Fertil Steril. 2003 Jun;79 Suppl 3:1659-61. Related Articles, Links
Comment in:
• Fertil Steril. 2004 Jan;81(1):226.
Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin.
Menon DK.
Department of Obstetrics and Gynecology, University Malaya Medical Centre, Kuala Lumpur, Malaysia.
[email protected]
OBJECTIVE: To document for the first time the successful treatment using human chorionic gonadotropin (hCG) and human menopausal gonadotropins (hMG) of anabolic steroid-induced azoospermia that was persistent despite 1 year of cessation from steroid use. DESIGN: Clinical case report. SETTINGS: Tertiary referral center for infertility. PATIENT(S): A married couple with primary subfertility secondary to azoospermia and male hypogonadotropic hypogonadism. The husband was a bodybuilder who admitted to have used the anabolic steroids testosterone cypionate, methandrostenolone, oxandrolone, testosterone propionate, oxymetholone, nandrolone decanoate, and methenolone enanthate. INTERVENTION(S): Twice-weekly injections of 10,000 IU of hCG (Profasi; Serono) and daily injections of 75 IU of hMG (Humegon; Organon) for 3 months. MAIN OUTCOME MEASURE(S): Semen analyses, pregnancy. RESULT(S): Semen analyses returned to normal after 3 months of treatment. The couple conceived spontaneously 7 months later. CONCLUSION(S): Steroid-induced azoospermia that is persistent after cessation of steroid use can be treated successfully with hCG and hMG.
J Clin Endocrinol Metab. 1985 Oct;61(4):746-52. Related Articles, Links
Male hypogonadotropic hypogonadism: factors influencing response to human chorionic gonadotropin and human menopausal gonadotropin, including prior exogenous androgens.
Ley SB, Leonard JM.
Although testosterone (T) therapy is sufficient for maturation and maintenance of secondary sex characteristics in hypogonadal men, gonadotropins are required for stimulation of spermatogenesis. Thirteen men with hypogonadotropic hypogonadism received treatment with hCG, followed in 12 by the addition of human menopausal gonadotropin (hMG). All initially had undetectable serum LH and FSH and low T levels and were azoospermic with small testes. During therapy, all achieved normal male levels of T. Twelve of 13 had marked and continuous increase in testicular volume. Three men had sperm in the ejaculate with hCG treatment alone. All but 1 patient developed sperm in their seminal fluid during combined hCG and hMG therapy. Two men achieved three pregnancies, and 2 more had semen that produced hamster oocyte penetration assays in the fertile range during the protocol period. Four of 5 who achieved sperm densities greater than 1 million/ml while receiving combined therapy maintained or increased sperm production while receiving continued hCG therapy after hMG was withdrawn. We examined the response to gonadotropin therapy of men who had received previous T therapy and those who had not. There were no differences in rapidity or degree of response, as assessed by rise in serum T, increase in testis volume, or maximal sperm density achieved. Multiple pituitary deficits and cryptorchidism were negative prognostic factors. In summary, the prognosis for successful stimulation of spermatogenesis in men with hypogonadotropic hypogonadism treated with hCG/hMG is good and not adversely affected by prior androgen treatment. Despite undetectable serum FSH levels, hCG treatment was sufficient to both initiate and maintain spermatogenesis in some patients
Urology. 2000 Oct 1;56(4):669. Related Articles, Links
Acquired hypogonadotropic hypogonadism presenting as decreased seminal volume.
Tash JA, McGovern JH, Schlegel PN.
James Buchanan Brady Urology Foundation, Department of Urology, The New York Presbyterian Hospital-Weill Medical College of Cornell University, New York, New York, USA.
A 32-year-old man with decreased ejaculatory volume was found to have acquired hypogonadotropic hypogonadism. Initial evaluation demonstrated castrate levels of testosterone with low serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels. Semen analysis revealed a volume of 0.35 cc and severe oligospermia. Administration of gonadotropin-releasing hormone (GnRH) did not effect an increase in LH or FSH, indicating a pituitary defect. Magnetic resonance imaging revealed a partially empty sella turcica. Treatment with human chorionic gonadotropin (hCG) alone resulted in normalization of testosterone levels, sperm concentration, and semen volume, as well as the successful conception and delivery of a healthy baby girl. The findings from this case demonstrate the importance of considering low serum testosterone levels in the evaluation of low semen volume, as well as the role of hCG alone as an infertility treatment for acquired hypogonadotropic hypogonadism.
