Serum Inhibin B as a Marker of Spermatogenesis

Inhibin B is produced by Sertoli cells, provides negative feedback on FSH secretion, and may prove to be an important marker for the functioning of seminiferous tubules. The purpose of the present study was to examine the relationship between the spermatogenic function of the testis of subfertile men and the plasma concentrations of inhibin B and FSH. These parameters were estimated in a group of 218 subfertile men. Serum inhibin B levels were closely correlated with the serum FSH levels (r 5 20.78, P , 0.001), confirming the role of inhibin B as feedback signal for FSH production. The spermatogenic function of the testis was evaluated by determining testicular volume and total sperm count. Inhibin B levels were significantly correlated with the total sperm count and testicular volume (r 5 0.54 and r 5 0.63, respectively; P , 0.001). Testicular biopsies were obtained in 22 of these men. Inhibin B was significantly correlated with the biopsy score (r 5 0.76, P , 0.001). Receiver operating characteristic analysis revealed a diagnostic accuracy of 95% for differentiating competent from impaired spermatogenesis for inhibin B, whereas for FSH, a value of 80% was found. We conclude that inhibin B is the best available endocrine marker of spermatogenesis in subfertile men. (J Clin Endocrinol Metab 83: 3110–3114, 1998) F is currently regarded as the most important endocrine parameter in the evaluation of male infertility (1). Its secretion can be suppressed by the testicular hormone inhibin, which is produced in Sertoli cells and may, therefore, be a serum marker for Sertoli cell function. Attempts to confirm this role of inhibin originally yielded contradictory results. Results of heterologous inhibin assays demonstrated that serum inhibin levels were stimulated with exogenous FSH and decreased after treatment with GnRH antagonists, radiotherapy-induced testicular damage, and testosterone (2–6). In contrast, a negative correlation between inhibin and FSH levels could not be shown, and inhibin levels in fertile controls and subfertile men with testicular disorders were not different (7). This discrepancy can now be explained on the basis of the aspecificity of the inhibin assay that was used. Inhibin is a dimer of an aand a b-subunit. Depending on the type of b-subunit, (bA or bB), inhibin A or inhibin B is formed. The antibodies used in the heterologous inhibin RIA were directed against the a-subunit, and they detected both dimeric inhibin and biologically inactive monomeric a-subunits (8). Since new specific sandwich assays for inhibin A, inhibin B, and uncombined a-subunits have been developed, studies have been undertaken to investigate the role of inhibins in male and female endocrinology. One major finding is that inhibin B is the physiologically important form of inhibin in the male, serum inhibin A levels being undetectable (9). The finding that castration results in undetectable inhibin B levels indicates that circulating inhibin B is produced by the testes (10). Furthermore, recent papers have reported a strong negative correlation between FSH and inhibin B in fertile and subfertile men (9, 11–14). Little information is available on the correlation of inhibin B with the severity of spermatogenic defects in subfertile men. So far, lower inhibin B levels were reported in a limited number of subfertile men, compared with fertile controls (10). More recently, inhibin B was found to be correlated with the sperm concentration in a study of 349 normal men (12) and in a mixed group of 65 men with normal and impaired spermatogenesis (13). The aim of this study was to further investigate the clinical value of inhibin B estimations in subfertile men and to correlate inhibin B levels with clinical history, testicular volume, testicular biopsy score, and sperm characteristics. Subsequently, we analyzed the additional value of inhibin B, compared with that of FSH, with special emphasis on the differentiation between normal and impaired spermatogenesis. Subjects and Methods