Atopic Dermatitis - treatment, symptoms and cause of Atopic Dermatitis

Atopic dermatitis (AD) is the cutaneous expression of the atopic state, characterized by a family history of asthma, hay fever, or dermatitis in up to 70% of patients. The criteria for the diagnosis of atopic eczema are shown in Table 56-1. The prevalence of atopic dermatitis is increasing worldwide, with a point prevalence in Norwegian school children as high as 23%.

The etiology of AD is only partially defined. There is a clear genetic predisposition. When both parents are affected by AD, over 80% of their children manifest the disease. When only one parent is affected, the prevalence drops to slightly over 50%. A number of genes have been tentatively linked to AD including genes coding for IgE, the high-affinity IgE receptor, mast cell tryptase, and interleukin (IL) 4. Patients with AD may display a variety of immunoregulatory abnormalities including increased IgE synthesis; increased specific IgE to foods, aeroallergens, bacteria, and bacterial products; increased expression of CD23 (low-affinity IgE receptor) on monocytes and B cells; impaired delayed type hypersensitivity reactions; and increased type II and decreased type I cytokine responses.

The clinical presentation often varies with age. Half of patients with AD present within the first year of life, and 80% present by 5 years of age. Some 80% ultimately coexpress allergic rhinitis or asthma later in life. The infantile pattern is characterized by weeping inflammatory patches and crusted plaques that occur on the face, neck, extensor surfaces, and groin. The childhood and adolescent pattern is marked by dermatitis of flexural skin, particularly in the antecubital and popliteal fossae. AD may resolve spontaneously in adults, but the dermatitis will persist into adult life in over half of individuals affected as children. The distribution of lesions may be similar to those seen in childhood. However, adults affected with AD frequently have localized disease, manifesting as hand eczema or lichen simplex chronicus.

Pruritus is a prominent characteristic of AD, and many of the cutaneous findings in affected patients are secondary to rubbing and scratching. Other cutaneous stigmata of AD are perioral pallor, an extra fold of skin beneath the lower eyelid (Dennie's line), increased palmar markings, and increased incidence of cutaneous infections, particularly with Staphylococcus aureus. Atopic individuals often have dry itchy skin, abnormalities in cutaneous vascular responses, and, in some instances, elevations in serum IgE.

Histologic examinaton of the skin affected by AD may demonstrate features of acute or chronic dermatitis. Immunopathology shows activated, memory T helper cells, which express the cutaneous lymphocyte antigen, the ligand for the inducible endothelial cell adhesion molecule E-selectin. AD skin lesions may also demonstrate IgE-bearing CD1a+ positive Langerhans cells, and these cells have been implicated in AD disease pathophysiology through mediation of hypersensitivity responses to environmental antigens.

Treatment of Atopic dermatitis

Therapy of AD should be based on avoidance of cutaneous irritants, adequate cutaneous hydration, judicious use of low- or midpotency topical glucocorticoids, and prompt treatment of secondarily infected skin lesions. Patients should be instructed to bathe using warm, but not hot, water and to limit their use of soap. Immediately after bathing while the skin is still moist, the skin should be lubricated with a low- or midpotency topical glucocorticoid in a cream or ointment base. Potent fluorinated topical glucocorticoids should not be used on the face or intertriginous areas. It takes a minimum of 30 g of glucocorticoid ointment to cover the entire body surface of an average adult.

Crusted and weeping skin lesions should be treated with systemic antibiotics with activity against S. aureus since secondary infection often exacerbates eczema. The frequency of macrolide-resistant organisms makes the use of penicillinase-resistant penicillins or cephalosporins preferable. Dicloxacillin or cephalexin (250 mg four times daily for 7 to 10 days) is generally adequate to decrease heavy colonization. As an adjunct, the use of triclosan-containing antibacterial washes and intermittent nasal mupirocin may be useful as prophylactic measures. The role of dietary allergens in atopic dermatitis is controversial, and there is little evidence that they play any role outside of infancy.

Control of pruritus is essential for treatment, since AD often represents "an itch that rashes." Antihistamines are useful to control the pruritus, but sedation may limit their usefulness. Unlike their effects in urticaria, nonsedating antihistamines are of little use since the effectiveness of antihistamines in the treatment of pruritus associated with AD is primarily related to their sedative effects as opposed to any specific action on histamine-mediated pathways.

Treatment with systemic glucocorticoids should be limited to severe exacerbations unresponsive to conservative topical therapy. In the patient with chronic AD, therapy with systemic glucocorticoids will generally clear the skin only briefly, but cessation of the systemic therapy will invariably be accompanied by return, if not worsening, of the dermatitis. Patients who do not respond to conventional therapies should be considered for patch testing to rule out allergic contact dermatitis. Immunotherapy with aeroallergens has not proven useful in AD, unlike its effect in allergic rhinitis and extrinsic asthma.