naloxone and Klinefelter-Syndrome

AIM TO THE STUDY: The investigation of the influence of anti-opioid drug on hypophyseal and gonadal hormones secretion in case of Klinefelter syndrome.. The naloxone test (0,4 mg iv) was performed in 14 patients with Klinefelter syndrome aged from 19 to 32 and in 12 age matched control subjects with azoospermia and normal spermatogenesis in testicular histology. The plasma levels of FSH, LH, prolactin, testosterone and estradiol were established before and after 30, 60, 60 and 120 minutes respectively, following the drug administration.. Basal FSH, prolactin and estradiol levels were significantly higher whereas basal testosterone was significantly lower in patients with Klinefelter syndrome than in the control group. After the naloxone administration the mean plasma prolactin level decreased significantly (p=0.01) in Klinefelter subjects. The respective diminution in control group was not significant. The levels of FSH and LH as well as testosterone and estradiol did not change during the naloxone test in both Klinefelter and control subjects.. The naloxone administration in Klinefelter syndrome caused the decrease in plasma prolactin levels but did not affect the plasma level of another hypophyseal and gonadal hormones. The opioid controlled gonadotropin secretion is altered in case of Klinefelter syndrome.

Topics: Adult; Estradiol; Follicle Stimulating Hormone; Humans; Hypothalamo-Hypophyseal System; Klinefelter Syndrome; Luteinizing Hormone; Male; Naloxone; Narcotic Antagonists; Prolactin; Testosterone

Plasma LH and FSH were measured every 20 min in a group of patients with Klinefelter's syndrome before and after placebo or naloxone administration (8 mg iv as a bolus followed by an infusion of 4 mg/h for 4 h) both in baseline conditions (N = 6) and during treatment with testosterone enanthate (200 mg im every two weeks; N = 4). The mean LH areas measured during saline infusion in baseline conditions (7888 +/- 758 IU/l per min mean +/- SEM) and during testosterone treatment (5042 +/- 2039 IU/l per min) were not significantly different from those measured during naloxone infusion (baseline 8317 +/- 818 IU/l per min; during testosterone treatment 5395 +/- 2007 IU/l per min). Similar results were obtained for FSH. These data suggest that in patients with Klinefelter's syndrome, the opioidergic inhibition of gonadotropin release is lacking and is not restored by testosterone replacement therapy.

Topics: Adult; Clinical Trials as Topic; Follicle Stimulating Hormone; Humans; Infusions, Intravenous; Klinefelter Syndrome; Luteinizing Hormone; Male; Naloxone; Random Allocation; Sodium Chloride; Testosterone

A study was performed on eight subjects with Klinefelter's syndrome to assess the relation between gonadal hormones and opioid inhibition of gonadotropin secretion through comparison of their gonadotropin response to naloxone (NAL) (0.3 mg/kg; 1/3 bolus iv. at time 0 and 2/3 iv. for 120 min) before and after testosterone propionate (TP) 100 mg/day im. for 5 days. Under basal conditions, NAL failed to induce a significant change in LH levels. After TP, however, despite unchanged basal LH levels (mean +/- S.E.M.: 27.0 +/- 3.4 vs 21.2 +/- 3.21 microU/ml), LH significantly increased in response to NAL. FSH did not respond to NAL either before or after TP administration, though FSH levels were significantly reduced by TP. These findings suggest that in man, as in animals, gonadal hormones regulate opioid inhibition of LH secretion. The negative feedback of testosterone and its ability to activate opioid inhibiting tone may be dissociated, in keeping with the view that gonadal hormones control gonadotropin secretion through the activation of distinct, albeit concomitant, mechanisms.

Topics: Adolescent; Adult; Endorphins; Estradiol; Follicle Stimulating Hormone; Humans; Klinefelter Syndrome; Luteinizing Hormone; Male; Naloxone; Pituitary Gland, Anterior; Testosterone