The effects of long-term (14-120 months) hCG-treatment of 17 male patients affected by isolated hypogonadotrophic hypogonadism (IHH) on testicular volume, plasma testosterone levels, and sperm concentration were assessed. Mean testicular volume increased from 3.8 +/- 0.2 (Mean +/- SEM) ml to a maximal of 14.9 +/- 1.1 ml after 22.2 +/- 2.3 months of hCG treatment. Maximal testicular volume correlated positively with the volume recorded before the patients had undergone any previous treatment. Testicular growth was also analysed by sorting the patients into two sub-groups according to whether their initial testicular volume was less than 4 ml (small testis subset, STS) or greater than or equal to 4 ml (large testis subset, LTS), supposedly indicating complete or partial gonadotrophin deficiency, respectively. Testicular volumes in the LTS group were always greater than those of the STS. Plasma testosterone levels reached adulthood values during hCG treatment and no statistically significant difference was detected between LTS and STS patients with IHH. Thirteen patients (70%) became sperm-positive during treatment with hCG alone; five out of eight (60%) were STS patients and eight out of nine (90%) were LTS. In addition, LTS patients always had a greater sperm output than did STS patients. Sperm concentration correlated positively with maximal testicular volume, but not with patient age, length of treatment, or initial testicular volume. The administration of hMG to eight of these patients caused an increase in testicular volume in two patients but the mean volume was not statistically different from that recorded at the end of treatment with hCG alone. Similarly, sperm concentration improved in three patients but again it did not differ significantly from that achieved in the course of hCG treatment. It is noteworthy that one patient became sperm-positive after the addition of hMG to his therapeutic regimen. Among sperm-positive patients attempting conception, seven out of 10 succeeded, two of whom were from the STS group. In summary, this study indicates that hCG alone is an effective treatment to induce complete spermiogenesis in IHH patients regardless of their initial testicular volume. However, a number of IHH patients may benefit from the addition of hMG in terms of testicular volume, sperm output, and pregnancy outcome.
The capacity to generate reactive oxygen species (ROS), both basally and after stimulation with the calcium ionophore A23187, was examined in the motile fraction of sperm isolated after swim-up from the semen of 10 naturally fertile men and three groups of infertile patients. The latter included: (1) men with a non-bacterial inflammation of the genital tract (n = 10); (2) men unable to impregnate their partners during an intra-uterine insemination programme (IUI) (n = 8) and their matched controls (n = 6); and (3) men with hypogonadotrophic hypogonadism (HH) who remained infertile after induction of spermatogenesis with gonadotrophin or gonadotrophin-releasing hormone therapy (n = 3) and their matched controls (n = 3). The levels of ROS production were elevated in the sperm of some infertile men with inflammation of the genital tract compared to those found in 10 naturally fertile men. In addition, sperm from those patients who remained infertile after an IUI programme produced higher amounts of ROS compared to their control group who became fertile. Similarly, the production of ROS by sperm from three patients with HH who remained infertile was significantly higher than those of the three men who became fertile. These data suggest that an excessive production of ROS by sperm may explain some cases of idiopathic male infertility.
TRH was administered as a 5-h constant rate iv infusion (5 micrograms/min) to seven healthy adult men. Serum samples were collected at regular intervals for measurement of PRL, TSH, and T3. Serum levels of PRL during TRH infusion increased sharply to maximum level by 40 min, and then, despite continued TRH stimulation, PRL levels declined gradually to a plateau value after 100 min. No further rise in serum PRL was observed when a bolus of 200 micrograms TRH was administered to three subjects after 240 min of infusion. Conversely, an iv bolus of sulpiride (25 mg), a dopaminergic antagonist, given to four subjects after 240 min, brought about a marked increase in serum PRL values above the plateau level. These results are consistent with the interpretation that down-regulation in PRL secretion which follows the initial peak of response most likely represents pituitary desensitization to TRH. During the infusion serum TSH increases in two phases. A first phase of secretion was observed by 40 min followed by a plateau, with a second phase of increase occurring between 80-180 min.
To assess the dynamics of the suppression and recovery of plasma gonadotropins and sex steroids during and after inhibition of pituitary-ovarian function by a long-acting agonist GnRH-analog (GnRH-A), eight patients with polycystic ovarian disease were treated with 12 micrograms/kg X day GnRH-A for 56 consecutive days. In response to GnRH-A, these patients had a sharp and pronounced decline of their initially elevated immunoreactive LH and bioactive LH (bioLH) levels. Plasma immunoreactive FSH levels declined more rapidly than did bioLH, but the FSH decline was less sustained. Plasma testosterone, androstenedione, and estrone (E1) levels also declined during GnRH-A administration. The pattern of plasma androgen decrease resembled that of bioLH. There was a positive correlation between bioLH and the two androgens (r = 0.85; P less than 0.05, by Spearman's rank correlation, for both hormones). Cessation of GnRH-A administration was followed by prompt progressive increases in gonadotropin and androgen concentrations to pretreatment values. FSH recovered faster than bioLH. BioLH plasma concentrations reached pretreatment values by day 28. The recovery of plasma androstenedione and testosterone levels correlated positively with that of bioLH. Although plasma E1 levels were higher during the recovery period than during treatment, they never reached the concentrations found during the basal period, whereas estradiol concentrations were slightly but not significantly higher than those in the basal period. As a consequence, the E1 to estradiol ratio, very high in the basal period, approximated unity during recovery. These data indicate that hyperandrogenism in polycystic ovarian disease is gonadotropin dependent and accompanied by a relative abundance of LH bioactivity basally and during GnRH-A administration. Thus, the relative increase in bioLH secretion appears to be independent of the rate of gonadotropin secretion and the circulating sex steroid concentrations.
Corticotropin-releasing hormone (CRH) has been shown capable of inhibiting hypothalamic gonadotropin-releasing hormone (GnRH) release through activation of an endogenous opioid peptide (EOP)-dependent mechanism. Recently, we have shown that prolactin (PRL) stimulates CRH release and inhibits GnRH release by hypothalami explanted from male rats. Thus, the present study was undertaken to investigate whether the inhibitory effect of PRL on GnRH release in vitro is mediated by CRH and/or EOP. To this aim, the release of GnRH in response to PRL was evaluated in presence of CRH9–41 α-helical (CRH9–41), a CRH receptor antagonist, and/or naloxone (NAL), a nonselective opioid receptor antagonist, using a static hypothalamic organ culture system which enabled us to evaluate immunoreactive GnRH (iGnRH) release from individually incubated longitudinally halved hypothalamic. As previously shown, PRL at the concentration of 100nmol/l inhibited basal iGnRH release by about 35%. CRH9–41 or NAL overcame the inhibitory effect of PRL on iGnRH release in a concentration-dependent fashion. The simultaneous co-incubation with both antagonists was not more effective than each single antagonist. CRH9–41 did not have any effect on basal iGnRH release whereas NAL, as previously reported, increased it. In addition, PRL at the concentration of 100 nmol/l stimulated basal hypothalamic β-endorphin (β-EP) release. In conclusion, these data show that antagonism to CRH receptors counteracts the suppressive effects of PRL upon GnRH release and that PRL is able to stimulate hypothalamic β-EP release in vitro.
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