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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 1 134-138
Copyright © 2000 by The Endocrine Society


Original Studies

Basal Inhibin B and the Testosterone Response to Human Chorionic Gonadotropin Correlate in Prepubertal Boys1

Kirsten Kubini, Milo Zachmann, Norbert Albers, Olaf Hiort, Markus Bettendorf, Joachim Wölfle, Frank Bidlingmaier and Dietrich Klingmüller

Department of Clinical Biochemistry, Division of Endocrinology (K.K., F.B., D.K.), and Department of Pediatrics (K.K., N.A., J.W.), University of Bonn, Bonn, Germany; Department of Pediatrics, University of Zurich (M.Z.), Zurich, Switzerland; Department of Pediatrics, University of Lubeck (O.H.), Lubeck, Germany; and Department of Pediatrics, University of Heidelberg (M.B.), Heidelberg, Germany

Address all correspondence and requests for reprints to: Dr. Kirsten Kubini, Department of Clinical Biochemistry, Division of Endocrinology, and the Department of Pediatrics, University of Bonn, Bonn, Germany.

During childhood, the quiescent phase of testicular activity, the hCG stimulation test is widely used to evaluate testicular function. Inhibin B, a gonadal peptide regulating FSH secretion, is an established marker of Sertoli cell function and spermatogenesis in adults. In contrast to the other hormones of the hypothalamo-pituitary-gonadal axis, inhibin B is also secreted in detectable amounts during childhood. The aim of this study was to determine whether basal inhibin B levels are able to predict prepubertal testicular function, so as to avoid a stimulation test. Inhibin B and testosterone before and after hCG stimulation were measured in 54 male children with various testicular disorders by an immunoassay specific for inhibin B. Basal inhibin B was compared to the testosterone increase after hCG. Inhibin B and the hCG-induced testosterone increment correlated strongly (r = 0.84; P < 0.0001). Patients with anorchia were clearly distinguishable from those with abdominal testes, having undetectable (inhibin B, < 15 pg/mL) respective normal inhibin B levels for age. Inhibin B and the testosterone response to hCG were low in boys with testicular damage (delayed diagnosis of cryptorchidism; after testicular torsion) and in patients with gonadal dysgenesis, but were normal or increased in children with androgen insensitivity syndrome. We conclude that basal inhibin B predicts the testosterone response to hCG in boys and therefore gives reliable information about both the presence and function of the testes. The diagnostic procedure in cryptorchidism may be reduced to a single inhibin B measurement. Furthermore, inhibin B levels show specific alterations in patients with sexual ambiguity, adding a valuable diagnostic tool to the complex differential diagnosis of male pseudohermaphroditism.




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