ATOPIC DERMATITIS

Characteristically, atopic dermatitis is a chronic disorder with a relapsing course, pruritis, variable presentation, and is associated with an atopic diathesis in 75 to 80% of afflicted patients.
The disorder may present with evidence of acute eczematous changes with micro-vesiculation, erosions and crusts or with more chronic lichenified plaques.
It may present as a generalized dermatitis or a more localized condition affecting the scalp, hands or feet.
This diversity makes the diagnosis of atopic dermatitis and its distinction from other eczematous dermatoses difficult.
Isolated findings and complications which can be associated with atopic dermatitis are misdiagnosed.
Conversely, other patients have eczematous dermatoses which actually represent cutaneous manifestations of systemic disorders which may be associated with malignancies, nutritional/metabolic and immunodeficiency states.
The dermatologist's approach to the differential diagnosis of eczema will be discussed in detail with special emphasis on the distinction of atopic dermatitis.
Attempting to explain the etiology of atopic dermatitis is far from easy.
Its association in families with atopic disorders may relate to the recent isolation of an autosomal dominant gene on chromosome 11q apparently responsible for IgE responsiveness in families with asthma and rhinitis.
The resolution of atopic-like dermatitis following bone marrow transplantation and the transfer of atopic dermatitis to a bone marrow recipient suggest an intrinsic dysregulation of the immune system in these individuals.
Classically atopic dermatitis has been associated with type IV hypersensitivity but the role of IgE mediated or type I hypersensitivity has been suggested for some time.
It is now hypothesized that "late phase reactions" occur in patients with allergic mediated atopic dermatitis, whereby the initial insult, involving mast cell degranulation with subsequent infiltration of neutrophils, basophils, and eosinophils is later replaced by lymphocytes and macrophages.
The presence of prior eosinophil infiltration is substantiated by documented presence of major basic protein in these infiltrates.
The presence of antigen specific IgE receptors on Langerhans cells in these infiltrates in atopic individuals and the mediation by cytokines (specifically IL-4 and gamma interferon) on these receptors provides a possible model to explain how chronic exposure to food and aeroallergens can precipitate a dermatitis.
Staphylococcal infection (or colonization) and superantigens may play a role in prolonging the eczematous changes.

The approach to therapy must be individualized to the needs of the patient

Bibliography

Examples of isolated findings that can be seen in atopic dermatitis:

.......................................	............................................
Keratosis pilaris Hand dermatitis........... Pityriasis alba	Perioroficial dermatitis Plantar juvenile dermatosis Frictional lichenoid dermatitis

Other associated conditions and complications of atopic dermatitis:
Secondary infections:

Bacterial	Fungal.......	Viral.........
	T. rubrum Candida P. ovale	Herpes simplex (Eczema Herpeticum) Verruca vulgaris Molluscum contagiosum

Ophthalmologic findings:

Keratoconus..........................Ectropion
Conjunctivitis.........................Subcapsular cataracts

Effects of therapy (ie., steroids))...........Growth retardation
Sleep disturbance..............................Psychosocial

Primary conditions:
Atopic dermatitis Asteatotic eczema Non-specific hand dermatitis Contact irritant dermatitis Contact allergic dermatitis Chronic eczema Nummular eczema Lichen simplex chronicus (neurodermatitis)	.....	Fungal infections Infestations (ie., scabies, lice) Autoeczematization Dyshidrotic eczema Airborn contact dermatitis Photoeczematous Prurigo nodularis Stasis dermatitis

Hodgkin's Thyroid disease Iron deficiency anemia Delusions of parasitosis

.....

Hepatic/renal disease Polycythemia vera Chronic urticaria Neurotic excoriations

Non-eczematous masqueraders of eczema:

Localized	....	Generalized
Bowen's Paget's Juvenile psoriasis Hypertrophic lichen planus		Erythroderma Rapid: Drug......... Lymphoma Contact (ie., T cell) SSSS...... Leukemia Gradual: Psoriasis...... Atopic dermatitis Pityriasis rubra pilaris Mycosis fungoides Histiocytosis X

Immunologic

Acquired immunodeficiency (HIV) Severe combined immunodeficiency Wiskott-Aldrich syndrome Ataxia telangiectasia X-linked agammaglobulinemia Hyper-IgE syndrome X-linked immunodefiency with hyper IgM Episodic lymphopenia with lymphocytotoxins

....

Selective IgA deficiency DiGeorge syndrome Nezelhoff's syndrome Letter-Siwe disease (histiocytosis X) Chronic granulomatous disease Leiner's disease Alopecia areata ?

Metabolic/nutritional Phenylketonuria Histidinemia Celiac sprue/gluten sensitive enteropathy Acrodermatitis enteropathica Hurler's syndrome Anhydrotic ectodermal dysplasia Hartnup's disease Pellagra Essential fatty acid deficiency Biotin deficiency Protein caloric malnutrition

....

Other Ichthyoses Ichthyosis vulgaris Netherton's syndrome Anhydrotic ectodermal dysplasia Dubowitz syndrome Migraine ?

Infant phase: birth to 2 yrs (mean 7.9 mos) cheeks, abdomen, ext surfaces of legs, irritabel and aggitated at night, prutitus, generalized papular eruption can erupt sparing the diaper area
Childhood phase: 2-12 yr, papules coalesce to plaques in flexural areas like neck, antecubital and popliteal fosae, and wrists and ankles. with extensive excoriations and lichenification
Adult phase: dorsal aspect of hands, upper eyelids, fexural extremities, more diffuse with increased scaling and decreased excoriations

Diagnostic Features of Atopic Dermatitis

Must have three or more major features:

Pruritus
Typical morphology and distribution
flexural lichenification or linearity in adults
facial and extensor involvement in infants and children
Chronic or chronically relapsing course
Personal or family history of atopy (asthma, allergic rhinitis, or atopic dermatitis)

Must also have three or more minor fatures:

Xerosis ( 50%) esp if humidity < 60%
Ichthyosis 37%, /*palmar hyperlinearity 1/3-1/2 /*keratosis pilaris
Immediate (type I) skin test reactivity 80%
Elevated serum IgE
Early age of onset
Tendency toward cutaneous infections (est. Staphyloccocal aureus and Herpes simplex)/impaired cell-mediated imnmunity
Tendency toward nonspecific hand or foot dermatitis
+Nipple eczema
+Cheilitis
Recurrent conjunctivitis
Dennie-Morgan infraorbital fold
Keratoconus
+Anterior subcapsular cataracts
Orbital darkening
Facial pallor/facial erythema
*Pityriasis alba
Itch when sweating
Intolerance to wool and lipid solvents
Perifollicular accentuation (generalized is pathognomonic)
Food hypersensitivity
Course influenced by environmental/emotional factors
*White dermatographism/delayed blanch 70%

ERYTHROMYCIN DRUG INTERACTIONS

THERAPEUTIC CONSIDERATIONS

Standard therapy:

Avoid harsh soaps
Liberal use of moisturize
Oral antihistamines

Consider secondary bacterial, fungal and/or herpes infection
Soaks with wet compress, remove them and allow areas to air dry

Topical corticosteriods

Systemic steroids
Occlusive suits ("Sauna suit")
Tars
Ultraviolet V phototherapy

Caution against dietary restriction without proof as this is usually not necessary!

Evening primrose oil
Eicosapentenoic Acid
Cyclosporin
Phosphodiesterase inhibitors

TP-5 (thymopoietin)
Thymostimulin (TP-1) injection
Interferon
IL-2
Chloroquin
Vitamin C and/or E
Ketotifen