The terms "dermatitis" and "eczema" are frequently used interchangeably. When the term "eczema" is used alone, it usually refers to atopic dermatitis (atopic eczema). "Eczematous" also connotes some scaling, crusting, or serous oozing as opposed to mere erythema. The term "dermatitis" is typically used with qualifiers (eg, "contact dermatitis") to describe several different skin disorders, the most common of which are discussed in this review. Atopic dermatitis is discussed separately. (See "Epidemiology, clinical manifestations, and diagnosis of atopic dermatitis (eczema)".)
Seborrheic dermatitis is a common problem of unknown etiology. Approximately 1 to 3 percent of adults have seborrheic dermatitis . The term is derived from the distribution of this disorder, in which erythematous, scaly patches develop in areas that are rich in sebaceous glands, such as the scalp, face, and upper trunk. The term "seborrhea" refers to excess oil secretion, although this finding is not uniformly present in patients with seborrheic dermatitis [2,3].
In infants, seborrheic dermatitis of the scalp is often called "cradle cap." (See "Cradle cap and seborrheic dermatitis in infants", section on 'Clinical manifestations'.)
Pathogenesis — The cause of seborrheic dermatitis is not completely understood. Evidence supports a causal role of the skin saprophytic species of Malassezia (formerly Pityrosporum ovale), which has been shown to colonize the skin of patients with this disorder . A host reaction to Malassezia yeasts or their metabolites is thought to contribute to the inflammatory response seen in seborrheic dermatitis .
Malassezia are lipid-dependent organisms which proliferate in sebum and are normal residents of the skin flora. Although increased numbers of yeasts have been reported in patients with seborrheic dermatitis , the number of Malassezia organisms present on the skin does not always correlate with the presence or severity of the disorder [3,5]. However, a contribution of Malassezia to the pathogenesis of seborrheic dermatitis is supported by the clinical response to antifungal therapies.