Sertoli cell-only syndrome (SCOS) is characterized by a lack of germ cells and thickened seminiferous tubule walls and is a frequent finding among men with non-obstructive azoospermia. Spermatogenesis is dependent upon the function and number of Sertoli cells (SC) to support the developing germ cells. Klinefelter syndrome is the most frequent genetic cause of SCOS and presents histological features in common with idiopathic SCOS. Aim of this study was to analyze the relationships between histological features and hormonal picture in SCOS patients (n: 37; AZ), Klinefelter patients (n: 14; KL) and vasectomized patients as a control group (n: 14; VA). Testicular tubule wall thickness was different in the three groups (P<0.05), with the highest values (12.2±0.9 μm) in KL and the lowest in VA (6.7±1.3 μm). Leydig cells number per grid was different between the three groups, with the highest number in KL (255.7±22.5) and the lowest in VA (48.1±16.4, P<0.001). The SC number per tubule was higher in AZ (44.5±2.8) compared with VA (21.8±6.6, P<0.001), whereas the difference did not reach significancy between KL (132.0±44.2) and either AZ or VA. Total testosterone levels were higher in VA (15.0±3.7 nmol/l) compared with KL (9.4±1.6 nmol/l, P<0.02) and AZ (12.8±0.7 nmol/l, P<0.05). A significant negative correlation between the Leydig cell number per grid and total testosterone levels (P<0.001) was found analyzing all patients together, but not single groups. SC number per tubule was positively related to total testosterone levels (P<0.001) and was negatively correlated with tubule walls thickness in AZ only (P<0.001). In conclusion, our data show that lower total testosterone levels are related to a higher number of Leydig cells, thicker tubule walls and a smaller tubule width in all the study groups, thus supporting the hypothesis of a major role of androgens on tubular structure maintenance regardless of genetic or environmental subject characteristics. SCOS patients seem to have lower total testosterone levels as a consequence of an impaired Leydig cells secretive activity.
03 - 07 May 2008
European Society of Endocrinology