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Anabolic androgenic steroids (AASs) are appearance and performance-enhancing drugs (APEDs) used in competitive athletics, in recreational sports, and by body-builders. The global lifetime prevalence of AASs abuse is 6.4% for males and 1.6% for women. Many AASs, often obtained from the internet and dubious sources, have not undergone proper testing and are consumed at extremely high doses and in irrational combinations, also along with other drugs. Controlled clinical trials investigating undesired side effects are lacking because ethical restrictions prevent exposing volunteers to potentially toxic regimens, obscuring a causal relationship between AASs abuse and possible sequelae. Because of the negative feedback in the regulation of the hypothalamic-pituitary-gonadal axis, in men AASs cause reversible suppression of spermatogenesis, testicular atrophy, infertility, and erectile dysfunction (anabolic steroid-induced hypogonadism). Should spermatogenesis not recover after AASs abuse, a pre-existing fertility disorder may have resurfaced. AASs frequently cause gynecomastia and acne. In women, AASs may disrupt ovarian function. Chronic strenuous physical activity leads to menstrual irregularities and, in severe cases, to the female athlete triad (low energy intake, menstrual disorders and low bone mass), making it difficult to disentangle the effects of sports and AASs. Acne, hirsutism and (irreversible) deepening of the voice are further consequences of AASs misuse. There is no evidence that AASs cause breast carcinoma. Detecting AASs misuse through the control network of the World Anti-Doping Agency (WADA) not only aims to guarantee fair conditions for athletes, but also to protect them from medical sequelae of AASs abuse., (© 2015 European Society of Endocrinology.)

Background: There is no systematic study on coiled sperm in semen, although they are commonly observed. This work characterizes coiled sperm in infertile men to understand the clinical implications and investigate the possible cause by osmotic swelling., Methods: Coiled sperm in semen from 439 infertile patients were quantified and their ultrastructure examined by electron microscopy. Hypo-osmotic swelling (HOS) and demembranation tests were performed to elucidate the nature of the coiling., Results: Semen from patients contained overall 3% of sperm with head-in-coil (HIC) and 8% other coiled forms, with 12% of patients having 20% or more such sperm. The percentage of coiled sperm (but not HIC) was correlated with age (R = 0.26, P = 0.003) and the epididymal secretory marker neutral alpha-glucosidase (R = 0.16, P < 0.001), and associated with heavy smoking and varicocele. Electron microscopy revealed coiling of tail filaments within the plasma membrane, resembling HOS. Some seminal coiled sperm and most sperm freshly coiled upon HOS could be opened by demembranation, while those that could not be opened were probably fixed in position by oxidation, which occurred more frequently in patients than semen donors., Conclusions: Sperm coiling in semen is common and independent of sperm quantity or hormonal status. Whereas HIC may have a genetic background, other coiled forms may be associated with a hostile endogenous milieu in the epididymis that causes swelling.

Context: The 46,XX male syndrome represents a rare, poorly characterized form of male hypogonadism., Objective: The objective of the study was to distinguish the 46,XX male syndrome from the more frequent 47,XXY-Klinefelter syndrome in regard to clinical, hormonal, and epigenetic features., Design: This was a case-control study., Setting: The study was conducted at a university-based reproductive medicine and andrology institution., Patients: Eleven SRY-positive 46,XX males were compared with age-matched controls: 101 47,XXY Klinefelter patients, 78 healthy men, and 157 healthy women [latter all heterozygous for androgen receptor (AR) alleles]., Interventions: There were no interventions., Main Outcome Measures: There was a comparison of phenotype, endocrine profiles, and X-chromosomal inactivation patterns of AR alleles., Results: The 46,XX males were significantly smaller than Klinefelter patients or healthy men, resembling female controls in height and weight. The incidence of maldescended testes was significantly higher than that in Klinefelter patients and controls. Gynecomastia was more frequent in comparison with controls, whereas there was a nonsignificant trend in comparison with Klinefelter patients. All XX males were infertile and most were hypogonadal. The inactivation patterns of AR alleles in XX males were significantly more skewed than in Klinefelter patients and women. Seven of 10 heterozygous XX male patients displayed an extreme skewing of more than 80% with no preference toward the shorter or longer AR allele. The length of the AR CAG repeat polymorphism was positively related to traits of hypogonadism., Conclusions: XX males are distinctly different from Klinefelter patients in terms of clinical and epigenetic features. Nonrandom X chromosome inactivation ratios are common in XX males, possibly due to the translocated SRY gene. The existence of a Y-chromosomal, growth-related gene is discussed.