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Bodybuilders, Anabolic Steroids and Male Factor:  Case Report

A couple presents for evaluation and treatment of infertility and the male is found to have a significant male factor. He has oligoasthenospermia: 1.3 x 10-6 /ml, 44% motile, and 12 % normal morphology (WHO, 1999). Her work-up is negative for any pathology. His social history appears to involve the use of anabolic steroids to enhance his body building. He denies use in the last 6 months. This may be important with respect to his current semen analysis, and the physician appears to have questions concerning his truthfulness on this subject.

Anabolic steroid use has been estimated to have affected 1-3 million Americans (1). The misuse of anabolic steroids is common in bodybuilders (2) where 55 % of elite power lifters had reported at one time using these drugs. When the organizations running the events such as the Olympic Committee test for steroid use, it is possible that its abuse potential drops but unfortunately not be completely eliminated. There appears to be little stopping the recreational bodybuilder using anabolic steroids to enhance their performance and physique. In a study of adolescent youth (age 14.9 +/- 1.0 years) in the United States, Durant et al (3) found that 6.5 percent reported using anabolic steroids without a physicianís prescription. Interestingly, these children were also likely to use other drugs such as cocaine, smokeless tobacco and marijuana. Anabolic steroids have addictive potential. The US Congress classified anabolic steroids as Schedule III (non-narcotic) class drugs of misuse in 1990, which may have lead to patients lack of acknowledging their use and hence incomplete data (2). Thus, it is possible that the current patient is still using them but is afraid of the social consequences.

Anabolic steroids have numerous effects on the body. The reproductive effects are seen in men by a dose dependent suppression of FSH and LH leading to suppression of the hypothalamic-pituitary axis (hypogonadotropic hypogonadism). Both LH and FSH are required for spermatogenesis. This results in decreased sperm counts, decreased motility, abnormal morphology, and testicular atrophy. It is possible that the elevated androgens also act suppressive locally in the testes. All of these were seen with this patient. It is important to discuss with the patient some of the other effects of anabolic steroids, as they may directly affect his health (2). Orally taken anabolic steroids, typically the C-17 alkylated anabolic steroids (methyltestosterone, metandienone, oxymetholone, oxandrolone, and stanozolol) are associated with liver toxicity and elevations in liver enzymes. These generally return to normal after the drug is discontinued. Serum lipid profiles may be altered which include increases in LDL and decreases in HDL. The increase in LDL may be associated with an increased potential for atherosclerosis. Blood pressure may increase due to increased fluid retention and volume retention. It is reasonable to assess the liver function, hepatic and cardiovascular function of the patient.

The reproductive effects of anabolic steroids are not permanent and may reverse with discontinuation of the medication. Gazvani et al (4) reported on the conservative management of azoospermia following anabolic steroid abuse in a case report of 4 men. The time from discontinuation to normal semen parameters ranged from 5 to 18 months. Thus, much variability existed. Turek et al (5) reported on a single case where the azoospermic male discontinued all anabolic steroids and began a regimen of trice weekly HCG injections (2000 IU) for 1 month followed by 3000 IU trice weekly for 3 additional months. The wife became pregnant by 3 months of therapy and the semen parameters normalized. It is of interest that a testis biopsy was performed which showed presence of all germinal precursor cells except mature spermatozoa indicating maturation arrest pattern. Pena et a (6) found that anabolic steroid induced azoospermia reversed 3 months after discontinuation in an HIV infected man undergoing IVF, again showing the variability of the return to normal spermatogenesis. With respect to the couple seeking care, several of the cases did return to normal semen parameters within 6 months. His unfortunately did not. The study using HCG injections and one published by Menon (7) where HCG and hMG injections were used resulted in pregnancy within a reasonable amount of time (3 and 7 months, respectively) without resorting to ART. Thus medical management should be suggested as least invasive approach.

If the couple does not wish to try more conservative therapy and wishes to proceed with ART in the near future, one could not be 100 % certain that anabolic steroids are the cause since many but not all have normalization in six months. It would be reasonable in that situation to consider further testing of the husband for other causes of oligozoospermia and provide appropriate genetic counseling. A karyotype analysis may reveal balanced translocations, chromosome inversions and sex chromosome abnormalities. While Klinefelterís syndrome (47, XXY) is the most common genetic problem affecting almost 15 % of azoospermic males, a significant proportion may be mosaics with limited sperm production. Not all Klinefelterís patients have the classic phenotype. Schlegel (8) reported on a phenotypically normal male (height 5í6Ē) with the condition. However, the patient in this case is unlikely to have 47, XXY. Microdeletions of the Y chromosome have been reported in infertile males and genetic testing is available at certain centers (9). The implications are that the offspring could be affected with the same genetic abnormality. While I was unable to find data on sperm DNA damage using a literature search, data does exist on DNA damage induced by anabolic steroids in skeletal muscle (10) where apoptosis was induced. Thus, it may be reasonable to assess the patientís semen for DNA damage prior to performing ART. Sperm DNA fragmentation lowers the pregnancy rate in IVF (11). This may be of significance in our counseling.


1. Wood A. Androgens in men: uses and misuses. 1996. NEJM. 334:707-14.

2. Kutscher EC, Lund BC, Perry PJ. Anabolic Steroids; a review for the clinician. 2002. Sports Med. 32(5):285-296.

3. Durant RH, Rickert VI, Ashworth CS, Newman C, Slavens G. Use of multiple drugs among adolescents who use anabolic steroids. 1993. NEJM. 328 (13):922-26.

4. Gazvani MR, Buckett W, Luckas MJM, Aird IA, Hipkin LJ, Lewis-Jones DI. Conservative management of azoospermia following steroid abuse. 1997. Hum. Reprod. 12(8):1706-1708.

5. Turek PJ, Williams RH, Gilbaugh JH, lipshutz LI. The reversibility of anabolic steroid-induced azoospermia. 1996. J Urol. 153(5):1628-30.

6. Pena JE, Thornton MH, Sauer MV. Reversible azoospermia: anabolic steroids may profoundly affect human immunodeficiency virus-seropositive men undergoing assisted reproduction. 2003. Obstet. Gynecol. 101:1073-5.

7. Menon DK. Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin. 2003. Fertil Steril. 79 S3:1659-61.

8. Schlegel PN. Clinically relevant and genetic evaluation of the infertile male. 2002. 15th Annual in vitro fertilization and embryo transfer course. Santa Barbara, pp. 371-394.

9. Huynd T, Mollard R, Trounson A. Selected genetic factors associated with male infertility. 2002 Hum. Repro. Update. 8(2): 183-198.

10. Abu-Shakra S, Alhalabi MS, Nachtman FC, Schemidt RA, Brusilow WS. Anabolic steroids induce injury and apoptosis of differentiated skeletal muscle. 1997. J. Neurosci. Res. 47(2):186-97.

11. Benchaib M, Braun V, Lornage J, Hadj S, Salle B, Lejeune H, Geurin JF. Sperm DNA fragmentation decreases the pregnancy rate in assisted reproductive technique. 2003. Hum. Repro. 18(5):1023-28.


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