INCREASED 17-OH-PROGESTERONE LEVELS FOLLOWING HCG STIMULATION IN MEN WITH IDIOPATHIC OLIGOZOOSPERMIA AND RAISED FSH-LEVELS

Leydig cell function was investigated in 71 men with idiopathic oligospermia and compared to 14 fertile controls by assessing the steroidogenic response to GnRH and the repetitive administration of hCG (1500 IU x3). The oligospermic men were divided into two groups according to their basal serum FSH values (FSH<8, n=35; FSH>8, n=36), this level being defined by the mean + 3 SD of the levels in normal men (3.71+4.08 mIU/ml). Oversecretion of LH was supported by the findings of: (a) higher basal LH levels (p<0.0001) in both oligospermic groups, although still within the normal range; (b) higher D-max LH and area LH (p<0.0001) levels in the FSH>8 group; (c) a strong position correlation (p<0.001) of the above parameters with the respective levels of FSH. No difference in basal testosterone levels was observed between the three groups, whereas basal levels of 17-OHP were significantly higher (p<0.05) in the group with FSH>8. The testosterone/LH ratio was significantly (p<0.0001) lower in the FSH>8 group, and was correlated inversely to the basal blood levels of FSH (p<0.0001) and to the area LH (p<0.04). After the hCG test, there was no difference in the testosterone and oestradiol response between the groups, whereas the secretion of 17-OHP and the ratio of 17-OHP/testosterone was significantly higher (p<0.0001) in the group with FSH>8 compared with the other two groups. Using multiple regression, the total production of 17-OHP and the 17-OHP/testosterone ratio were found to be correlated positively with FSH levels. These results support the view that in men with idiopathic oligozoospermia associated with severe Sertoli cell dysfunction there is parallel oversecretion of LH and compensated dysfunction of the Leydig cells, as indicated by oversecretion or accumulation of 17-OHP after hCG administration, and also by the low testosterone/LH ratio. This is possibly due to alterations in intratesticular paracrine factors deriving from the Sertoli cells, as suggested by the positive correlation between the altered steroidogenic indices and blood FSH levels.