Generalized skin diseases

Eczema and dermatitis

The terms eczema and dermatitis are often used interchangeably to denote an inflammatory process in the skin that involves the upper dermis and epidermis. The epidermis exhibits swelling of the keratinocytes and accumulation of fluid between them (spongiosis). In the severe form of spongiosis, blisters form within the epidermis. Childhood eczema in black children frequently is seen as a follicular eruption of pinhead-sized papules. In chronic forms of eczema or dermatitis the prominent changes are thickening of the epidermis and marked hyperkeratosis (thickening of the outer horny layer of the epidermis). These changes lead to lichenification (see above), roughening and scaling of the skin surface, and itching. The function of the horny layer as an impervious barrier may be seriously impaired, with two important consequences: loss of water from the skin leads to desiccation of the horny layer, which in turn leads to cracking, increased scaling, and soreness; and loss of the barrier function causes increased absorption of medications applied to the surface of the skin. For example, the enhanced absorption of topically applied corticosteroids may cause toxic changes in the skin and in distant organs and tissues.

Dermatitis is classified into several different types, including contact dermatitis, atopic dermatitis, and seborrheic dermatitis. Contact dermatitis may be further classified as allergic or nonallergic. Nonallergic contact dermatitis occurs in response to skin irritants, is common in industrial settings (occupational dermatitis), and usually affects the hands. Acids, alkalis, dirty oils, detergents, solvents, and even repeated exposure to water are among the numerous causes. Genetic predisposition undoubtedly plays a part, however, which explains why some workers, but not others, suffer from occupational dermatitis, despite equal exposure.

Allergic contact dermatitis is a less common cause of occupational skin disease but is frequently found among the general population. Like primary irritant contact dermatitis, it can be produced and studied under controlled conditions, and therefore more is known about the underlying pathogenic mechanisms. Allergic contact dermatitis occurs only in persons who have, after previous exposure, become sensitized to the offending antigen. Common antigens include nickel, chromium, rubber, and paraphenyline diamine. The dendritic Langerhans cells of the epidermis are responsible for recognizing the antigen, which is usually bound to a homologous protein or polypeptide. This information, conveyed to the local lymph glands via the lymphatic vessels, leads to the formation of specifically sensitized lymphocytes. On subsequent exposure to the offending antigen, these and other secondarily recruited cells release chemical mediators (lymphokines) that evoke dermatitis in the exposed skin. Sensitization usually persists, although it may decline with old age.

Allergic contact dermatitis is usually suspected from the distribution of the rash, which corresponds to the areas of skin exposed to the antigen. For example, red-tipped match contact allergic dermatitis is caused by phosphorous sesquisulfide released as a vapour following the striking of a match. In pipe and cigarette smokers who use this type of match, the area affected is the side of the face, explained by the smoker’s habit of cupping the match and matchbox in the hands during the process of striking. The diagnosis of allergic contact dermatitis is confirmed by a patch test, in which minute concentrations of suspect antigens are placed on areas of the skin. An accurate diagnosis of allergic contact dermatitis is important because the condition can be cured by avoiding contact with the offending substance.

Atopic dermatitis, which affects a small number of infants, is one of several genetically linked disorders that include asthma, hay fever, and urticaria. This group of atopic diseases is characterized by sensitization of the skin to a wide range of common antigens. In addition to eczematous changes, persons with atopic dermatitis may also often have diminished, absent, or paradoxical cutaneous vascular reactions to vasodilating and vasoconstricting drugs; impaired immunity to fungal and viral infections; and cataracts in the lenses of the eyes. Although there is some controversy over the causes of atopic dermatitis, the role of genetics is undisputed. About 70 percent of patients have a family history of eczema, asthma, or hay fever. Most patients begin to suffer symptoms during the first six months of life, and there is evidence that ingestion of dairy products during this period may precipitate development of atopic dermatitis in a predisposed infant. There is no real evidence that food plays a significant role in the development of atopic dermatitis in older children and adults. The disease usually improves during the second decade of life, although it sometimes persists in adults and may even appear then for the first time.

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Seborrheic dermatitis is a less common form of chronic dermatitis that characteristically affects the scalp and other hairy areas, the face, and flexural areas (groin, armpits, skin behind the ears, the cleft between the buttocks). It is frequently associated with infection of the skin by yeasts and bacteria, but a causal relationship with these organisms has not been established. There is no evidence of increased greasiness of the skin (seborrhea). Dandruff is a mild form of seborrheic dermatitis that affects most people at some time during their lives. The scaliness of the scalp associated with dandruff is caused by the intermittent shedding of dead stratum corneum cells, which in health are shed continuously.