The Etiology of Seborrheic Dermatitis

Despite the high rate of occurrence of seborrheic dermatitis, very little is known about its cause. However, several factors (e.g., hormone levels, fungal infections, nutritional deficits, neurogenic factors) are associated with the condition. The possible hormonal link may explain why the condition appears in infancy, disappears spontaneously, then reappears more prominently after puberty. A more causal link seems to exist between seborrheic dermatitis and the proliferation of Malassezia species (e.g., Malassezia furfur, Malassezia ovalis) found in normal dimorphic human flora. Yeasts of this genus predominate and are found in seborrheic regions of the body that are rich in sebaceous lipids (e.g., head, trunk, upper back). A causal relationship is implied because of the ability to isolate Malassezia in patients with seborrheic dermatitis and by its therapeutic response to anti-fungal agents. A similar link has been suggested in studies of patients with seborrheic dermatitis that is associated with acquired immunodeficiency syndrome (AIDS). Seborrheic dermatitis also may be associated with nutritional deficiencies, but to date there is no established connection.

An altered essential fatty acid pattern may be important in the pathogenesis of infantile seborrheic dermatitis. Serum essential fatty acid patterns from 30 children with the condition suggested a transient impaired function of the delta-6 desaturase enzyme.12 A neurogenic theory for the development of seborrheic dermatitis may account for its association with parkinsonism and other neurologic disorders, including postcerebrovascular accidents, epilepsy, central nervous system trauma, facial nerve palsy, and syringomyelia induced by neuroleptic drugs with extrapyramidal effects.7 It may be confined to the syringomyelia-affected area or to the paralyzed side in a patient with hemiplegia. However, no neurotransmitters have been identified in this context.

Adolescent and adult seborrheic dermatitis usually starts as mild greasy scaling of the scalp with erythema and scaling of the nasolabial folds or the postauricular skin. The scaling often is concurrent with an oily complexion and appears in areas of increased sebaceous gland activity (e.g., auricles, beard area, eyebrows, trunk [flexure and inframammary areas]. Sometimes the central face is involved. Blepharitis, with meibomian gland occlusion and abscess formation, otitis externa, and coexistent acne vulgaris or pityriasis versicolor, may be evident.

Two types of seborrheic dermatitis may appear on the chest-a common petaloid type and a rarer pityriasiform type. The former starts as small, reddish-brown follicular and perifollicular papules with greasy scales. These papules become patches that resemble the shape of flower petals or a medallion (medallion seborrheic dermatitis). The pityriasiform type often has generalized macules and patches that resemble extensive pityriasis rosea. These patches rarely produce an eruption so generalized that it causes erythroderma.

In infants, seborrheic dermatitis may present as thick, greasy scales on the vertex of the scalp (cradle cap). The condition is not pruritic in infants, as it is in older children and adults.

Typically, acute dermatitis (characterized by oozing and weeping) is absent. The scales may vary in color, appearing white, off-white, or yellow. Infants with large, dry scales often have psoriasiform seborrheic dermatitis. This presentation often is the only sign of seborrheic dermatitis in infants and usually occurs in the third or fourth week after birth. However, the scalp, central face, forehead, and ears may have fine, widespread scaling. The dermatitis may become generalized. The flexural folds may be involved, often with a cheesy exudate that manifests as a diaper dermatitis that also may become generalized. Generalized seborrheic dermatitis is uncommon in otherwise healthy children and usually is associated with immunodeficiencies. Immunocompromised children with generalized seborrheic dermatitis often have concomitant diarrhea and failure to thrive (Leiner's disease); therefore, infants with these symptoms should be evaluated for immunodeficiencies.