Inhibin B levels in azoospermic subjects with cytologically characterized testicular pathology

BACKGROUND AND OBJECTIVE Inhibin B, a heterodimeric glycoprotein of gonadal origin, is the most important circulating form of inhibin in human males and an inverse relationship between inhibin B and FSH plasma levels was been recently observed. Azoospermia represents the end-point of different kinds of testicular damage, ranging from a normal spermatogenic pattern (obstructive forms) to the complete absence of germ cells (Sertoli Cell Only Syndrome, SCOS). Furthermore, azoospermia may be related to maturational disturbances at different levels (spermatogonial, spermatocytic, spermatidic). To better define the relationship between testicular damage and inhibin levels and to evaluate the diagnostic Value of this hormone in the management of subjects with azoospermia, we performed specific inhibin B assays in a group of azoospermic subjects affected by different kinds of testicular pathology. PATIENTS Eighty-nine azoospermic men were studied by testicular ultrasound examination, fine needle aspiration of the testes and hormonal parameters (FSH, LH and testosterone, inhibin B). Thirty normo-zoospermic subjects were considered as controls for seminal and hormonal parameters. DESIGN AND RESULTS On the basis of cytological analysis five different testicular appearences were identified in azoospermic patients: (i) Sertoli cell only syndrome (SCOS); (ii) Severe hypospermatogenesis; (iii) Spermatogonial and/or spermatocytic arrest; (iv) Spermatidic arrest; (v) Normal germ line (obstructive forms). No difference in LH and testosterone levels was found among the different groups. A significant negative correlation was present between inhibin B and FSH both in azoospermic men (r=-0.503, P<0.0001) and normozoospermic controls (r= -0.361, P<0.05). Groups characterized by obstructive azoospermia and spermatidic arrest showed inhibin B concentrations similar to normozoospermic subjects (130.7 +/- 73.5, 160.3 +/- 35.1 and 148.5 +/- 46.8 ng/l, respectively), while groups characterized by SCOS, severe hypospermatogenesis and spermatogonial and/or spermatocytic arrest showed mean inhibin B concentrations significantly lower than controls (56.5 +/- 56.0, 57.9 +/- 31.2; 48.9 +/- 16.7 ng/l, respectively). In the group of SCOS, 8 out of 42 subjects (19.0%) showed inhibin B concentrations within the normal range despite high FSH levels. CONCLUSIONS This study demonstrated that, in humans, spermatids play an important role in the mechanism regulating inhibin B secretion by Sertoli cells. The significance of this hormone as a diagnostic parameter in azoospermic patients does not seem to be specific because it does not permit discrimination between obstructive forms or spermatidic arrest. Furthermore, despite an evident clinical, cytological and hormonal pattern for SCOS, inhibin B levels are normal in some of these patients. The significance of this latter result remains to be elucidated.