Index

Abstract

The role of androgens is central in the pathogenesis of acne vulgaris. Androgenproduction leads to an increase in sebum production by sebaceous glands. Beforethe onset of puberty, the adrenal glands produce increasing amounts of dehy-droepiandrosterone sulfate (DHEAS), which becomes metabolized in the skin tomore potent hormones [e.g., testosterone and dihydrotestosterone (DHT)] by theenzymes sulfotransferase, 3b-hydroxysteroid dehydrogenase (3b-HSD), 17b-HSD, and 5a-reductase (5a-R) (1). Onset of acne lesions tends to coincide with the onset of puberty during which there is an increase in the production of androgens thatresults in excessive sebum production (2-6). Accumulation of sebum and kerati-nous material within pilosebaceous follicles blocks and dilates the follicularinfundibulum resulting in the formation of microcomedones. Microcomedonesprovide an anaerobic, lipid-rich medium for the proliferation of Propionibacteriumacnes. Consequently, P. acnes induces an inflammatory reaction by releasingchemotactic factors that attract lymphocytes and neutrophils, activating Toll-likereceptors and inducing follicular keratinocyte secretion of interleukin-1 leading tokeratinocyte proliferation (7,8). Interestingly, the serum levels of DHEAS corre-late with the severity of comedonal acne in prepubertal females (9,10). Addi-tionally, although still within normal limits, the serum level of circulatingandrogens is significantly increased in women with acne compared with womenwithout acne (11,12). The severity of acne may also be related to the sexualmaturity of males and females, which may be associated to an increase in sensi-tivity of the sebaceous gland to androgens (13,14). Thus, androgens play aprominent role in the pathogenesis of acne vulgaris and treatment modalitiesaimed at minimizing their effects may be required.