Testicular responses to hCG stimulation at varying doses in men with spinal cord injury

Abstract

Study design Prospective Objectives To test whether provocative stimulation of the testes identifies men with chronic spinal cord injury (SCI), a population in which serum testosterone concentrations are often depressed, possibility due to gonadal dysfunction. To accomplish this objective, conventional and lower than the conventional doses of human chorionic gonadotropin (hCG) were administered. Methods Thirty men with chronic SCI [duration of injury >1 year; 18 and 65 years old; 16 eugonadal (>12.1 nmol/l) and 14 hypogonadal (≤12.1 nmol/l)] or able-bodied (AB) men [11 eugonadal and 27 hypogonadal] were recruited for the study. Stimulation tests were performed to quantify testicular responses to the intramuscular administration of hCG at three dose concentrations (i.e., 400 IU, 2000 IU, and 4000 IU). The hCG was administered on two consecutive days and blood was collected for serum testosterone in the early morning prior to each of two injections; subjects returned on day 3 for a final blood sample collection. Results The average gonadal response in the SCI and AB groups to each dose of hCG was not significantly different in the hypogonadal or eugonadal subjects, with the mean serum testosterone concentrations in all groups demonstrating an adequate response. Conclusions This work confirmed the absence of primary testicular dysfunction without additional benefit demonstrated of provocative stimulation of the testes with lower than conventional doses of hCG. Our findings support prior work that suggested a secondary testicular dysfunction occurs in a majority of those with SCI and depressed serum testosterone concentrations.

Administration of increasing doses of gonadotropin-releasing hormone in men with spinal cord injury to investigate dysfunction of the hypothalamic–pituitary–gonadal axis

“… 18 Because serum T responses to standard hCG stimulation testing was not significantly different for able-bodied or SCI men, regardless of gonadal status, it was suggested that the preponderance of hypogonadism identified in men with SCI is probably associated with hypothalamic-pituitary dysfunction, and not end-organ failure. 19 …”

“… 18 The testicular response to a conventional dose of human chorionic gonadotropin (hCG; 4000 IU) or with lower doses of hCG (400 and 1000) in those with SCI was generally appropriate, regardless of whether the participants had low or normal serum testosterone levels. 18 , 19 Of note, whether an individual with SCI was hypogonadal or eugonadal was not predictive of whether the person would respond with an appropriate clinical response to the standard stimulation dose of hCG. The authors speculated that because peripheral stimulation to hCG was essentially normal in those with SCI that a more subtle central problem due to insufficient hypothalamic drive to gonadotropin release should be considered.…”

Activity-Based Physical Rehabilitation with Adjuvant Testosterone to Promote Neuromuscular Recovery after Spinal Cord Injury

“…After SCI, 45–60% of men exhibit low T (hypogonadism, T < 300 ng/dL) [ 91 , 92 , 93 ] that results, in-part, from secondary testicular dysfunction [ 94 ] and impairments in the hypothalamic-pituitary axis [ 95 , 96 ]. Hypogonadism is ~four times more prevalent after SCI than in able-bodied men [ 7 ], with T concentrations remaining >25% below that of age-matched healthy men for an extended duration after SCI [ 91 , 97 ].…”

Spinal cord injury and male infertility—a review of current literature, knowledge gaps, and future research

“…There is also an association between severity of injury (complete SCI) and an increased risk of hypogonadism ( 44 , 47 ). Bauman et al compared testicular response to human chorionic gonadotropin (hCG) stimulation in SCI men and able bodied men, and found that SCI men had adequate and equal response; thus concluding that the hypogonadal state in SCI is not due to primary testicular failure ( 48 ). Naderi et al also showed that hypogonadism seen in SCI is likely a centrally mediated failure of the hypothalamic-pituitary-testis axis ( 42 ).…”