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 a nd 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 (obstruc tive forms) to the complete absence of germ cells (Sertoli Cell Only Syndro me, SCOS). Furthermore, azoospermia may be related to maturational disturba nces at different levels (spermatogonial, spermatocytic, spermatidic). To b etter define the relationship between testicular damage and inhibin levels and to evaluate the diagnostic Value of this hormone in the management of s ubjects with azoospermia, we performed specific inhibin B assays in a group of azoospermic subjects affected by different kinds of testicular patholog y. 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 test icular appearences were identified in azoospermic patients: (i) Sertoli cel l only syndrome (SCOS); (ii) Severe hypospermatogenesis; (iii) Spermatogoni al and/or spermatocytic arrest; (iv) Spermatidic arrest; (v) Normal germ li ne (obstructive forms). No difference in LH and testosterone levels was fou nd among the different groups. A significant negative correlation was prese nt between inhibin B and FSH both in azoospermic men (r=-0.503, P<0.0001) a nd normozoospermic controls (r= -0.361, P<0.05). Groups characterized by ob structive azoospermia and spermatidic arrest showed inhibin B concentration s similar to normozoospermic subjects (130.7 +/- 73.5, 160.3 +/- 35.1 and 1 48.5 +/- 46.8 ng/l, respectively), while groups characterized by SCOS, seve re hypospermatogenesis and spermatogonial and/or spermatocytic arrest showe d 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 SC OS, 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 imp ortant role in the mechanism regulating inhibin B secretion by Sertoli cell s. The significance of this hormone as a diagnostic parameter in azoospermi c patients does not seem to be specific because it does not permit discrimi nation between obstructive forms or spermatidic arrest. Furthermore, despit e an evident clinical, cytological and hormonal pattern for SCOS, inhibin B levels are normal in some of these patients. The significance of this latt er result remains to be elucidated.