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Effects of Chemotherapy-Induced Testicular Damage on Inhibin, Gonadotropin, and Testosterone Secretion: A Prospective Longitudinal Study

Department of Obstetrics and Gynaecology (E.M.W.), Monash University, Clayton, Victoria 3168, Australia; School of Biological and Molecular Sciences (N.P.G.), Oxford Brookes University, Oxford; Department of Obstetrics and Gynaecology (S.C.R.), University of Edinburgh, Edinburgh EH3 9EW; Department of Haematology (A.C.P.), University of Edinburgh, Western General Hospital; Department of Medicine (F.C.W.W.), University of Manchester, Manchester Royal Infirmary and Department of Reproductive Medicine (F.C.W.W.), St Mary’s Hospital, Manchester, United Kingdom

Address correspondence and requests for reprints to: Dr. E.M. Wallace, Department of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia. E-mail: Euan.Wallace{at}med.monash.edu.au

To investigate the role of inhibin in the control of follicle-stimulating hormone (FSH) secretion, we have measured levels of immunoreactive inhibin (ir-inhibin), inhibin B, Pro-C containing inhibins, FSH, luteinizing hormone (LH), and testosterone in twelve men with hematological malignancies before, during, and after chemotherapy.

Inhibin B levels fell significantly by 1 month from a mean ± SE baseline level of 273.2 ± 32.8 pg/mL, reaching a nadir of 52.6 ± 15.3 pg/mL at 4 months (P < 0.0001). FSH levels increased within the first month from a baseline level of 3.9 ± 0.6 IU/L, reaching a peak level of 22.4 ± 3.3 IU/L at 4 months (P < 0.0001). FSH and inhibin B were significantly and inversely correlated (r = 0.69, P < 0.0001). Pro-C containing inhibin levels increased significantly (P < 0.05) at 3 months and were significantly and positively correlated with FSH (r = 0.38, P = 0.002). LH levels increased significantly but to a much lesser extent than FSH, the increase becoming evident only 4 months after treatment commenced (P < 0.03). Levels of ir-inhibin and testosterone remained unchanged throughout the study.

These data provide strong support to the hypothesis that inhibin B is the physiologically important form of inhibin in men, negatively regulating FSH secretion at the pituitary. Furthermore, they suggest that FSH stimulates inhibin -subunit secretion by the testis.

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