This article reviews current knowledge concerning the dermatologic manifestations of
biotin deficiency.
Biotin is a water-soluble
vitamin that acts as an essential cofactor for four carboxylases, each of which catalyzes an essential step in intermediary metabolism. For example,
acetyl-CoA carboxylase catalyzes the rate-limiting step in
fatty acid elongation. In infants, children, and adults, deficiency of
biotin causes
alopecia and a characteristic scaly, erythematous
dermatitis distributed around body orifices. The
rash closely resembles that of
zinc deficiency. Candida albicans often can be cultured from the skin lesions.
Biotinidase deficiency, an inborn error, causes
biotin deficiency, probably as a consequence of unpaired intestinal absorption, cellular salvage, and renal reclamation of
biotin;
biotinidase deficiency causes dermatologic manifestations similar to
biotin deficiency. There is evidence that impaired
fatty acid metabolism secondary to reduced activities of the
biotin-dependent carboxylases (especially
acetyl-CoA carboxylase) plays an etiologic role in the dermatologic manifestations of
biotin deficiency.
Candida infections secondary to impaired immune function might also contribute to the
dermatitis of
biotin deficiency.