1-5-09 Eczemas Eczema=dermatitis.

It is a generic term that includes the following conditions: atopic dermatitis, allergic contact dermatitis, and irritant contact dermatitis. Dermatitis means skin inflammation. In practice, it refers to a specific pattern of skin inflammation with epidermal changes resulting from scratching and rubbing. It is a histopathology pattern of tiny fluid collections in the epidermis. Triggers of eczema include: Clothing: choose cotton over wool Airborne irritants: chlorine and cigarette smoke exacerbate eyelid involvement Hormonal: menstrual flaring, preganancy, parturition, menopause Sweathing: causes pruritis scratching more eczema Dry, cold winters (some may also experience exacerbations during the summer) Season of birth Animal exposure during first few months of life Exposure to viral infections Atopic dermatitis (AD) is a chronic inflammatory disease of the skin frequently seen in the pediatric age group. Characterized by itching (pruritis), dry skin, scaly skin, erythema, edema, scaling, excoriations, oozing, lichenification (aka lichen simplex chronicus) Crusted rash appears most commonly on face, scalp, hands, arms, feet and legs Small bumps open and weep when scratched There is thickening of the skin due to the chronic nature of AD A component of the atopic triad (atopic dermatitis, asthma, allergic rhinitis) Associated with these presentations: Dennie-Morgan folds are multiple creases of the lower eyelid that can result from any chronic dermatitis around the eyes. Hyperlinearity of the palms can also be seen Ichthyosis Vulgaris: diagnostic of keratinization, with dry rectangular scales and accentuated palm creases affecting the extensor aspects of arms and legs. X-linked Ichthyosis: occurs exclusively in males, with darker and larger areas that affect both extensor and flexor areas; improves with age Hertoghes Sign: lateral part of the prow is alopeicic due to chronic rubbing Pretty common immune-related inflammatory skin disorder, with a 10-20% prevalence in Western industrialized countries Immunologic abnormalities in AD characterized by increased IgE production with a TH2 response (psoriasis is TH1). Increased basophils and spontaneous histamine release Decreased cytotoxic CD8 number and function Increased CD23 expression on B cells and monocytes Chronic macrophage activation with increased GM-CSF, PGE2, and IL-10 Decreased numbers of TH1-like cells producing IFN-gamma There are greater numbers of activated eosinophils in chronic AD than in acute

AD The TH2 profile involves IL-4 and IL-10 TH2 cells suppress macrophage activity, activate eosinophils, induce isotype switching to IgE and IfG4, and downregulate TH1 (via IL-10) Antimicrobial peptides defensins (HBD-2) and cathelicidins (LL37) are decreased in atopics (unlike psoriasis, which has normal levels Thus, theres a propensity for S. aureus infection

Multi-factorial etiology that includes: interactions between genes and environment, family history w/ strong correlation w/ siblings, and AD genes localized to chromosomes known to control immune response and inflammation Begins early in life: seen in infancy in 50-75% of cases Clearance rate of 60% of cases by age 16, but relapses do occur in adulthood Prognosis worsens with severe childhood disease, early onset, concomitant family history of asthma/allergic rhinitis (think atopic triad!), biparental history of AD Theories that AD results from clean living Various foods can exacerbate AD, the most common being eggs, peanuts, milk, fish, soybeans, and wheat In adults, milk-induced eczema and casein-specific T cells are commonly found. The flare is often delayed by 24 hours. No reliable test exists to delineate cause/effect for dietary agents; RAST and prick tests are used to exclude an IgE-mediated food allergy Morbidity: psychological problems, itch-scratch cycle, sleeplessness, poor concentration on work or school, repeated treatments/time/financial costs Clinical phases of AD: Infantile phase (0-2 years) Onset at 3 mo, with involvement of the face and scalp. After 6 months, limb folds and hands become involved. Red, crusty, weeping patches with excoriations seen on both cheeks and extensor surfaces of extremities Chronically relapsing and remitting Childhood phase (2-12 years) Papules in flexural regions Persistent rubbing leads to lichenified plaques and excoriations Adult phase (puberty onwards) Flexural lichenified eczema with facial involvement in periorbital regions seen. Upper trunk, shoulders, scalp affected with chronic remission/ exacerbation. In summary Childhood AD involves antecubital, popliteal, flexors, eyelids, face, and neck. Its associated with growth retardation in severe cases alongside psychological disturbances. Adult AD has less characteristic distribution, but commonly involves hands and wrist. It is characterized by dry, excoriated, lichenified lesions. Stress, anxiety, and depression can worsen the condition. Diagnosis of AD requires 3+ of the following major criteria: Pruritis (keep in mind that psoriasis usually does NOT itch) Typical morphology and distribution Chronic/chronically relapsing course Personal or family history of atopy Treatment of AD involves three strategies: Avoid triggers: anxiety/stress, allergens (irritants, soaps, detergents, cigarette smoke, house dust mites, grass pollens), climactic factors (temperature/ perspiration, low humidity environments, wool), food allergens (eggs, milk,

peanuts, soybeans, tree nuts, fish wheat, prolonged breast feeding), infections (eczema herpeticum, molluscum contagiosum, HPV, superficial fungal infections, S. aureuswhich is found in over 90% of AD patients!) Control dry skin: emmolients (moisturizers, baths with added lubricants) Treat the inflammation: topical (glucocorticosteroids, immunomodulators, newer non-steroidal TIMstacrolimus and pimecrolimus), systemic treatments (oral antihistamine, oral antibiotic, systemic steroid, phototherapy, cytotoxic drugs), mild tars Topical steroid therapy has several limitations including: questionable efficacy, skin side effects (atrophy, telangiectasia, striae, perioral dermatitis), risk of cataract and glaucoma, cushing syndrome and growth retardation, HPA-axis suppression (adrenal insufficiency) There is also topical steroid phobia (people worried about skin thinning, non-specific long-term effects, and absorption/effect on growth)

In summary: Always consider secondary infection, especially with S. aureus or HSV For adults with new onset eczema, inquire about history of eczema as a child as well as exposure to offending allergens In adults with known AD but changes in pattern/severity, consider contact allergies Patients with AD need discussions regarding bathing, soaps, emollients, itching, sleeping, clothing, pets

Allergic contact dermatitis (ACD) Nickel: common in gold jewelry, the most common contact allergen on patch tests Adhesive dermatitis is common in hospitalized patients; treat with topical steroids Allergen comes into contatct with previously sensitized skin Evokes a type IV cell-mediated delayed hypersensitivity reaction A TH1 disease Acute and chronic cases are well demarcated and localized to the site of contact with allergen Varied morphology Individuals can be exposed to the allergen for years before finally developing hypersensitivity (remember, its delayed and requires previously sensitized skin) Once sensitized, even minute slight exposures can cause frequent outbreak Most common causes: poison ivy/oak/sumac, Ni/Au, Balsam of Peru, Neomycin/ Bacitracin, fragrance, thimerosol, formaldehyde and formaldehyde-releasing preservative Systemic contact dermatitis generally involves a chemical which the patient has had a prior contact allergy; the paitent is then exposed to the same chemical via a systemic route (injection or oral, IV or intranasal) Textile dermatitis is usually due to dyes, such as blue dyes or resins used to prevent shrinking. More common in women, in areas where clothing fits more tightly Airborne contact dermatitis: most notable in exposed areas, inducing ACD thats lichenified and dry Most commonly affects face, eyelids, V of the neck, arms, and legs Most commonly caused by plants (esp Compositae allergen), resins, woods, plastics, rubbers, glues, metals, pharm chemicals, insecticide, and pesticide Most commonly seen occupationally induced Irritant contact dermatitis (ICD) Most common form of occupational skin disease Occurs when the normal epidermal barrier is disrupted and secondary inflammation develops Caused by both mechanical and chemical factors Clinical types: chemical burns, irritant reactions, that are either chronic or acute Severity depends on type of irritant, environmental factors (humidity, temp), and host factors (age, sex, pre-existing skin condition, anatomic region exposed, sebaceous activity) Occurs without prior exposure, and is a direct toxic effect of the irritant on the skin Most commonly affected areas are the hands and face, since they are exposed

Most common irritants: water, skin cleansers, industrial cleaning agents, acids and alkalis, oils, organic solvents, redox agents, plants, animal products Clinical effects of these irritants include: dermatitis, ulcerations, acneiform, mililiaria (small itchy rashes), disorders of pigmentation, alopecia, urticaria, granulomas Treatment: remove irritant, moisturizers, barrier cream, topical gluticocoritcoid, oral antihistamine

Contrasting ICD and ACD ACD is less common than ICD ACD is type IV delayed hypersensitivity cell mediated reaction, while ICD is nonimmunologic ACD involves thousands of allergens (no shit) while ICD does not ACD is diagnosed with patch testing, while ICD is diagnosed with patient history and clinical exam.