Seborrheic dermatitis

The etiology of SD is unclear with no consensus for a unifying hypothesis.[1] SD may be hormonally dependent, explaining why the condition arises in infancy, disappears spontaneously in childhood, and then re-emerges after puberty when sebaceous glands are hormonally reactivated. SD probably represents a proliferation of the resident Malassezia furfur species, although M globosa and M restricta have been identified in cases of SD.[6] These are human saprophytes that sometimes switch from yeast to the pathogenic mycelial form. Several factors have been implicated in this switch.[7] The contribution of M furfur may result from the saprophyte's lipase activity, the release of inflammatory free fatty acids, and activation of the alternative complement pathway. Tissue culture in both adults and AIDS patients with SD tends to support this conclusion, together with the good therapeutic response to antifungal agents. Culture of SD in infants aged 4-16 weeks revealed M furfur to be the dominant organism. M furfur is also found more commonly in infants with SD than in those with atopic dermatitis, other infantile dermatoses, or those who are otherwise healthy.

An explosive, often generalized, onset of SD may be a marker for HIV infection, regardless of age. It can present as a central facial rash, similar to that associated with systemic lupus erythematosus. SD tends to manifest early in persons with AIDS, appearing in 25% to 50% of those affected, and is more likely to develop in those with diminished T-cell function.[8] The association between SD and neurologic disorders (such as parkinsonism and stroke), and the fact that neuroleptic drugs with parkinsonian adverse effects can induce SD, may mean SD has a neurogenic etiology. However, no specific neurotransmitters have been identified in the regions to which SD is often confined (e.g., the cutaneous areas affected by syringomyelia or the overlying skin on the paralyzed side of hemiplegics). Increased pooled sebum in affected areas may produce localized areas of SD, accounting for the characteristic pattern of distribution in skin folds and areas with a high density of sebaceous glands. A number of medications may flare or induce SD. They include psychotropic drugs, such as phenothiazines, cimetidine, and various immunosuppressants, such as auranofin and gold.

Wearing face masks during the Coronavirus disease 2019 (COVID-19) pandemic has been associated with several facial dermatoses including seborrheic dermatitis.[9][10]

The M furfur fungus metabolizes triglycerides naturally found in sebum through its lipase activity. This results in the formation of the lipid byproduct oleic acid. When oleic acid filters through the top layer of the epidermis (the stratum corneum), inflammation can occur causing its erratic cleavage. This accounts for the characteristic clinical finding of erythematous, flaky skin. In infantile SD an analysis of the serum essential fatty acid patterns suggests transient impaired function of the enzyme delta 6-desaturase.[11]

Scalp seborrheic dermatitis

Inflammatory patches with a superficial greasy scale. Scale may be scraped away to reveal inflamed skin.

Medallion seborrheic dermatitis

Oval inflammatory patches with a superficial greasy scale on anterior chest and sometimes face; uncommon, although more frequent in African-American patients.[2]

Erythrodermic seborrheic dermatitis

Generalized erythema with fine scaling and occasional severe itching.

Cradle cap

Erythematous, scaly distribution over scalp. This type is seen in infancy.

Dandruff

Also known as pityriasis capitis. Characteristic white flaky deposits are found on clothing and in hair.

Pathophysiology