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Inhibin B: A Marker for the Functional State of the Seminiferous Epithelium in Patients with Azoospermia Factor c Microdeletions

University Department of Growth and Reproduction, Rigshospitalet (L.F.-L., H.L., A.M.A., E.C., N.E.S., E.R.-D.M.), DK-2100 Copenhagen, Denmark; Andrology Unit, Department of Clinical Physiopathology, University of Florence (C.K.), Florence, Italy; The Fertility Clinic, Herlev University Hospital (S.B.), DK-2730 Herlev, Denmark; and Reproduction, Fertility, and Populations, Institut Pasteur (C.K., K.M.), 75724 Paris, France

Address all correspondence and requests for reprints to: Dr. Lone Frydelund-Larsen, University Department of Growth and Reproduction, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. E-mail: lfl{at}biobase.dk.

Abstract

Testicular production of inhibin B is believed to be dependent on the presence of germ cells within the seminiferous tubules. However, this association has recently been questioned in patients with deletions of azoospermia factor (AZF) on the Y chromosome. We have addressed this problem in 442 unselected infertile/subfertile patients (excluding obstructive and iatrogenic forms) who were analyzed for Yq microdeletions. AZFc microdeletions were found in 16 patients (3.8% of the total infertile group, but 9% of the subgroup with azoospermia or severe oligozoospermia with sperm concentration <1 x 10⁶/ml). The reproductive hormone profiles in patients with AZFc microdeletions were analyzed and compared with those in infertile patients without microdeletions and those in fertile control individuals. The mean serum inhibin B concentration in the patients with AZFc microdeletions (39.5 ± 36.0 pg/ml) was significantly lower than that in the group of infertile patients without microdeletions (134.6 ± 88.5 pg/ml). However, no significant difference was found compared with that in a matched group of infertile patients with comparably low sperm counts (72.6 ± 75.5 pg/ml). Bilateral testicular biopsies in the AZFc-deleted patients revealed a variable histological pattern suggestive of a progressive depletion of seminiferous epithelium. An association between testicular pathology and the reproductive hormone profile was found; the more severe forms had lower inhibin B and higher FSH levels. Importantly, if Sertoli cell-only tubules were prevalent in the biopsy, inhibin B was invariably undetectable. In patients with bilateral spermatocytic arrest, inhibin B remained within the normal range, which is consistent with a role of spermatocytes in the maintenance of inhibin B secretion. Our data support the view that, in contrast to recently published data, in patients with AZF microdeletions the serum concentration of inhibin B is dependent upon the functional interaction between Sertoli cells and spermatocytes and/or spermatids.

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