Abstract
Anabolic steroid associated male infertility is a little known but potentially treatable form of drug related infertility. We report on a bodybuilder with a 5-year history of steroid use who was azoospermic. He underwent successful gonadotropin replacement and conception was achieved 3 months after therapy was initiated. Important diagnostic and therapeutic considerations in steroid-induced infertility are discussed.
Key Words: infertility, male; anabolic steroids; oligospermia; hypogonadism; semen
For more than 40 years anabolic steroids have been used by athletes to improve strength and performance.[SUP][1][/SUP] In these settings supranormal amounts of androgenic steroids have ranged from 10 to 40-fold above physiological replacement doses.[SUP]2 and 3[/SUP] The use of exogenous anabolic steroids is a controversial drug problem of epidemic proportion. Official use of these drugs is limited to medical prescription since steroids are restricted as schedule III substance under the anabolic steroid control act of 1990.[SUP][4][/SUP]
As derivatives of testosterone, anabolic steroids greatly affect the male pituitary-gonadal axis. A hypogonadal state can be induced that is characterized by decreased serum testosterone concentrations, testicular atrophy and impaired spermatogenesis. These effects result from the negative feedback of androgens on the hypothalamic-pituitary axis and possibly from local suppressive effects of excess androgens on the testis.[SUP]2, 5 and 6[/SUP]Serum follicle-stimulating hormone and luteinizing hormone concentrations are also low in this steroid-induced state of hypogonadotropic hypogonadism. With impaired sperm production semen quality decreases and infertility often results. Frequently users of anabolic steroids seek medical attention because of infertility.[SUP][2][/SUP] However, little literature exists on the treatment of steroid-induced infertility.[SUP]3 and 6[/SUP] We report a case of azoospermia induced by exogenous steroids that responded to the judicious use of replacement hormones for several months.
Case Report
A 34-year-old man had a 4-year history of primary infertility and decreased libido. His 24-year-old wife had recently undergone evaluation by a gynecologist and was considered healthy. The patient described a 5-year history of intermittent androgenic steroid use for bodybuilding that had ended 5 years before referral. He had commonly used 2 or 3 steroid preparations together in 14 to 16-week cycles followed by an equal peroid of abstinence. More than 5 different steroids were used, the most common being injectable nandrolone decanoate and oral stanozolol. Because of a documented low serum testosterone concentration 3 years after discontinuing steroid use, and endocrinologist had treated him with 2,000 units human chorionic gonadotropin 3 times weekly without any effect on libido or sperm counts. Beginning 2 years before referral after the discontinuation of human chorionic gonadotropin the patient was treated with 200 mg. testosterone cyprionate intramuscularly weekly. The dose was decreased until a stable low-normal serum testosterone concentration was achieved. Libido improved on testosterone. A year before referral testosterone therapy was tapered and the patient remained azoospermic. He was referred for continued evaluation.
The patient was muscular, 6 feet 2 inches tall and weighed 230 pounds. Physical examination showed normal secondary sexual characteristics. Inspection of the genitalia revealed a normal phallus along with bilaterally descended and markedly atrophic testes. Bilateral grade 1 varicoceles were noted. The vasa deferentia and epididymides were normal and no hernias or rectal abnormalities were palpated. Laboratory examination of the semen revealed a normal volume of ejaculate that was azoospermic and fructose-positive. A pellet of centrifuged semen contained no sperm. Serum testosterone levels documented on referral to our clinic are shown in Figure 1. Serum concentrations of follicle-stimulating hormone and luteinizing hormone were in the normal range.
<dl class="figure" id="fig1" data-t="f" style="border: 1px solid rgb(215, 215, 215); font-size: 13px; margin: 24px 0px 15px; padding: 6px; vertical-align: baseline; border-radius: 3px;"><dt class="autoScroll" data-style="height:274px;width:374px;" style="border: 0px; margin: 12px 0px 0px; padding: 0px; vertical-align: baseline; overflow-y: hidden; overflow-x: auto;">
</dt><dd id="labelCaptionfig1" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline; color: rgb(92, 92, 92);">Figure 1. Serum testosterone concentration pattern. hCG, human chorionic gonadotropin. U, units, BID, twice daily.
</dd><dd class="menuButtonLinks" style="border: 0px; margin: 0px; padding: 6px 0px 0px; vertical-align: baseline; text-align: right; position: relative; color: rgb(92, 92, 92);">Figure options
</dd></dl>
Treatment began with discontinuation of all exogenous medications. Serum testosterone was then measured Figure 1. Serum gonadotropins remained normal during this period. Magnetic resonance imaging to rule out a pituitary tumor showed a normal pituitary gland. Testis biopsy was performed to exclude the possibility of testis failure secondary to fibrosis or the Sertoli-cell-only syndrome, either of which would have precluded further hormonal therapy. Biopsy revealed normal seminiferous tubule density and the presence of germ cells at all levels of maturation except mature spermatozoa Figure 2. There was a marked decrease in the density of spermatid forms consistent with a diagnosis of late complete maturation arrest. Leydig cells appeared normal.
<dl class="figure" id="fig2" data-t="f" style="border: 1px solid rgb(215, 215, 215); font-size: 13px; margin: 24px 0px 15px; padding: 6px; vertical-align: baseline; border-radius: 3px;"><dt class="autoScroll" data-style="height:173px;width:260px;" style="border: 0px; margin: 12px 0px 0px; padding: 0px; vertical-align: baseline; overflow-y: hidden; overflow-x: auto;">
</dt><dd id="labelCaptionfig2" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline; color: rgb(92, 92, 92);">Figure 2. Testis biopsy demonstrates presence of all germinal precursor cells except mature spermatozoa, indicative of maturation arrest pattern. Decrease in expected density of small round spermatid forms is also noted (arrows), suggesting that arrest is late in spermatogenic cycle. H & E, reduced from X200.
</dd><dd class="menuButtonLinks" style="border: 0px; margin: 0px; padding: 6px 0px 0px; vertical-align: baseline; text-align: right; position: relative; color: rgb(92, 92, 92);">Figure options
</dd></dl>
Therapy was initiated with 2,000 units human chorionic gonadotropin 3 times weekly for 4 weeks followed by 3,000 units human chorionic gonadotropin 3 times weekly for 3 months based on the gonadotropin and testosterone response. Serum luteinizing hormone concentrations increased but follicle-stimulating hormone remained in the normal range during treatment. Tamoxifen (10 mg. twice daily) was prescribed to minimize human chorionic gonadotropin-induced gynecomastia.[SUP][7][/SUP] Serial semen parameters are listed in Table 1.
<dl id="tbl1" data-t="t" class="table " data-label="tbl1" style="border: 1px solid rgb(215, 215, 215); font-size: 13px; margin-right: 0px; margin-bottom: 15px; margin-left: 0px; padding: 6px; vertical-align: baseline; border-radius: 3px;"><dd class="lblCap" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline; color: rgb(92, 92, 92);">Serial semen parameters
</dd><dd class="table" title="Serial semen parameters" style="border: 0px; margin: 12px 0px 0px; padding: 1px; vertical-align: baseline; color: rgb(92, 92, 92); overflow-x: auto; overflow-y: hidden; max-width: 600px;">
<tbody>
</tbody></dd><dd class="menuButtonLinks" style="border: 0px; margin: 0px; padding: 6px 0px 0px; vertical-align: baseline; text-align: right; position: relative; color: rgb(92, 92, 92);">Table options
</dd></dl>
The wife successfully became pregnant 3 months after therapy was begun. The semen analysis closest to the time of conception revealed a sperm concentration of 26 X 10[SUP]6[/SUP]sperm per cc with a 60 percent motile fraction. Two months later because of the development of painful gynecomastia, human chorionic gonadotropin was discontinued and testosterone was given intramuscularly.
Discussion
The nonmedical use of anabolic steroids by athletes is a potentially significant cause of infertility in male adolescents and adults. It has been estimated that 3 to 12 percent of male athletes of high school age in the United States have used steroids.[SUP][1][/SUP] The incidence of steroid use is 14 percent in college athletes and 30 to 75 percent in professional athletes or bodybuilders.[SUP][8][/SUP] The patterns of anabolic steroid administration are largely unstandardized and complex. Frequently, oral and parenteral hormones are used in what is referred to as “stacking” in an effort to maximize steroid receptor binding and increase the desired effects.[SUP][1][/SUP] By staggering the courses of different anabolic steroids athletes hope to avoid tolerance or “plateauing” to any single preparation.[SUP][1][/SUP]Steroids are usually cycled or used for 6 to 12 weeks followed by abstinence for several weeks. In addition, within each cycle steroid doses can be increased and then decreased to maximize responses, which is a process called "pyramiding."[SUP][1][/SUP] Steroid doses range from 1.5 to 2.0 times that of replacement therapy for endurance runners to 30 to 40 times this amount for competitive bodybuilders or power lifters.[SUP]1, 2 and 3[/SUP] Unfortunately, steroid illegality combined with a wide variability in usage patterns has precluded the accurate medical assessment of steroid benefits and side effects.
Infertility with anabolic steroid use commonly presents as oligospermia or azoospermia along with abnormalities of sperm motility and morphology.[SUP]2, 3, 6 and 9[/SUP] As with many of the other steroid side effects the semen parameter deficits are thought to be reversible and, consequently, the discontinuation of all steroids is an appropriate first course of therapy. Although early studies suggested that the endocrine imbalance induced by anabolic steroids is reversible,[SUP]1, 9 and 10[/SUP] more recent reports in athletes have cast doubt on this theory.[SUP]6 and 11[/SUP] In 1 study abnormally low testosterone and gonadotropin levels were documented 2.5 years after steroid use was discontinued.[SUP][6][/SUP]
When semen parameters and endocrine balance are not restored 6 months after the cessation of steroid use or when the discontinuation of steroids is not possible, we elect to treat patients in a manner similar to that used for the Kallman syndrome, hypophysectomy or other forms of hypogonadotropic hypogonadism. In these diseases there is a lack of follicle-stimulating hormone and luteinizing hormone production, and a low serum testosterone concentration similar to the findings in athletes taking anabolic steroids.[SUP]2 and 5[/SUP] Treatment for virilization in these patients involves weekly doses of intramuscular testosterone. However, the induction of spermatogenesis requires treatment with gonadotropins or gonadotropin analogues, including intramuscular injections of human chorionic gonadotropin[SUP]6, 11 and 12[/SUP] and human menopausal gonadotropin.[SUP][12][/SUP] Subsequently, spermatogenesis can be maintained by human chorionic gonadotropin injections alone.
A possible factor in the return of complete spermatogenesis in our patient was the removal of exogenous testosterone. It is not known whether there is a beneficial effect on spermatogenesis with the addition of tamoxifen to human chorionic gonadotropin therapy. When used to treat men with oligospermia this estrogen receptor blocker may alter gonadotropin secretion and improve spermatogenesis as well as possibly stimulate endogenous testosterone production.[SUP]13 and 14[/SUP] Because our patient remained azoospermic after the cessation of steroids and testosterone, assessment included testis biopsy. Commonly used in the evaluation of azoospermia, testis biopsy offers information on the state of the germinal epithelium to assist in planning therapy and can often be helpful when the fertility history of a patient beyond steroid use is unclear. As seen in Figure 2, biopsy demonstrated a late maturation arrest pattern without evidence of spermatozoa on intraoperative touch imprint evaluation.
Generally, once therapy is initiated fertility rates in hypogonadotropic hypogonadal patients are impressive.[SUP]6 and 12[/SUP] In a study of men with idiopathic hypogonadotropic hypogonadism treatment with human chorionic gonadotropin alone or in combination with human menopausal gonadotropin resulted in 40 pregnancies among 22 patients (92 percent) with a mean conception time of 7.6 months after sperm were first noted in the ejaculate.[SUP][12][/SUP] Mean sperm concentration at conception was 16 X 10[SUP]6[/SUP] sperm per ml. with a mean motile fraction of 38 percent. These values are considered subnormal by World Health Organization standards.[SUP][15][/SUP] In fact, 5 pregnancies (16 percent) occurred with sperm densities less than 1 X 10[SUP]6[/SUP] sperm per ml. The semen parameters of our patient are listed in Table 1.
The unpredictability in the recovery of spermatogenesis with anabolic steroid use is due to several factors. Steroid use is largely clandestine and is likely to be withheld from the treating physician. The large number of drugs and protocols complicates the assessment of drug impact on fertility. In addition, the preexisting fertility states of these patients may be unclear. However, as we have shown, treatment for correctly diagnosed anabolic steroid-induced infertility can be successful.
REFERENCES
Anabolic steroid associated male infertility is a little known but potentially treatable form of drug related infertility. We report on a bodybuilder with a 5-year history of steroid use who was azoospermic. He underwent successful gonadotropin replacement and conception was achieved 3 months after therapy was initiated. Important diagnostic and therapeutic considerations in steroid-induced infertility are discussed.
Key Words: infertility, male; anabolic steroids; oligospermia; hypogonadism; semen
For more than 40 years anabolic steroids have been used by athletes to improve strength and performance.[SUP][1][/SUP] In these settings supranormal amounts of androgenic steroids have ranged from 10 to 40-fold above physiological replacement doses.[SUP]2 and 3[/SUP] The use of exogenous anabolic steroids is a controversial drug problem of epidemic proportion. Official use of these drugs is limited to medical prescription since steroids are restricted as schedule III substance under the anabolic steroid control act of 1990.[SUP][4][/SUP]
As derivatives of testosterone, anabolic steroids greatly affect the male pituitary-gonadal axis. A hypogonadal state can be induced that is characterized by decreased serum testosterone concentrations, testicular atrophy and impaired spermatogenesis. These effects result from the negative feedback of androgens on the hypothalamic-pituitary axis and possibly from local suppressive effects of excess androgens on the testis.[SUP]2, 5 and 6[/SUP]Serum follicle-stimulating hormone and luteinizing hormone concentrations are also low in this steroid-induced state of hypogonadotropic hypogonadism. With impaired sperm production semen quality decreases and infertility often results. Frequently users of anabolic steroids seek medical attention because of infertility.[SUP][2][/SUP] However, little literature exists on the treatment of steroid-induced infertility.[SUP]3 and 6[/SUP] We report a case of azoospermia induced by exogenous steroids that responded to the judicious use of replacement hormones for several months.
Case Report
A 34-year-old man had a 4-year history of primary infertility and decreased libido. His 24-year-old wife had recently undergone evaluation by a gynecologist and was considered healthy. The patient described a 5-year history of intermittent androgenic steroid use for bodybuilding that had ended 5 years before referral. He had commonly used 2 or 3 steroid preparations together in 14 to 16-week cycles followed by an equal peroid of abstinence. More than 5 different steroids were used, the most common being injectable nandrolone decanoate and oral stanozolol. Because of a documented low serum testosterone concentration 3 years after discontinuing steroid use, and endocrinologist had treated him with 2,000 units human chorionic gonadotropin 3 times weekly without any effect on libido or sperm counts. Beginning 2 years before referral after the discontinuation of human chorionic gonadotropin the patient was treated with 200 mg. testosterone cyprionate intramuscularly weekly. The dose was decreased until a stable low-normal serum testosterone concentration was achieved. Libido improved on testosterone. A year before referral testosterone therapy was tapered and the patient remained azoospermic. He was referred for continued evaluation.
The patient was muscular, 6 feet 2 inches tall and weighed 230 pounds. Physical examination showed normal secondary sexual characteristics. Inspection of the genitalia revealed a normal phallus along with bilaterally descended and markedly atrophic testes. Bilateral grade 1 varicoceles were noted. The vasa deferentia and epididymides were normal and no hernias or rectal abnormalities were palpated. Laboratory examination of the semen revealed a normal volume of ejaculate that was azoospermic and fructose-positive. A pellet of centrifuged semen contained no sperm. Serum testosterone levels documented on referral to our clinic are shown in Figure 1. Serum concentrations of follicle-stimulating hormone and luteinizing hormone were in the normal range.
<dl class="figure" id="fig1" data-t="f" style="border: 1px solid rgb(215, 215, 215); font-size: 13px; margin: 24px 0px 15px; padding: 6px; vertical-align: baseline; border-radius: 3px;"><dt class="autoScroll" data-style="height:274px;width:374px;" style="border: 0px; margin: 12px 0px 0px; padding: 0px; vertical-align: baseline; overflow-y: hidden; overflow-x: auto;">
</dd><dd class="menuButtonLinks" style="border: 0px; margin: 0px; padding: 6px 0px 0px; vertical-align: baseline; text-align: right; position: relative; color: rgb(92, 92, 92);">Figure options
</dd></dl>
Treatment began with discontinuation of all exogenous medications. Serum testosterone was then measured Figure 1. Serum gonadotropins remained normal during this period. Magnetic resonance imaging to rule out a pituitary tumor showed a normal pituitary gland. Testis biopsy was performed to exclude the possibility of testis failure secondary to fibrosis or the Sertoli-cell-only syndrome, either of which would have precluded further hormonal therapy. Biopsy revealed normal seminiferous tubule density and the presence of germ cells at all levels of maturation except mature spermatozoa Figure 2. There was a marked decrease in the density of spermatid forms consistent with a diagnosis of late complete maturation arrest. Leydig cells appeared normal.
<dl class="figure" id="fig2" data-t="f" style="border: 1px solid rgb(215, 215, 215); font-size: 13px; margin: 24px 0px 15px; padding: 6px; vertical-align: baseline; border-radius: 3px;"><dt class="autoScroll" data-style="height:173px;width:260px;" style="border: 0px; margin: 12px 0px 0px; padding: 0px; vertical-align: baseline; overflow-y: hidden; overflow-x: auto;">
</dd><dd class="menuButtonLinks" style="border: 0px; margin: 0px; padding: 6px 0px 0px; vertical-align: baseline; text-align: right; position: relative; color: rgb(92, 92, 92);">Figure options
</dd></dl>
Therapy was initiated with 2,000 units human chorionic gonadotropin 3 times weekly for 4 weeks followed by 3,000 units human chorionic gonadotropin 3 times weekly for 3 months based on the gonadotropin and testosterone response. Serum luteinizing hormone concentrations increased but follicle-stimulating hormone remained in the normal range during treatment. Tamoxifen (10 mg. twice daily) was prescribed to minimize human chorionic gonadotropin-induced gynecomastia.[SUP][7][/SUP] Serial semen parameters are listed in Table 1.
<dl id="tbl1" data-t="t" class="table " data-label="tbl1" style="border: 1px solid rgb(215, 215, 215); font-size: 13px; margin-right: 0px; margin-bottom: 15px; margin-left: 0px; padding: 6px; vertical-align: baseline; border-radius: 3px;"><dd class="lblCap" style="border: 0px; margin: 0px; padding: 0px; vertical-align: baseline; color: rgb(92, 92, 92);">Serial semen parameters
</dd><dd class="table" title="Serial semen parameters" style="border: 0px; margin: 12px 0px 0px; padding: 1px; vertical-align: baseline; color: rgb(92, 92, 92); overflow-x: auto; overflow-y: hidden; max-width: 600px;">
| Period | Volume (normal 1.5–5.0) | Concentration (normal greater than 60 × 10[SUP]6[/SUP]) | % Motility (normal greater than 60) | Forward Progression (range 1–4) | |
|---|---|---|---|---|---|
| 3 mos. before referral | 3.0 | 0 | 0 | 0 | |
| At referral | 1.5 | 0 | 0 | 0 | |
| During human chorionic gonadotropin therapy: | |||||
| At 3 mos. | 3.0 | 26 × 10[SUP]6[/SUP] | 60 | 2.5 | |
| At 4 mos. | 0.2 | 40 × 10[SUP]6[/SUP] | 65 | 2.5 | |
| 2 mos. after human chorionic gonadotropin therapy | 1.5 | 40 × 10[SUP]6[/SUP] | 60 | 2.5 |
<tbody>
</tbody>
</dd></dl>
The wife successfully became pregnant 3 months after therapy was begun. The semen analysis closest to the time of conception revealed a sperm concentration of 26 X 10[SUP]6[/SUP]sperm per cc with a 60 percent motile fraction. Two months later because of the development of painful gynecomastia, human chorionic gonadotropin was discontinued and testosterone was given intramuscularly.
Discussion
The nonmedical use of anabolic steroids by athletes is a potentially significant cause of infertility in male adolescents and adults. It has been estimated that 3 to 12 percent of male athletes of high school age in the United States have used steroids.[SUP][1][/SUP] The incidence of steroid use is 14 percent in college athletes and 30 to 75 percent in professional athletes or bodybuilders.[SUP][8][/SUP] The patterns of anabolic steroid administration are largely unstandardized and complex. Frequently, oral and parenteral hormones are used in what is referred to as “stacking” in an effort to maximize steroid receptor binding and increase the desired effects.[SUP][1][/SUP] By staggering the courses of different anabolic steroids athletes hope to avoid tolerance or “plateauing” to any single preparation.[SUP][1][/SUP]Steroids are usually cycled or used for 6 to 12 weeks followed by abstinence for several weeks. In addition, within each cycle steroid doses can be increased and then decreased to maximize responses, which is a process called "pyramiding."[SUP][1][/SUP] Steroid doses range from 1.5 to 2.0 times that of replacement therapy for endurance runners to 30 to 40 times this amount for competitive bodybuilders or power lifters.[SUP]1, 2 and 3[/SUP] Unfortunately, steroid illegality combined with a wide variability in usage patterns has precluded the accurate medical assessment of steroid benefits and side effects.
Infertility with anabolic steroid use commonly presents as oligospermia or azoospermia along with abnormalities of sperm motility and morphology.[SUP]2, 3, 6 and 9[/SUP] As with many of the other steroid side effects the semen parameter deficits are thought to be reversible and, consequently, the discontinuation of all steroids is an appropriate first course of therapy. Although early studies suggested that the endocrine imbalance induced by anabolic steroids is reversible,[SUP]1, 9 and 10[/SUP] more recent reports in athletes have cast doubt on this theory.[SUP]6 and 11[/SUP] In 1 study abnormally low testosterone and gonadotropin levels were documented 2.5 years after steroid use was discontinued.[SUP][6][/SUP]
When semen parameters and endocrine balance are not restored 6 months after the cessation of steroid use or when the discontinuation of steroids is not possible, we elect to treat patients in a manner similar to that used for the Kallman syndrome, hypophysectomy or other forms of hypogonadotropic hypogonadism. In these diseases there is a lack of follicle-stimulating hormone and luteinizing hormone production, and a low serum testosterone concentration similar to the findings in athletes taking anabolic steroids.[SUP]2 and 5[/SUP] Treatment for virilization in these patients involves weekly doses of intramuscular testosterone. However, the induction of spermatogenesis requires treatment with gonadotropins or gonadotropin analogues, including intramuscular injections of human chorionic gonadotropin[SUP]6, 11 and 12[/SUP] and human menopausal gonadotropin.[SUP][12][/SUP] Subsequently, spermatogenesis can be maintained by human chorionic gonadotropin injections alone.
A possible factor in the return of complete spermatogenesis in our patient was the removal of exogenous testosterone. It is not known whether there is a beneficial effect on spermatogenesis with the addition of tamoxifen to human chorionic gonadotropin therapy. When used to treat men with oligospermia this estrogen receptor blocker may alter gonadotropin secretion and improve spermatogenesis as well as possibly stimulate endogenous testosterone production.[SUP]13 and 14[/SUP] Because our patient remained azoospermic after the cessation of steroids and testosterone, assessment included testis biopsy. Commonly used in the evaluation of azoospermia, testis biopsy offers information on the state of the germinal epithelium to assist in planning therapy and can often be helpful when the fertility history of a patient beyond steroid use is unclear. As seen in Figure 2, biopsy demonstrated a late maturation arrest pattern without evidence of spermatozoa on intraoperative touch imprint evaluation.
Generally, once therapy is initiated fertility rates in hypogonadotropic hypogonadal patients are impressive.[SUP]6 and 12[/SUP] In a study of men with idiopathic hypogonadotropic hypogonadism treatment with human chorionic gonadotropin alone or in combination with human menopausal gonadotropin resulted in 40 pregnancies among 22 patients (92 percent) with a mean conception time of 7.6 months after sperm were first noted in the ejaculate.[SUP][12][/SUP] Mean sperm concentration at conception was 16 X 10[SUP]6[/SUP] sperm per ml. with a mean motile fraction of 38 percent. These values are considered subnormal by World Health Organization standards.[SUP][15][/SUP] In fact, 5 pregnancies (16 percent) occurred with sperm densities less than 1 X 10[SUP]6[/SUP] sperm per ml. The semen parameters of our patient are listed in Table 1.
The unpredictability in the recovery of spermatogenesis with anabolic steroid use is due to several factors. Steroid use is largely clandestine and is likely to be withheld from the treating physician. The large number of drugs and protocols complicates the assessment of drug impact on fertility. In addition, the preexisting fertility states of these patients may be unclear. However, as we have shown, treatment for correctly diagnosed anabolic steroid-induced infertility can be successful.
REFERENCES
- 1
- S.E. Lukas
- Current perspectives on anabolic-androgenic steroid abuse.
- Trends Pharmacol. Sci., 14 (1993), p. 61
- Article
| PDF (1461 K)
| View Record in Scopus
| Citing articles (94)
- 2
- B.H. Kilshaw, R.A. Harkness, B.M. Hobson, A.W.M. Smith
- The effects of large doses of the anabolic steroid, methandrostenolone, on an athlete.
- Clin. Endocrinol., 4 (1975), p. 537
- View Record in Scopus
| Full Text via CrossRef
| Citing articles (19)
- 3
- U.A. Knuth, H. Maniera, E. Nieschlag
- Anabolic steroids and semen parameters in bodybuilders.
- Fertil. Steril., 52 (1989), p. 1041
- View Record in Scopus
| Citing articles (45)
- 4
- Schedules of controlled substances; anabolic steroids.
- Federal Register, 56: Rules and Regulations., U. S. Government Printing Office, Washington, D. C. (February 13, 1991)
- 5
- P. Holma, H. Adlercreutz
- Effect of an anabolic steroid (metandienon) on plasma LH, FSH, and testosterone and on the response to intravenous administration of LRH.
- Acta Endocrinol., 83 (1976), p. 856
- View Record in Scopus
| Full Text via CrossRef
| Citing articles (18)
- 6
- J.P. Jarow, L.I. Lipshultz
- Anabolic steroid-induced hypogonadotropic hypogonadism.
- Amer. J. Sports Med., 18 (1990), p. 429
- View Record in Scopus
| Full Text via CrossRef
| Citing articles (54)
- 7
- D. Fairlamb, E. Boesen
- Gynaecomastia associated with gonadotropin-secreting carcinoma of the lung.
- Postgrad. Med. J., 53 (1977), p. 269
- View Record in Scopus
| Full Text via CrossRef
| Citing articles (15)
- 8
- C.E. Yesalis
- Epidemiology and patterns of anabolic-androgen steroid use.
- Psychiatr. Ann., 22 (1992), p. 7
- View Record in Scopus
| Full Text via CrossRef
| Citing articles (27)
- 9
- P.K. Holma
- Effects of an anabolic steroid (metandienone) on spermatogenesis.
- Contraception, 15 (1977), p. 151
- Article
| PDF (663 K)
| View Record in Scopus
| Citing articles (30)
- 10
- H.A. Haupt
- Anabolic steroids and growth hormone.
- Amer. J. Sports Med., 21 (1993), p. 468
- View Record in Scopus
| Full Text via CrossRef
| Citing articles (50)
- 11
- H. Martikainen, M. Alen, P. Rahkila, R. Vihko
- Testicular responsiveness to human chorionic gonadotropin during transient hypogonadotropic hypogonadism induced by androgenic/ anabolic steroids in power athletes.
- J. Steroid Biochem., 25 (1986), p. 109
- Article
| PDF (499 K)
| View Record in Scopus
| Citing articles (26)
- 12
- A.S. Burris, R.V. Clark, D.J. Vantman, R.J. Sherins
- A low sperm concentration does not preclude fertility in men with isolated hypogonadal hypogonadism after gonadotropin treatment.
- Fertil. Steril., 50 (1988), p. 343
- View Record in Scopus
| Citing articles (59)
- 13
- J.E. Damber, L. Abramsson, M. Duchek
- Tamoxifen treatment of idiopathic oligozoospermia: effect on hCG-induced testicular steroidogenesis and semen variables.
- Scand. J. Urol. Nephrol., 23 (1989), p. 241
- View Record in Scopus
| Full Text via CrossRef
- 14
- K. Sterzik, B. Rosenbusch, D. Grab, M. Heyden, K. Lichtenberger, A. Wolf
- Die Behandlung der Oligozospermie mit Tamoxifen fuhrt zu keiner Verbesserung der Spermienqualitat.
- Zentrabl. Gynakol., 113 (1991), p. 683
- View Record in Scopus
- 15
- WHO Laboratory Manual for the Examination of Human Semen and Semen-Cervical Mucus Interaction (3rd ed.), Cambridge University Press, New York (1992), p. 44 appendix 1A
- From the Scott Department of Urology, Baylor College of Medicine, Houston, Texas.
