Use of oral contraceptives in the management of acne

The pathogenesis of acne (the most common disorder involving the sebaceous gland) originates from increased sebum production by the sebaceous gland followed by colonization of the hair follicle with Propionibacterium acnes, hyperkeratinization of the upper follicle, and release of inflammatory mediators into the skin. Androgens are the main stimulators of sebum production. Androgens originate from the gonads and adrenal glands, but can also be locally produced within the sebaceous gland from dehydroepiandrosterone sulfate. In the presence of high androgen levels, which can be either a normal pattern of adolescence or a consequence of gonadal or adrenal disease, overproduction of sebum triggers the pathogenesis of acne which, mainly in adolescent women, has deleterious psychological consequences. Estrogens exert the opposite action on sebum production, probably due to the reduction of androgen availability, a direct consequence of estrogen-related increased production of hepatic sex hormone-binding globulin (SHBG). The inhibition of the hypothalamus-pituitary axis induced by oral contraceptives is followed by reduced androgen production. Oral contraceptives containing ethinyl estradiol, which has strong estrogenic activity, amplify the hypoandrogenic effect via estrogen-related stimulation of SHBG. The hypoandrogenic effect of oral contraceptives is modulated by the progestin compound. Progestins derived from 19-nortestosterone bind androgenic receptors, whereas others exert antiandrogenic properties by antagonizing the binding of androgens to their receptors, reduce 5a-reductase, and do not bind SHBG. Through this last effect, SHBG is freely available to bind androgens, and the same progestin is totally free to exert its antiandrogenic properties. After correct evaluation of the cause of acne, appropriate management can be undertaken using oral contraceptives containing low daily doses of ethinyl estradiol (20 or 30 mu g) associated with a progestin compound, such as cyproterone acetate, drospirenone, or chlormadinone acetate, the antiandrogenic activity of which has been demonstrated by many studies in animals and in humans.