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Eczema usually refers to atopic dermatitis. When used in nonatopic settings, eczema is synonymous with dermatitis and requires a qualifying term to be useful (contact dermatitis, stasis dermatitis, or contact eczema, stasis eczema). 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 by allergic exema, eczema, dermatitis, rash.
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 on a exema, eczema, dermatitis, rash
The pathogenesis of atopic dermatitis is not entirely understood. Atopy is characterized immunologically by high concentrations of serum IgE, a high incidence of IgE-mediated response by skin test to common inhaled antigens, decreased numbers of immunoregulatory T cells, defective antibody-dependent cellular
The role of cytokines in atopic dermatitis appears to be important and continues to be studied; current theory suggests that atopic patients have a predominance of T cells of the Th2 type and produce high amounts of the cytokine interleukin 4 (IL- 4), which in turn can stimulate B cells to make IgE antibodies. Cytokine production by T cells may be modulated by monocytes, which are found in increased numbers in lesional skin of atopic patients. Trigger factors such as Staphylococcus aureus, Pityrosporum ovale, house dust mites, as well as neurocutaneous influences may also affect immune responses that lead to the development of dermatitis.
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
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
The management of atopic dermatitis centers around
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
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.
To control pruritus, the adjunctive use of antihistamines is usually helpful. Considerable trial and error may be required to identify the antihistamine best for the individual patient. In contrast to allergic rhinitis, the nonsedating H1 blockers are of limited value in most cases of atopic dermatitis but can be tried in patients
Controlling exacerbating factors is helpful in the acute phase and in long-term management. The exacerbating factors most important to avoid are low humidity
Reducing colonization with S. aureus may help prevent exacerbations. Antiseptic cleansers such as chlorhexidine, as well as topical corticosteroids and UVB phototherapy, have all been shown to
Controlling house dust mite populations has
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. On the basis of controlled food challenge studies, elimination of dietary milk, wheat, eggs, soy, peanuts, and fish have been recommended in
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. Hypersensitivity to topical hydrocortisone has
The patient with allergic contact dermatitis usually complains of intense itching in the area of exposure, followed by the development of a pruritic dermatitis. The exposure can antedate the dermatitis by 2 weeks if it is the result of a primary sensitization. In these cases, the immunologic sensitization
Clinical findings include erythema, edema, papules, vesicles, and serous oozing in the involved areas. One often sees a sharply outlined configuration corresponding to the area of skin exposure. For example, in poison oak or ivy dermatitis, there are frequently linear streaks of dermatitis corresponding to areas of contact with the plant resin. The extent of the dermatitis reflects the source of exposure, i.e., cosmetics on the face, nickel where jewelry is worn, rubber where elastic bands contact the skin, and points of
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 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 are
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
Mild irritants produce erythema, chapped skin, dryness and fissuring. Pruritus can range from mild to extreme, but pain is also a common symptom especially
Treatment goals in irritant contact dermatitis are to restore a normal epidermal barrier and then protect it from the irritating substance. Reduced exposure to soap and water, use of emollient creams or ointments, and use of gloves in hand dermatitis may control chronic irritant contact dermatitis. In more severe cases, corticosteroid ointments under
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."
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
In mild cases, medium to potent topical corticosteroids can control outbreaks. Limited courses of systemic corticosteroids are occasionally required in difficult cases. There may be a place for patch testing to nickel, chromium, or cobalt, and an attempt to eliminate environmental and dietary metal exposure. Local treatments with PUVA, UVA, or superficial X-ray have
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
Patients usually report one to several patches of itchy skin that gradually enlarge in size, usually to a maximum of 3 to 5 cm. An important differentiating feature is
Round patches of erythema, scaling, and occasional crust or exudate are suggestive of nummular dermatitis. The term nummular translates literally to "coin shaped." The distribution is usually extensor areas of extremities, the back, and buttocks. The differential diagnosis includes psoriasis and tinea corporis. A potassium hydroxide examination of any scaly lesions is indicated to exclude fungal
The elimination of drying factors (see section on xerotic dermatitis) is important in long-term management. To reduce acute inflammation, potent topical corticosteroids under occlusive dressings or intralesional corticosteroid injections (triamcinolone 5 mg/mL or betamethasone 6 mg/mL) may be necessary.
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
In lichen simplex chronicus, there is thickened skin with erythema and accentuation of skin lines (lichenification). Usually there is only one area of involvement. Common sites include the extremities, posterior neck, buttocks, vulva, scrotum, and anal area. In prurigo nodularis, there are several to multiple nodules, 0.5 to
The treatment of lichen simplex chronicus consists of breaking the itch-scratch cycle. Potent corticosteroids under occlusion may be successful. Intralesional corticosteroid injections and cryotherapy with liquid nitrogen may be required in nodular cases although the treatment of prurigo nodularis is frequently