Eczema is a type of dermatitis and these terms are often used synonymously (atopic eczema or atopic dermatitis). Eczema is a reaction pattern that presents with variable clinical findings and the common histologic finding of spongiosis (intercellular edema of the epidermis)
Atopic dermatitis (AD) is the cutaneous expression of the atopic state, characterized by a family history of asthma, allergic rhinitis, or eczema. The prevalence of AD is increasing worldwide.
Atopic dermatitis (AD) is clinically charecterized by
1. Pruritus and scratching
2. Course marked by exacerbations and remissions
3. 4. Personal or family history of atopy (asthma, allergic rhinitis, food allergies, or eczema)
4. Lesions typical of eczematous dermatitis
5. Clinical course lasting longer than 6 weeks
6. Lichenification of skin
The etiology of AD is only partially defined, but there is a clear genetic predisposition. When both parents are affected by AD, >80% of their children manifest the disease. When only one parent is affected, the prevalence drops to slightly over 50%. Patients with AD may display a variety of immunoregulatory abnormalities including increased IgE synthesis, increased serum IgE, and impaired delayed-type hypersensitivity reactions.
Treatment
Therapy of AD should include avoidance of cutaneous irritants, adequate moisturizing through the application of emollients, judicious use of topical anti-inflammatory agents, and prompt treatment of secondary infection. Patients should be instructed to bathe no more often than daily using warm or cool water, and to use only mild bath soap. Immediately after bathing while the skin is still moist, a topical anti-inflammatory agent in a cream or ointment base should be applied to areas of dermatitis, and all other skin areas should be lubricated with a moisturizer.
Low- to midpotency topical glucocorticoids are employed in most treatment regimens for AD.
Secondary infection of eczematous skin may lead to exacerbation of AD. Crusted and weeping skin lesions may be infected with S. aureus. When secondary infection is suspected, eczematous lesions should be cultured and patients treated with systemic antibiotics active against S. aureus.
Control of pruritus is essential for treatment, since AD often represents "an itch that rashes." Antihistamines are most often used to control pruritus, and mild sedation may be responsible for their antipruritic action. Sedation may also limit their usefulness; however, when used at bedtime, sedating antihistamines may improve the patient's sleep.
Treatment with systemic glucocorticoids should be limited to severe exacerbations unresponsive to topical therapy
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