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Journal of Clinical Endocrinology & Metabolism Vol. 70, No. 5 1414-1419 doi:10.1210/jcem-70-5-1414 Copyright © 1990 by the Endocrine Society. Serum Inhibin Concentrations before and during Gonadotropin Treatment in Men with Hypogonadotropic Hypogonadism: Physiological and Clinical Implications*ROBERT I. MCLACHLAN ,
DAVID M. FINKEL,
WILLIAM J. BREMNER and
PETER J. SNYDER
Medical Service, Veterans Administration Medical Center (R.I.M., W.J.B.), and the Department of Medicine, and Population Center for Research in Reproduction, University of Washington School of Medicine (R.I.M., W.J.B.) Seattle, Washington 98108 Address all correspondence and requests for reprints to: William J. Bremner, M.D., Ph.D., Veterans Administration Medical Center, Medical Service (111), 1660 South Columbian Way, Seattle, Washington 98108. We measured by RIA the inhibin concentrations in the sera of 20 men with hypogonadotropic hypogonadism before and during treatment with gonadotropins in order to determine the role of gonadotropins in the control of inhibin secretion and the utility of the serum inhibin concentration in assessing the spermatogenic response to gonadotropin treatment in these patients. Before treatment the mean serum inhibin concentration in the 20 hypogonadotropic men as a group (391 ± 49 U/L) was significantly lower (P < 0.001) than that in 27 normal men (741 ± 52 U/L). In the 7 men whose hypogonadism was of postpubertal onset, the mean serum inhibin concentration (559 ± 69 U/L) was not significantly lower than that in normal men. In the 13 men whose hypogonadism was of prepubertal onset, the serum inhibin level was significantly lower [381 ± 74 U/L (P < 0.01) in the 7 without a history of cryptorchidism and 207 ± 46 U/L (P < 0.01) in the 6 with a history of cryptorchidism]. All 20 patients were azoospermic or severely oligospermic and had distinctly subnormal serum testosterone concentrations, even those whose serum inhibin values were normal. In the 7 patients with postpubertal hypogonadism, treatment with hCG alone for 6 months increased the serum testosterone concentration and maximum sperm count to normal, even though the previously normal inhibin concentration was not increased further. In the 13 patients with prepubertal hypogonadism, treatment with hCG alone increased the serum inhibin concentration, and combined treatment with hCG and human menopausal gonadotropin (hMG) increased inhibin further, to well within the normal range (742 ± 143 U/L) in the patients without a history of cryptorchidism and to just within the normal range (487 ± 96 U/L) in those with such a history. In the 7 patients with prepubertal hypogonadism but no history of cryptorchidism, treatment with hCG and hMG increased the maximum sperm count to normal in 5. In the 6 patients with prepubertal hypogonadism who did have a history of cryptorchidism, hCG and hMG treatment produced a normal sperm count in only 1. Of 12 patients whose serum inhibin level was more than 300 U/L before treatment, 11 developed a normal maximum sperm count in response to treatment, but of 8 patients whose inhibin concentration was less than 300 U/L before treatment, only 2 developed a normal sperm count in response to treatment (P < 0.01). We conclude that 1) both FSH and LH independently stimulate inhibin secretion; 2) normal Sertoli cell function, as judged by the serum inhibin concentration, appears to be necessary, but not sufficient, for spermatogenesis; and 3) the pretreatment serum inhibin concentration predicts the spermatogenic response to gonadotropin treatment.
* This work was supported by NIH Grants HD-13869, RR-40, and P-50-HD-12629 and the V.A.
Received September 29, 1989. This article has been cited by other articles:
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Neil Hamilton Fairley Fellow of the Australian National Health and Medical Research Council. 
