Click here to view next page of this article

EXEMA DERMATITIS

Exema usually refers to atopic dermatitis. When used in nonatopic settings, exema is synonymous with dermatitis and requires a qualifying term to be useful (contact dermatitis, stasis dermatitis, or contact eczema, stasis exema). The term allergic usually refers to an immunologically mediated process in response to an allergen. Allergic contact dermatitis is mediated in part by T-cell activation following exposure to certain antigens contacted by the skin. Urticaria, an allergic disease mediated by IgE antibodies in response to specific antigens. Atopic dermatitis is frequently considered an allergic dermatitis. Elevated serum IgE levels plus the coexistence of IgE-mediated diseases seen in atopy (allergic rhinitis and asthma) suggest that atopic dermatitis is triggered.

ATOPIC DERMATITIS

Atopy (atopic dermatitis, asthma, or hay fever) is present in 8% to 25% of persons. Evidence supports a genetic basis for the disease. A family history of respiratory atopy can be obtained in almost 50% of patients with atopic dermatitis. Maternal atopy poses a significantly higher risk of infantile atopy than does paternal atopy, and chromosome studies have suggested that the trait for atopy may be inherited.

Pathophysiology

The pathogenesis of atopic dermatitis is not entirely understood. Atopy is characterized immunologically by high concentrations of serum IgE, a high incidence.

History

A suggestive history includes onset of a dermatitis at an early age (most patients have manifestations of atopic dermatitis by age 5-7), pruritus, a chronic recurring course, and a positive family history.

Examination

Papules, erythema, excoriations and lichenification are the hallmarks of atopic dermatitis. Unlike many skin diseases where the recognition of a primary lesion is helpful in making the diagnosis, atopic dermatitis does not present with a characteristic primary lesion; the distribution and collection of skin findings are more important in the diagnosis. In adults, flexural areas (neck, antecubital fossae and popliteal fossae) are most commonly involved.

Treatment

With recent advances in understanding the immunology of atopic dermatitis, new therapies have focused on immune regulation.

In the acute management of atopic dermatitis, topical corticosteroids and emollients are the primary therapeutic modalities. For mild disease, a low-potency corticosteroid cream is effective. For more severe disease, a medium-potency corticosteroid cream or ointment may be needed. Those patients with pustules should be evaluated with cultures and treated with oral antibiotics. Acute exacerbations in patients with moderately severe disease can sometimes be aborted by a short course of systemic corticosteroids (e.g., prednisone 40-60 mg/day for 3-4 days, then 20-30 mg/day for 3-4 days).

The management of chronic severe atopic dermatitis is a challenge for even the most skilled dermatologist. The use of chronic systemic corticosteroids may be necessary and requires monitoring for complications such as glaucoma, osteoporosis, and opportunistic infections. The most severe cases require combinations of treatments that can include systemic corticosteroids, ultraviolet light therapy, and cyclosporine. Phototherapy with UVB, UVA, and psoralens plus UVA (PUVA) have been shown to be successful in controlling the dermatitis and may reduce corticosteroid requirements. Although treatment with PUVA may produce the best results, patient preference favors combined use of UVB and UVA. Cyclosporine in doses of 3 mg/kg/day to 6 mg/kg/day is effective in severe atopic dermatitis. Monthly monitoring of serum cyclosporine levels, renal function, and blood pressure is essential. Other modalities with potential future use include interferon gamma, thymopentin, immunotherapy with antigen-antibody complexes, and mixtures of Chinese herbs.

Immunotherapy in atopic disease is indicated in allergic rhinitis and asthma but has not been successful in the treatment of atopic dermatitis. Atopic patients have allergic responses to multiple allergens including aeroallergens, and the elimination of these is frequently not feasible.

ALLERGIC CONTACT DERMATITIS

Allergic contact dermatitis occurs when a delayed (type IV) hypersensitivity to a substance develops following skin contact with that substance. This can occur after one exposure or after years of repeated exposures to an antigen. The antigen, usually of low molecular weight, binds to epidermal proteins and is presented

The most common sensitizers in North America are poison ivy and poison oak. Many other categories of chemical substances, both natural and synthetic, have the capability of sensitizing individuals and causing allergic contact dermatitis. Other common sensitizers in the United States include neomycin, nickel, fragrances such as balsam of Peru, preservatives such as quaternium 15 found in topical medications and cosmetics, components in rubber, and chemicals in shoes, both leather and synthetic.

Diagnosis

A good history plus the skin morphology and distribution usually allow the diagnosis of allergic contact dermatitis to be made. Elimination of suspected substances may suffice, but patch testing is necessary in chronic cases to identify specific allergens. Commercially available patch test kits can add to the testing of the

Treatment

Treatment of the acute phase of allergic contact dermatitis depends on the severity of the dermatitis. When there is serous oozing and vesicles, wet to dry compresses with water or aluminum acetate (Burow's solution) help dry the skin and allow subsequent application of topical medications. Topical corticosteroids  

IRRITANT CONTACT DERMATITIS

Irritant contact dermatitis is a multifactorial syndrome resulting from the effects of physical, mechanical, or chemical irritation of the skin. A common occupational problem, irritant contact dermatitis occurs when the normal epidermal barrier is disrupted and secondary inflammation develops. Most irritant substances are those used on a daily basis in most living and work environments. These generally are low-grade irritants that require repeated exposure to produce a dermatitis (soapy water, cleansers, rubbing alcohol). Some irritants are highly caustic, producing severe dermatitis after minimal exposure (bleach, strong acids, alkalis). Although anyone can develop irritant contact dermatitis, those with compromised skin (atopic dermatitis, dry skin) and those with light-colored or "fair" skin are at

Examination

Mild irritants produce erythema, chapped skin, dryness and fissuring. Pruritus can range from mild to extreme, but pain is also a common symptom especially when erosions and fissures are present. The hands are the usual site for irritant contact dermatitis. The web spaces of the fingers trap irritating substances and may

XEROTIC DERMATITIS

Xerotic (asteatotic) dermatitis is a form of mild irritant dermatitis that occurs in areas of dry skin. As the skin loses hydration, the stratum corneum becomes scaly and develops small cracks that gradually enlarge to form patches of erythema with scaling. The name given to this superficial cracking is "erythema craquele." These areas are usually intensely pruritic, and are worsened by low humidity and exposure to hot water, soap, or solvents. Pretibial areas are most common, but

DYSHIDROTIC DERMATITIS (POMPHOLYX, DYSHIDROSIS)

Dyshidrotic dermatitis is an intensely pruritic chronic recurrent dermatitis of unknown etiology that typically involves the palms and soles. The term dyshidrotic implies a malfunction of eccrine sweating, although this has not consistently been found. A recent study, however, demonstrated 2.5 times the perspiration volume

NUMMULAR DERMATITIS

Nummular dermatitis is a chronic pruritic skin eruption consisting of circular raised patches of erythematous scaly skin. Patients and doctors frequently misdiagnose nummular dermatitis as tinea corporis because of the circular shape of the lesions that suggests tinea corporis. The etiology is not known, although

NEURODERMATITIS

Neurodermatitis is defined broadly as the skin changes that occur from scratching. Subsets within this category include lichen simplex chronicus, which refers to thickened patches of skin that develop as a result of chronic scratching, and prurigo papularis or nodularis which consist of multiple individual papules or nodules induced by scratching and picking. There is always pruritus in the areas of scratching, but frequently no primary cause for the itching can be identified.