Introduction

• The terms eczema and dermatitis are used interchangeably, denoting a

polymorphic inflammatory reaction pattern, involving the epidermis and dermis.
• There are many types of eczema, and they are varying in the clinical findings and
the course of the disease.
• In acute dermatitis, the findings are often pruritis, erythema, and vesiculation.
• While in chronic dermatitis pruritus, xerosis, lichenification,
hyperkeratosis/scaling, and ± fissuring
•
• Eczema:
• 1. Endogenous: atopic dermatitis
• 2. Exogenous: contact dermatitis (allergic, irritant)
 Atopic dermatitis

• Atopic dermatitis (AD) is

• an inflammatory skin disease that typically manifests for the first time in early
childhood.
• Although it often improves during adolescence, it may also become a chronic
condition that extends into adulthood.
• Age of Onset: First 2 months of life and by the first year in 60% of patients;
30% by age 5, and only 10% between age 6 and 20 years. Rarely AD as an
adult.
• Genetic Aspects: The inheritance pattern is not yet ascertained. However, in
one series, 60% of adults with AD had children with AD. The prevalence in
children was higher (81%) when both parents had AD.
• Gender: Slightly more common in males than in females.
• • Prevalence: 7% - 15%
 Atopic dermatitis

• Etiologies, and predisposing factors:

•

• Microbial agents: Exotoxins of Staphylococcus aureus acting as superantigens. Also group A

streptococcus, rarely fungus (candida).

• auto-allergens: Sera of patients with AD contain IgE antibodies directed at human proteins. The
release of these auto-allergens from damaged tissue could trigger IgE or T-cell responses, suggesting
maintenance of allergic inflammation.

• Foods: Infants and children, but not adults, have flares of AD with eggs, milk, peanuts, soybeans,
fish, and wheat.

• Sessional variations: it gets worse during the winter and improves during the summer.

• clothing: Pruritus flares after taking off clothing. Wool is an important trigger. Also the fur of pets
and some carpets.
 Atopic dermatitis

• Pathogenesis:
• It is basically an interaction of the skin barrier, genetic, environmental, pharmacologic, and skin
immunologic factors
• Skin barrier disruption due to impaired filaggrin production, reduced ceramide levels, and
increased transepidermal water loss; dehydration of skin
• . It is type 1 hypersensitivity reaction (IgE-mediated) that started when interaction happens
between the body and the listed above antigens.
• Mast cells and basophils get sensitized by IgE that is bound to the antigens and they release
vasoactive substances.
• The epidermal Langerhans has a high affinity for IgE receptors which participate in the
initiation of an eczema-like reaction. The process has two phases;
• • acute inflammation which is associated with mainly IL 4 and IL13 expression.
• • Chronic inflammation is associated with IL5, granulocyte-macrophage colony-stimulating
factor, IL12, and interferon-γ.
 Atopic dermatitis

• Clinical manifestations
• Skin symptoms:
• • PRURITUS
• • Constant scratching leads to a vicious cycle of itch -> scratch -> rash -> itch -> scratch.
• Other symptoms of atopy: allergic rhinitis, obstruction of nasal passage, …
• Skin lesions:
• • Acute: Poorly defined erythematous patches, papules, and plaques with or without scale. Edema with widespread
• involvement; skin appears "puffy" and edematous. Erosions: moist, crusted, linear or punctate, resulting from scratching.
• Secondarily infected sites: S. aureus. Oozing erosions and/or pustules. Skin is dry, cracked, and scaly.
• • Chronic:
• 1. Lichenification (thickening of the skin with accentuation of skin markings), follicular lichenification (espedally in brown
• and black persons).
• 2. Fissures: painful, especially flexures. Often on the palms, fingers, and soles.
• 3 Dennie-Morgan fold (fold of skin under the lower eyelid, due to chronic eyelid dermatitis).
• 4 Ichthyosis vulgaris (fish like dry scales in the leg, and often thickened skin.
• 5 Keratosis pilaris (spine papules in the upper arm and thigh).
• 6. Distribution. Predilection for the flexures, front and sides of the neck, eyelid, forehead, face, wrists and dorsa of the feet
• and hands. Generalized in severe disease.
• 7 White" Dermatographism. Stroking of involved skin will not lead to redness as in normal skin but to blanching;delayed blanch to
cholinergic agents.
 Atopic dermatitis

• Age-related features:
 Atopic dermatitis
Taking history from the patient
• • History of the patient:
• ask about the skin lesion..
• -When did it start?
• -What aggravates the problem? Food- clothing- soup - sun exposure.
• -If there are vesicles ask about them to differentiate between the other forms of eczema like irritant
• contact dermatitis or nummular eczema where vesicles could appear.
• constitutional symptoms: ask about fever
• and past medical history:
• -Ask about hereditary diseases.
• -Ask about of allergy “asthma, hay fever, rhinitis, conjunctivitis, eczema”
• -History of urticarias to roll out and put as last DD, “the lesions come, stay for few hours,
• then go and it can be chronic for years”.
• Family history:
• -You have to ask if there are any allergic diseases in the family like asthma, allergic rhinitis, conjunctivitis, eczema, hay fever, and any history of anaphylaxis.
• Social history: ask if the condition affects his performance in any way.
• Travel history:
• -Ask about any history of traveling to exclude scabies
• to differentiate between AD and scabies
• scabies lesions will be the same as AD lesions, but present in the digital finger spaces there will be excoriation, more itching in this area, as well as the genital areas, are involved also there will
other members of the family have the same
• condition” so the history of scabies has to be rolled out.

• Examination:
• There are important signs must focus on
• • Face: whitish or hypopigmented scaly patches “Pityriasis alba”
• • Eye:
• -Extra fold below the eye “Dennie–Morgan fold”
• -periorbital pigmentation.
• -loss of the lateral eyebrows.
• -keratoconjuctivites, dryness of the eye is rare.
• -the cornea will become a cone shape “Keratoconus”
• -cataract.
• • Neck: hyperpigmentation “dirty neck sign”.
• • Leg: dryness, fish-like scales, ichthyosis “Ichthyosis Vulgaris”
• • Palms: increase in numbers of lines “hyperlinear palms”
• • Arms and thighs: Keratosis pilaris, when you run your fingers in these areas there will be spinney small papules. It can also come in normal skin.
 Atopic dermatitis
• Differential diagnosis
• Psoriasis
• Contact dermatitis
• Scabies
• Laboratory investigations:
• bacterial Culture: Colonization with S. aureus is very common, in severe cases look for
• MERSA colonization.
• Viral Culture: Rule out herpes simplex virus (HSV) infection in crusted lesions.
• blood Studies: Increased IgE in serum, eosinophilia. HSV antigen detection for diagnosis of acute HSV
infection.
• Skin biopsy: will show spongiosis.

• Complications:
• AD can be complicated with infections like S. aureus or viruses like herpes virus “eczema herpeticum
which has a bad prognosis”
• Prognosis:
• -If
left untreated it may persist for months to years.
• -spontaneous remission could present in more than 40%.
• -Occasionally recurrence attacks may present.
• -30-50% of the patients develop asthma with or without hay fever .
 Atopic dermatitis
• Management;
• Avoid rubbing and scratching. And avoid emotional stress and sweating.
• Acute
• - Wet dressings.
• - Topical glucocorticoids + topical or oral antibiotics.(firist line treatment)
• - Oral H1-antihistamines (Hydroxyzine).
• Subacute and Chronic
• Moisturizer application
• Topical glucocorticoids.:don’t use it for long duration since it causes skin atrophy
• When the patient gets better, replace the steroids with Calcineurin inhibitors (maintenance)- used for children
less than 8 years and we cant use at beginning thereby .
• UV phototherapy (maintenance):Children 10 years old or above can undergo phototherapy.
• For chronic, add keratinolytic like salicylic acid
In severe intractable disease; Systemic glucocorticoids.
• In sever cases when all other treatments fail; cyclosporine (used for adult, without renal
problem or hypertension).
• And Biologic agent Dupilumab directed against IL4,IL13
• Ig E target drugs – omalizumab
l ‫ملخص ل‬Treatment
Irritant contact dermatitis & Allergic
contact dermatitis
 Irritant contact dermatitis:

• Treatment measures:
• - Avoid irritant or caustic chemical(s) by wearing protective clothing (i.e., goggles,
• shields, and gloves).
• - If contact does occur, wash with water or weak neutralizing solution.
• -Barrier creams.
• -In occupational ICD that persists despite adherence to the above measures, change of
• job may be necessary.
• Acute case:
• -Identify and remove the etiologic agent.
• -Wet dressings with Burow’s solution, changed every 2–3 h.
• - Larger vesicles may be drained, but tops should not be removed.
• - Topical glucocorticoid preparations.
• - In severe cases, systemic glucocorticoids may be indicated, Prednisone: 2-week
• course.
• Subacute and chronic:
• -Remove etiologic/pathogenic agent.
• -Potent topical glucocorticoids (betamethasone dipropionate or clobetasol propionate)
• -adequate lubrication. As healing occurs, continue with lubrication.
• -Calcineurin acid inhibitors are not effective in ICD.
• -In chronic ICD of hands, a “hardening effect” can be achieved in most cases with
• topical (soak or bath) PUVA therapy.
• -
• Systemic treatment:
• we can use systemic retinoid but with caution to contraindications.
 Allergic contact dermatitis:
• Treatment measures:
• -Termination of Exposure. Identify and remove the etiologic agent.
• -Topical Therapy: Topical glucocorticoid ointments/gels.
• -Larger vesicles may be drained, but tops should not be removed.
• -Wet dressings with cloths soaked in Burow’s solution changed every 2–3 h.
• -Pimecrolimus and tacrolimus (Calcineurin acid inhibitors) are effective in ACD but to a lesser degree than
glucocorticoids.
• Systemic treatment:
• -Glucocorticoids are indicated if it is severe case or airborne ACD.
• -In airborne ACD where complete avoidance of allergen may be impossible, immunosuppression with oral
cyclosporine may become necessary.

• Calcininerun acid inhibitor are not effictife in Irritant contact dermatitis

• Most important-> Allergic Contact Dermatitis (ACD).
• It tends to involve surrounding skin & spread beyond affected site "immunological“
• Appear after 12 to 72 hours after exposure
• .You should know some names for the causative agents "metal salts, dyes, plant products, jewelry, nickel
sulfate
• hair dye Hair dye-> The allergy is to PPD "Para-phenyene-diamine" and benzene
• .Most important -> Patch test
• Know how patch test is done ? the results? when we read the results? after 48-72 hours
• .Patch test Should be delayed until the dermatitis has subsided for at least 2 weeks.
• Why? to avoid false positive results because the body is active during the acute eczema, so may give
positive results for unsensitized agents.
• Prior to patch test, the patient should stop antihistamine and systemic steroid drugs at least 72 h
‫ملخص‬
 seborrheic dermatitis

• Introduction
• A very common chronic dermatosis characterized by redness and scaling and occurring
• in regions where the sebaceous glands are most active, such as the face and scalp, the
presternal area, and in the body folds.
• Epidemiology
• - Occur Infancy (within the first months), puberty, most between 20 and 50 years or older.
• - More common in Males Pathogenesis -Hereditary diathesis - Caused by Malassezia furfur
• -There is an increase in incidence in Parkinson disease and facial paralysis and in
immunosuppressed patients
• - Intractable SD should be a clue to the existence of HIV disease
• Clinical manifestation :
• - Pruritus which increased by perspiration
• - Gradual onset
• Description of Skin lesion : Orange-red or white dry scaling macules
• ,papules or patches, sharply marginated
• Manifestation depending on site - Ear : sticky crusts, and fissures
• - Trunk: yellowish-brown patches over the sternum common
• - Body folds: erythematous eruption; erosions and fissures
• - Genitalia: yellow crusts and psoriasiform lesions.
 seborrheic dermatitis

• DDX:
• *Mild psoriasis vulgaris
• *impetigo (rule out by smears for bacteria)
• *dermatophytosis, pityriasis versicolor, intertriginous candidiasis (rule out dermatophytes and yeasts by potassium hydroxide KOH).
• (Extra-note>> How to do KOH test: A doctor or nurse takes a sample by lightly
• scraping the infected area. Sometimes the doctor will use a swab. The sample is then placed on a slide with potassium hydroxide
(KOH) solution and is gently heated. This solution slowly dissolves the skin cells but not the fungus)
• *subacute lupus erythematosus (rule out by biopsy)
• seborrheic" papules in secondary syphilis (rule out Treponema pallidum by darkfield); syphilis serology
• Laboratory Studies
• Dermatopathology.
• Focal parakeratosis, moderate acanthosis, spongiosis
• A characteristic feature is neutrophils at the tips of the dilated follicular openings, which appear as crusts/ scales.
• Course and Prognosis
• -The condition improves in the summer and flares in winter
• -Recurrences and remissions, especially on the scalp,
• -Infantile and adolescent SD disappears with age
• Management
• initial therapy followed by chronic maintenance therapy
• Initial Therapy Topical 1- Removal of the crusts *Infantile: with warm olive oil compresses
• Eyelids: with a cotton ball dipped in diluted baby shampoo.
• 2- 2% ketoconazole shampoo,
• 3- 2.5% hydrocortisone cream or clobetasol propionate (in resistant cases)
• 4- For body folds > Castellani Paint but staining is a problem, Pimecrolimus cream, 1%; tacrolimus ointment, 0.03%
• 5- For eyelids > Sodium sulfacetamide ointment
 seborrheic dermatitis

• Systemic 1- 13-cis-retinoic acid orally, Caution: Contraception should be used in females of childbearing age
• 2- In milder cases, itraconazole 100 mg
• Maintenance Therapy
• Ketoconazole 2% shampoo
• 1% pimecrolimus cream and 0.03% tacrolimus ointment
 Reffrences
• Note 220,217,216
• fitzpatrick color atlas 8th edition 8th edition