Low dose flutamide in the treatment of acne vulgaris in women with or without oligomenorrhea or amenorrhea.

Abstract

Background: In the skin, the expression of androgen action is dependent on the reduction of testosterone to dihydrotestosterone mediated by the enzyme 5 alpha-reductase. Additionally, an exaggeration of this peripheral metabolism has been associated with acne in women.

Methods: Fifty-two women with acne vulgaris but without hirsutism were recruited in this study, including 42 with oligomenorrhea or amenorrhea (Group 1) and 10 with regular menstrual cycles (Group 2). As a control, another 15 oligomenorrheic women without acne were also studied (Group 3). Flutamide combined with sequential estrogen-progestogen preparations was given to patients in Group 1. In Group 2, flutamide alone was administered. In Group 3, the women were treated with sequential estrogen-progestogen.

Results: In Groups 1 and 2, a significant decrease in the number of inflammatory lesions was found at the end of 3 and 6 months of treatment, and even after discontinuation of therapy for 6 months. Before treatment, patients in Group 1 showed signs of biochemical hyperandrogenism, including elevated levels of serum testosterone (T), androstenedione (A), and dehydroepiandrosterone sulfate (DHEA-S), as well as a decreased level of sex hormone-binding globulin (SHBG). A decrease in circulating T and A, and an elevation in serum SHBG were found 3 and 6 months after treatment in Group 1. In Group 2, clinical improvement of acne was achieved by flutamide alone without alteration in circulating androgens (including T, A, and DHEA-S). Similarly, no change in serum androgens was observed in the women of Group 3 after treatment.

Conclusion: A low dose of flutamide (250 mg/day) in association with or without estrogen-progestogen is effective for the clinical improvement of acne vulgaris in women with or without oligomenorrhea or amenorrhea. However, the effectiveness on hyperandrogenic symptoms by antiandrogens may or may not be reflected by the suppression of serum androgens.