❖ Adult (Initial Therapy)
➢ Scalp
■ Shampoos
● Selenium sulfide
Equal effectiveness
● Zinc pyrithione
Leave in place for 3-5 mins, then completely rinse out of hair
● Tar
Improvement w/i 4-6 weeks
● 2% ketoconazole
■ Glucocorticoid solution/lotion/gel + medicated shampoo (ketoconazole/tar)
■ 1% pimecrolimus cream
➢ Face and trunk
■ Ketoconazole shampoo, 2%
■ Glucocorticoid cream and lotions
● 2% ketoconazole cream
● 1% pimecrolimus cream
● 0.03% or 0.1% tacrolimus ointment
 Treatment
❖ Adult (Initial Therapy)
➢ Eyelids
■ Gentle removal of crust in the morning by cotton ball dipped in diluted baby shampoo
■ Sodium sulfacetamide in a suspension containing 0.2% prednisolone and 0.12%
phenylephrine
Sodium sulfacetamide ointment
2% ketoconazole cream
1% pimecrolimus cream
0.03% tacrolimus ointment
➢ Skin folds
■ 2% ketoconazole cream (main)
■ Castellani paint → staining
■ 1% pimecrolimus cream
■ 0.03% or 0.1% tacrolimus ointment
➢ Systemic therapy
■ Only for very severe cases
■ 13-cis-retinoic acid, 0.5 - 1 mg/kg, oral – for more severe cases
■ Itraconazole, 100mg BD, 2 consecutive days, once a month – for milder cases
■ Contraception for childbearing age females https://pubmed.ncbi.nlm.nih.gov/15449823/#:~:text=Seborrhea%20has%20been%20less%
20well,condition%20using%20combined%20oral%20contraceptives
.
 Treatment
❖ Adult (Maintenance Therapy)
➢ Shampoos
■ 2% ketoconazole
■ Tar
➢ Cream
■ Ketoconazole
■ 1 to 2.5% hydrocortisone → monitor for signs of atrophy
■ 1% pimecrolimus
➢ Ointment
■ 0.03% tacrolimus
03 Contact Dermatitis
 Introduction
● A generic term to acute or chronic inflammation reactions to substances that come in contact with
the skin
● Can be acute (a single episode) or chronic (persistent)
● Two major types of contact dermatitis
➢ Irritant contact dermatitis (ICD)
➢ Allergic contact dermatitis (ACD)
 Irritant Contact Dermatitis (ICD)
3a
Introduction & Epidemiology

Introduction
● A form of skin inflammation caused by contact with substances and/or environmental factors
that injure the skin, damaging the skin barrier
● A localized disease confined to areas exposed to irritants
● Hands are the most commonly affected area

Epidemiology
● Most common form of occupational skin disease (80%)
● However, can occur in anyone being exposed to a substance irritant or toxic to the skin
 Aetiology
Aetiologic Agents Predisposing Factors Occupational Exposure

Abrasives, cleaning agents Atopy Medical, dental or vet

services

Oxidizing and/or reducing Fair skin Housekeeping, hairdressing,

agents cleaning, floral arranging

Plants and animal enzymes, Low temperature, low Agriculture, horticulture,

secretions humidity forestry

Desiccant powder, dust and Mechanical irritant Printing, painting,

soil engineering, fishing

Excessive exposure to water Occlusion Food preparation and

catering
 Pathogenesis
Pathogenesis
● Irritants (both chemical and physical), if applied for sufficient time and in adequate concentration
● The initial reaction is usually limited to the site of contact with the irritant

➢ Acute ICD
➔ Result from direct cytotoxic damage to keratinocytes

➢ Chronic ICD
➔ Results from repeated exposures that cause damage to cell membranes, disrupting the skin
barrier and leading to protein denaturation and then cellular toxicity
 Clinical Manifestations (Acute ICD)
Clinical Symptoms Skin Findings
● Subjective symptoms ● Minutes after exposure or delayed up to ≥ 24h
(burning, stinging or ➔ Lesion ranged from erythema to vesiculation and caustic burn
with necrosis
smarting)
➔ Sharply demarcated erythema and superficial oedema
➔ In more severe reactions, vesicles and blisters → erosions and/or
➔ Immediate-type Stinging frank necrosis
○ Occur within
seconds after ❖ No papules
exposure
❖ Distribution - isolated, localized, or generalized
➔ Delayed-type stingings
○ Occur within 1-2 ❖ Duration - days to weeks
Constitutional Symptoms
mins, peaking at 5-
● Only in widespread acute ICD
10 mins, fading by “acute illness” syndrome, fever
30 mins may occur
 Clinical Manifestations (Chronic ICD)
Skin Findings
Clinical Symptoms
● Dryness → chapping → erythema → hyperkeratosis and scaling →
● Stinging fissures and crusting
● Smarting ➔ Lesion is ill-defined borders, lichenification

● Burning ❖ Distribution
● Itching ○ Usually on the hands (usually starting from finger web
spaces → sides and dorsal surface of the hands → palm)
● Pain (as fissures develops)
❖ Duration - months to years

Constitutional Symptoms
● None, except when infection
occurs
 Laboratory Investigations

Histopathology Patch Tests

➢ Acute ICD ● Negative in ICD
○ Epidermal cell necrosis
○ Presence of neutrophils,
vesiculation and necrosis

➢ Chronic ICD
○ Acanthosis
○ Hyperkeratosis
○ Lymphocytic infiltrate
 Special Form of ICD
➔ Hand dermatitis
◆ Often sensitization to allergens (nickel, chromate salt) occurs later, and then ACD is superimposed in
ICD
◆ In such cases, the eruption may spread beyond the hands and may even generalized

➔ Airborne ICD
◆ Characteristically on the face, neck, anterior chest and arms
◆ Most frequent causes are irritating dust and volatile chemicals

➔ Pustular and acneiform ICD

◆ ICD may target follicles and become pustular and papulopustular
◆ Results from metals, mineral oils, greases, cutting fluids and naphthalenes
 Differential Diagnosis
● Allergic contact dermatitis
● Psoriasis
● Atopic dermatitis

Course & Prognosis

● Healing usually occurs within 2 weeks of removal of noxious stimuli
● In more chronic cases, 6 weeks or longer
● In the setting of occupational ICD, only one-third of individuals have complete
remission
● Atopic individuals have a worse prognosis
 Management

Prevention
● Avoid irritant or caustic chemical(s) by wearing protective clothing
● If contact does occur, wash with water or weak neutralizing solution
● Barrier creams
● In occupational ICD that persists in spite of adherence to the preceding
measures, a change of job may be necessary
 Management (Cont)
Acute Subacute & Chronic
● Identify and remove the etiologic ● Remove etiologic/pathogenic
agent agent
● Apply wet dressings with Burow’s ● Potent topical glucocorticoids
solution, changed every 2-3h (betamethasone dipropionate /
● Large vesicles may be drained
clobetasol propionate) and
● Topical class I-II glucocorticoids
adequate lubrication
preparations
● In chronic ICD of the hands, a
● In severe cases, systemic
“hardening effect” can be
glucocorticoids may be indicated
○ Prednisone - 2-week course, achieved in most cases with
60mg initially, tapering by topical (soak or bath) PUVA
steps of 10mg therapy
Systemic Treatment
● Alitretinoin - 0.5 mg/kg body
weight po for up to 6 months
● Observe CIs to systemic
retinoids
 Allergic Contact
3b Dermatitis
 Introduction
● A form of dermatitis caused by an allergic reaction to a material (allergen), in
contact with the skin

● A systemic disease defined by hapten-specific T-cell mediated inflammation

● An eczematous (papules, vesicles, or pruritic) dermatitis

● Caused by re-exposure to a substance to which the individual has been sensitized

● The allergen is harmless to people that are not allergic to it

● Also known as contact allergy

 Epidemiology & Pathogenesis
Epidemiology
● Accounts for 7% of occupational related
illnesses in US
● Non-occupational ACD 3x greater than
occupational ACD
● Age of onset - all ages, but uncommon in
young children and individual >70 years

Pathogenesis
● A classic, delayed, cell-mediated
hypersensitivity reaction
 Allergens
● Contact allergens are diverse and range from metal salts to antibiotics
and dyes to plant products
 Clinical Manifestation
● Eruptions starts in a sensitized individual 48h or days after contact with the allergen
● Repeated exposures lead to a crescendo reaction
● The site of the eruption is confined to the site of exposure

Symptoms
● Intense pruritus
● In severe cases, stinging and pain

Constitutional Symptoms
● “Acute illness” syndrome, including fever (only seen in severe ACD)
 Skin Lesions
Acute Subacute Chronic

Well-demarcated erythema Plaques of mild erythema Plaques of lichenification,

and oedema with showing small, dry scales, scaling with satellite, small,
superimposed closely spaces sometimes associated with firm, rounded or flat topped
papules or non-umbilicated small, red, pointed, or rounded papules, excoriations and
vesicles erythematous firm papules and pigmentation
scales

In severe reactions, bullae,

confluent erosions exuding
serum and crusts
Distribution of lesions
➔ Shoe dermatitis
◆ Isolated, localized
to one region
➔ Plant dermatitis
◆ Generalized
 Laboratory Investigations

Dermatopathology Patch Tests

➔ Acute ❖ +ve patch test
○ Prototype of spongiotic
○ Erythema and papules
dermatitis, with intercellular
oedema (spongiosis), ○ Possibly vesicles
lymphocytes and confined to the test site
eosinophils in the epidermis
○ Monocytes and histiocytes ★ Patch tests should be delayed
infiltration in the dermis
until the dermatitis has subsided
➔ Chronic for at least 2 weeks and should
○ Spongiosis + acanthosis be performed on a previously
○ Elongation and broadening uninvolved site
of papillae
○ Hyperkeratosis
○ Lymphocytic infiltrate
 Special Form of ACD
➔ Allergic phytodermatitis (APD)
◆ Occurs in sensitized individuals after exposure to a wide variety of plant allergens
◆ Characterized by an acute, very pruritic, eczematous dermatitis, often in a linear arrangement
◆ In US, poison ivy / oak are by far the most common plant implicated

➔ Systemic ACD
◆ After systemic exposure to allergen to which the individual had prior ACD
◆ A delayed T-cell mediated reaction
◆ Examples: ACD to ethylenediamine → subsequent reaction to aminophylline; poison ivy dermatitis →
subsequent reaction to ingestion of cashew nuts; antibiotics, sulfonamides, propylene glycol, metal ions,
sorbic acid and fragrances

➔ Airborne ACD
◆ Contact with airborne allergens in exposed body sites, notably the face including the eyelids, “V” of the
neck, arms and legs
◆ Prolonged repetitive exposure leads to dry, lichenified ACD with erosions and crusting
◆ Caused by plant allergens, especially from compositae, natural resins, woods, and essential oils volatizing
from aromatherapy
 Differential Diagnosis
● Irritant contact dermatitis ● Epidermal dermatophytosis
● Fixed drug eruption
● Atopic dermatitis ● Phytophotodermatitis
● Seborrhoeic dermatitis
● Psoriasis
Course & Prognosis
● Evolution of ACD - duration of ACD varies, resolving in around 1-2 weeks, but becomes worse as
long as the allergen continues to come into contact with the skin
● Acute. Erythema → papules → vesicles → erosions → crusts → scaling
● Chronic. Papules → scaling → lichenification → excoriations
 Management

Termination of exposure ● Identify and remove the etiologic agent

Topical therapy ● Topical glucocorticoids ointments/gel (class I-III)

● Pimecrolimus and tacrolimus

Systemic therapy ● Glucocorticoids , indicated in severe and airborne ACD

○ Prednisone: 70mg in adults, tapering by 5-10mg over a
1- to 2-week period
● In airborne ACD, where complete avoidance of allergen may be
impossible, immunosuppression with oral cyclosporine may
become necessary
Differences between ICD & ACD
THANK YOU