Mlg. Anapliotou et al., INCREASED 17-OH-PROGESTERONE LEVELS FOLLOWING HCG STIMULATION IN MEN WITH IDIOPATHIC OLIGOZOOSPERMIA AND RAISED FSH-LEVELS, International journal of andrology, 17(4), 1994, pp. 192-198
Leydig cell function was investigated in 71 men with idiopathic oligos
permia and compared to 14 fertile controls by assessing the steroidoge
nic response to GnRH and the repetitive administration of hCG (1500 IU
x3). The oligospermic men were divided into two groups according to t
heir basal serum FSH values (FSH<8, n=35; FSH>8, n=36), this level bei
ng defined by the mean + 3 SD of the levels in normal men (3.71+4.08 m
IU/ml). Oversecretion of LH was supported by the findings of: (a) high
er basal LH levels (p<0.0001) in both oligospermic groups, although st
ill 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<0.00
1) of the above parameters with the respective levels of FSH. No diffe
rence in basal testosterone levels was observed between the three grou
ps, 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 th
e basal blood levels of FSH (p<0.0001) and to the area LH (p<0.04). Af
ter the hCG test, there was no difference in the testosterone and oest
radiol response between the groups, whereas the secretion of 17-OHP an
d 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 mul
tiple regression, the total production of 17-OHP and the 17-OHP/testos
terone ratio were found to be correlated positively with FSH levels. T
hese results support the view that in men with idiopathic oligozoosper
mia associated with severe Sertoli cell dysfunction there is parallel
oversecretion of LH and compensated dysfunction of the Leydig cells, a
s indicated by oversecretion or accumulation of 17-OHP after hCG admin
istration, 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 t
he altered steroidogenic indices and blood FSH levels.