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Relationships between FSH, inhibin B, anti-Mullerian hormone, and testosterone during long-term treatment with the GnRH-agonist histrelin in patients with prostate cancer

¹ Reproductive Endocrinology and Genetics Unit, Department of Obstetrics and Gynecology
² Department of Urology, Shaare-Zedek Medical Center, The Hebrew University, PO Box 3235, Jerusalem 91031, Israel
³ Institute of Hormone Research, Ben Gurion University of the Negev, Jerusalem, 92548 Israel

(Correspondence should be addressed to T Eldar-Geva; Email: gevat{at}szmc.org.il)

Objectives: Medical castration with long-acting GnRH-agonist (GnRHa) is a well-established treatment for metastatic prostate cancer. Our aim was to explore the relationships between FSH, inhibin B, anti-Mullerian hormone (AMH), and testosterone during treatment with an implant releasing GnRHa.

Design: Analysis of hormone levels in frozen serum samples.

Methods: Ten patients aged 77±7 (means±S.E.M.) years with prostate cancer were treated with the GnRHa histrelin for at least a year. Two weeks prior to insertion and for 3–4 months following removal the patients were treated with the antiandrogen flutamide. Serum inhibin B, FSH, testosterone, and AMH levels were measured retrospectively.

Results: FSH, inhibin B, and testosterone increased during antiandrogen administration and levels fell after implant insertion. Four weeks post insertion, FSH gradually increased while inhibin B and testosterone remained fully suppressed. AMH levels did not change during antiandrogen treatment, but increased following implant insertion and remained elevated for the duration of implant use. Following removal, FSH and testosterone increased, inhibin B remained low, while AMH decreased.

Conclusions: The secondary increase in FSH following initial suppression with the implant is probably related to impaired inhibin B secretion. The lack of inhibin B response to the secondary increase in FSH suggests that long-term exposure of Sertoli-cells to GnRHa impairs their function. This effect appears to be selective since unlike inhibin B, AMH increased. In the absence of testosterone, FSH has a role in AMH regulation.