Anabolic Steroid-Associated Infertility: A Potentially Treatable and Reversible Cause of Male Infertility

Abstract

Anabolic steroid abuse has become a major public health problem around the world. Olympic athletes, professional athletes, college and high school students utilize these drugs for their muscle and strength building benefits. However, the short and long term effects on reproductive and sexual function have not been reported in a series of patients. Pharmacologic doses of testosterone-based drugs cause drops in endogenous testosterone production and result in impairment of spermatogenesis. Classically, patients actively taking anabolic steroids present with severe oligospermia or azoospermia, with a suppressed hypothalamic-pituitary axis. The objective of this study is to evaluate the clinical characteristics and outcomes of male infertility patients with a history of anabolic steroid abuse. Retrospective chart review of infertility patients with history of anabolic steroid abuse from a single male infertility clinic. Chart review was performed on patients from one infertility clinic from 1995-2005. All patients with a history of illicit anabolic steroid use at the present time or in the past were included. Data collection was performed regarding patient age, temporal relationship to steroid abuse, semen parameters, hormonal parameters and subsequent treatment and outcome if available. Patients were excluded if they were prescribed testosterone from other physicians for “treatment of hypogonadism.” A review of charts in patients presenting to a single infertility clinic revealed 15 patients with a clear reportable history of self-administered anabolic steroid abuse. The average patient age was 33 yrs. The average number of years since anabolic steroid use was 5.3 yrs[range: actively using (5 patients) to 19 years prior to presentation]. The average number of cycles of anabolic steroids utilized ranged from one to many years of continuous anabolic steroid use. 11/15 pts presented with typical low testosterone, low follicle stimulating hormone and low luteinizing hormone levels. Of the other 4 patients, one had non-obstructive azoospermia, one had an epididymal obstruction, one had a vasectomy with testis biopsy showing diminished spermatogenesis and one had vasal atresia with normal hormonal parameters. Of classic anabolic patients, 81% (9/11) of patients were azoospermic, 19% (2/11) of patients were mildly or moderately oligospermic and 55% (6/11) of patients had history of prior paternity. Azoospermia was reversible with either cessation of anabolic steroids or gonadotropin replacement in 78% (7/9) of patients. 71% (5/7) of patients required gonadotropin therapy for return of spermatogenesis and 29% (2/7) of patients had spontaneous return of spermatogenesis after cessation of anabolic steroids. Anabolic steroid-associated infertility typically follows a pattern of hypogonadotropic hypogonadism that usually results in azoospermia. Not all patients with a history of anabolic steroid abuse are infertile and these data do not allow global conclusions to be drawn regarding all patients who have abused anabolic steroids. Treatment is available for infertile patients who have abused anabolic steroids, which includes rebound spermatogenesis with cessation of drugs, treatment with gonadotropins or possibly testis sperm retrieval/ICSI.