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Successful treatment of anabolic steroid-induced azoospermia
Fertil Steril. 2003 Jun;79 Suppl 3:141-3.
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
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.Clinical case report.Tertiary referral center for infertility.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.Twice-weekly injections of 10,000 IU of hCG (Profasi; Serono) and daily injections of 75 IU of hMG (Humegon; Organon) for 3 months.Semen analyses, pregnancy.Semen analyses returned to normal after 3 months of treatment. The couple conceived spontaneously 7 months later.Steroid-induced azoospermia that is persistent after cessation of steroid use can be treated successfully with hCG and hMG.
A 27-year-old woman was referred by her general practitioner because of a 1-year history of primary subfertility. Her 37-year-old husband, who worked as a security guard, was an amateur bodybuilder and had been lifting weights regularly for the past 20 years. He had taken part in several regional level bodybuilding competitions. He admitted starting to use anabolic steroids to enhance his muscle mass and strength 10 years previously. In this time he had used more than seven different types of steroid, all of which he obtained illegally.
He explained that he used steroid combinations for usually a few months before taking a short break and then commencing another course of steroids. The longest sustained course he took was for 8 months when he took twice weekly injections of testosterone cypionate (amounting to 1 gram per week) combined with both daily Dianabol tablets (methandrostenolone; he started on 10 mg/day and then increased the dose to 60 mg/day) and daily Anavar tablets (oxandrolone at 20 mg/day). He admitted to also using Sustanon injections (testosterone propionate), Anadrol tablets (oxymetholone), Deca-Durabolin injections (nandrolone decanoate), and Primobolan Depot injections (methenolone enanthate).
During this period of time he had noticed a marked testicular atrophy as well as some erectile dysfunction (he described only partial erections which were difficult to maintain). He had not been on any medication in the past 1 year, had no other past medical history of note, and did not smoke or drink alcohol. On examination his skeletal muscle mass was found to be greatly increased. His secondary sexual characteristics were normal, although he had demonstrable gynecomastia. His testicles were of a low volume (2 to 3 mL) but were firm and nontender. There were no varicoceles present.
His serum gonadotropin and testosterone levels were low (FSH 0.5 U/L, LH 0.9 U/L, testosterone: 7 nmol/L). His serum prolactin level was normal. A urinary drug screen failed to identify any illicit substances; this was consistent with his story of having stopped taking the anabolic steroids 1 year previously when the couple decided to start a family. Three semen analyses (the third repeated 3 months after the second) showed a complete azoospermia with normal ejaculate volumes and liquefaction times.
We provided him with injections of human chorionic gonadotropins (hCG; Profasi; Serono) three times a week at a dose of 10,000 IU together with daily injections of human menopausal gonadotropin (hMG, Humegon; Organon) at a dose of 75 IU per day. After just 1 month of this treatment there was a dramatic improvement in his semen analyses, which showed a count of 8 million sperm/mL, motility of 48%, and 60% with normal morphology. His serum gonadotropin and androgen levels were normal at this time (FSH 5 U/L, LH 8 U/L, testosterone: 21 nmol/L). We continued this regimen for 2 months more and then rechecked his semen analyses. The sperm count was 23 million sperm/mL; motility was 45%, and 50% had normal morphology. We stopped the drug regimen and rechecked his semen analyses and serum testosterone levels 3 months later. The semen analysis was normal, as were the testosterone levels.
The goal of treating anabolic steroid–induced azoospermia is to restore endocrine function. Endocrine medications that are targeted specifically to ameliorate hypothalamic-pituitary-gonadal function have been well described and include testosterone esters, hCG, synthetic analogues of GnRH, and antiestrogens [5]. Human chorionic gonadotropin used alone has been reported to be successful in treating this group of patients [6 and 7]. In these cases, testicular function, once back to normal, continued even after the hCG was stopped. Although administering hMG seems appropriate given the hypogonadotropic results in this patient, it is not clear if exactly the same response could not have been achieved using hCG alone. Indeed the speed of recovery of endocrine function in our patient did not seem to be any faster than in reported cases using hCG alone [6].
There is no consensus on the ideal dosage of hCG or hMG in the treatment of this condition. We choose this dosage regimen empirically, with a mind to increase the dose further if subsequent semen analyses failed to show a response. Further study is needed to identify the optimal treatment in these patients
Fertil Steril. 2003 Jun;79 Suppl 3:141-3.
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
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.Clinical case report.Tertiary referral center for infertility.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.Twice-weekly injections of 10,000 IU of hCG (Profasi; Serono) and daily injections of 75 IU of hMG (Humegon; Organon) for 3 months.Semen analyses, pregnancy.Semen analyses returned to normal after 3 months of treatment. The couple conceived spontaneously 7 months later.Steroid-induced azoospermia that is persistent after cessation of steroid use can be treated successfully with hCG and hMG.
A 27-year-old woman was referred by her general practitioner because of a 1-year history of primary subfertility. Her 37-year-old husband, who worked as a security guard, was an amateur bodybuilder and had been lifting weights regularly for the past 20 years. He had taken part in several regional level bodybuilding competitions. He admitted starting to use anabolic steroids to enhance his muscle mass and strength 10 years previously. In this time he had used more than seven different types of steroid, all of which he obtained illegally.
He explained that he used steroid combinations for usually a few months before taking a short break and then commencing another course of steroids. The longest sustained course he took was for 8 months when he took twice weekly injections of testosterone cypionate (amounting to 1 gram per week) combined with both daily Dianabol tablets (methandrostenolone; he started on 10 mg/day and then increased the dose to 60 mg/day) and daily Anavar tablets (oxandrolone at 20 mg/day). He admitted to also using Sustanon injections (testosterone propionate), Anadrol tablets (oxymetholone), Deca-Durabolin injections (nandrolone decanoate), and Primobolan Depot injections (methenolone enanthate).
During this period of time he had noticed a marked testicular atrophy as well as some erectile dysfunction (he described only partial erections which were difficult to maintain). He had not been on any medication in the past 1 year, had no other past medical history of note, and did not smoke or drink alcohol. On examination his skeletal muscle mass was found to be greatly increased. His secondary sexual characteristics were normal, although he had demonstrable gynecomastia. His testicles were of a low volume (2 to 3 mL) but were firm and nontender. There were no varicoceles present.
His serum gonadotropin and testosterone levels were low (FSH 0.5 U/L, LH 0.9 U/L, testosterone: 7 nmol/L). His serum prolactin level was normal. A urinary drug screen failed to identify any illicit substances; this was consistent with his story of having stopped taking the anabolic steroids 1 year previously when the couple decided to start a family. Three semen analyses (the third repeated 3 months after the second) showed a complete azoospermia with normal ejaculate volumes and liquefaction times.
We provided him with injections of human chorionic gonadotropins (hCG; Profasi; Serono) three times a week at a dose of 10,000 IU together with daily injections of human menopausal gonadotropin (hMG, Humegon; Organon) at a dose of 75 IU per day. After just 1 month of this treatment there was a dramatic improvement in his semen analyses, which showed a count of 8 million sperm/mL, motility of 48%, and 60% with normal morphology. His serum gonadotropin and androgen levels were normal at this time (FSH 5 U/L, LH 8 U/L, testosterone: 21 nmol/L). We continued this regimen for 2 months more and then rechecked his semen analyses. The sperm count was 23 million sperm/mL; motility was 45%, and 50% had normal morphology. We stopped the drug regimen and rechecked his semen analyses and serum testosterone levels 3 months later. The semen analysis was normal, as were the testosterone levels.
The goal of treating anabolic steroid–induced azoospermia is to restore endocrine function. Endocrine medications that are targeted specifically to ameliorate hypothalamic-pituitary-gonadal function have been well described and include testosterone esters, hCG, synthetic analogues of GnRH, and antiestrogens [5]. Human chorionic gonadotropin used alone has been reported to be successful in treating this group of patients [6 and 7]. In these cases, testicular function, once back to normal, continued even after the hCG was stopped. Although administering hMG seems appropriate given the hypogonadotropic results in this patient, it is not clear if exactly the same response could not have been achieved using hCG alone. Indeed the speed of recovery of endocrine function in our patient did not seem to be any faster than in reported cases using hCG alone [6].
There is no consensus on the ideal dosage of hCG or hMG in the treatment of this condition. We choose this dosage regimen empirically, with a mind to increase the dose further if subsequent semen analyses failed to show a response. Further study is needed to identify the optimal treatment in these patients
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