ABSTRACT
The role of androgens is central in the pathogenesis of acne vulgaris. Androgen
production leads to an increase in sebum production by sebaceous glands. Before
the onset of puberty, the adrenal glands produce increasing amounts of dehy-
droepiandrosterone sulfate (DHEAS), which becomes metabolized in the skin to
more potent hormones [e.g., testosterone and dihydrotestosterone (DHT)] by the
enzymes 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 that
results in excessive sebum production (2-6). Accumulation of sebum and kerati-
nous material within pilosebaceous follicles blocks and dilates the follicular
infundibulum resulting in the formation of microcomedones. Microcomedones
provide an anaerobic, lipid-rich medium for the proliferation of Propionibacterium
acnes. Consequently, P. acnes induces an inflammatory reaction by releasing
chemotactic factors that attract lymphocytes and neutrophils, activating Toll-like
receptors and inducing follicular keratinocyte secretion of interleukin-1 leading to
keratinocyte 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 circulating
androgens is significantly increased in women with acne compared with women
without acne (11,12). The severity of acne may also be related to the sexual
maturity 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 a
prominent role in the pathogenesis of acne vulgaris and treatment modalities
aimed at minimizing their effects may be required.
