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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
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 Initially, the restoration of the integrity of the skin as a barrier to infection and allergen exposure requires intensive rehydration and lubrication.
 Isolated findings and complications which can be associated with atopic dermatitis are misdiagnosed.
 The use of antihistamines to break the itch-scratch cycle' and topical mild corticosteroids are often helpful but caution regarding the use of fluorinated steroid use cannot be overemphasized especially in covered and intertriginous areas and on the face.
 When considering the use of mid-potency topical or systemic corticosteroids a dermatologic consultation should be considered.
 One must look for evidence of superinfection or infestation and treat accordingly.
 Tar, ultraviolet phototherapy, dietary manipulation, and evening primrose oil are considerations.
 One should also consider psychosocial contributing factors in evaluating these patients.
 Allergic evaluation and the use of agents like phosphodiesterase inhibitors, immunosuppressants, immune modulators, vitamins C and E and mast cell stabilizers are more controversial
Examples of isolated findings that can be seen in atopic dermatitis:
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Keratosis pilaris
Hand dermatitis...........
Pityriasis alba
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Perioroficial dermatitis
Plantar juvenile dermatosis
Frictional lichenoid dermatitis
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Other associated conditions and complications of atopic dermatitis:
Secondary infections:
Bacterial
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Fungal.......
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Viral.........
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T. rubrum
Candida
P. ovale
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Herpes simplex (Eczema Herpeticum)
Verruca vulgaris
Molluscum contagiosum
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Ophthalmologic findings:
Keratoconus..........................Ectropion
Conjunctivitis.........................Subcapsular cataracts
Other:
Effects of therapy (ie., steroids))...........Growth retardation
Sleep disturbance..............................Psychosocial
Conditions characterized by eczematous dermatitis:
Primary conditions:
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Atopic dermatitis
Asteatotic eczema
Non-specific hand dermatitis
Contact irritant dermatitis
Contact allergic dermatitis
Chronic eczema
Nummular eczema
Lichen simplex chronicus (neurodermatitis)
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Fungal infections
Infestations (ie., scabies, lice)
Autoeczematization
Dyshidrotic eczema
Airborn contact dermatitis
Photoeczematous
Prurigo nodularis
Stasis dermatitis
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Pruritic diseases with secondary eczematous changes:
Hodgkin's
Thyroid disease
Iron deficiency anemia
Delusions of parasitosis
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Hepatic/renal disease
Polycythemia vera
Chronic urticaria
Neurotic excoriations
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HIV infection
Non-eczematous masqueraders of eczema:
Localized
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Generalized
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Bowen's
Paget's
Juvenile psoriasis
Hypertrophic lichen planus
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Erythroderma
Rapid:
Drug......... Lymphoma
Contact (ie., T cell)
SSSS...... Leukemia
Gradual:
Psoriasis...... Atopic dermatitis
Pityriasis rubra pilaris
Mycosis fungoides
Histiocytosis X
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Other conditions associated with "atopic-like" dermatitis:
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
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Selective IgA deficiency
DiGeorge syndrome
Nezelhoff's syndrome
Letter-Siwe disease (histiocytosis X)
Chronic granulomatous disease
Leiner's disease
Alopecia areata ?
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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
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Other
Ichthyoses
Ichthyosis vulgaris
Netherton's syndrome
Anhydrotic ectodermal dysplasia
Dubowitz syndrome
Migraine ?
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Phases of Atopic Dermatitis
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%
Adapted from Hanifin and Rajka Acta DermVenereol (Suppl).1980;92:44-7.
* = common; +=uncommon but specific
ERYTHROMYCIN DRUG INTERACTIONS
INCREASED ACTIVITY
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DECREASED ACTIVITY
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Theophylline
Carbamazepine
Cyclosporine
Na warfarin
Digoxin
Disopyramide
Methylprednisone
Trazolam
Alfentanil
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Clindomycin
Lincomycin
Sulfonamides
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THERAPEUTIC CONSIDERATIONS
Standard therapy:
Discuss realistic expectations
Keep the plan as simple as possible.
Write out instructions for patients on an education handout.
Must control xerosis and itching
Avoid harsh soaps
Liberal use of moisturize
Oral antihistamines
If oozing or infected:
Consider secondary bacterial, fungal and/or herpes infection
Soaks with wet compress, remove them and allow areas to air dry
Control inflammatation if above is ineffective:
Topical corticosteriods
Consider advanced therapy if above is ineffective:
Systemic steroids
Occlusive suits ("Sauna suit")
Tars
Ultraviolet V phototherapy
Evaluation for psychosocial, dietary and/or environmental factors
Caution against dietary restriction without proof as this is usually not necessary!
Controversial:
Evening primrose oil
Eicosapentenoic Acid
Cyclosporin
Phosphodiesterase inhibitors
Investigational:
TP-5 (thymopoietin)
Thymostimulin (TP-1) injection
Interferon
IL-2
Chloroquin
Vitamin C and/or E
Ketotifen
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