Abstract. The present work investigates the sex hormone profiles in 50 male patients with liver cirrhosis of different etiology according to the degree of liver dysfunction. The only hormonal impairment in well-compensated cirrhotics (group A) was an increase in mean serum concentrations of estrone, androstenedione, and sex hormone binding globulin. In decompensated cirrhotic patients with ascites (group B), low mean levels of total and free testosterone were found along with normal gonadotropins mean levels. Estrone and androstenedione levels were still elevated, whereas sex hormone binding globulin levels were not different from controls. In decompensated cirrhotics patients with encephalopathy (group C), total and free testosterone mean levels were lower than in group B, and LH mean levels were elevated; estrone levels were markedly high, but androstenedione levels were subnormal; sex hormone binding globulin concentrations were again not different from controls. The few patients with high prolactin levels belonged primarily to this group. Estradiol mean levels were not significantly elevated in any of the groups. It is concluded that the various hormonal patterns of gonadal failure and of the impairment of steroid metabolism and transport, observed in cirrhosis, can be attributed to the degree of liver dysfunction.

In order to investigate the possible relationship of hyperprolactinemia to psychological distress in patients undergoing chronic hemodialysis, 19 uremic women were evaluated by a semistructured interview and administered the Kellner Symptom Questionnaire. Group A (10 uremic women with hyperprolactinemia) did not differ significantly in anxiety, depression, somatization and hostility from group B (9 normoprolactinemic uremic women). Both groups rated themselves more depressed and hostile than a normal control group of 10 women, and hyperprolactinemic patients were also significantly more anxious than the normal controls.

The investigation of a sample of 99 women on maintenance hemodialysis has shown the presence of sexual disturbances to a great extent: the rate of sexual intercourse and the ability to reach orgasm were significantly lower than in age-matched control women. 80% declared a reduction in their sexual desire and the frequency of intercourse was also lower as compared to the period prior to dialysis. Ageing decreased the sexual activity in both the ill and healthy population, but in uremic patients the sexual activity ended at an earlier age. The patients with hyperprolactinemia reported lower frequencies of intercourse and lower percentages of orgasm than normoprolactinemic ones. The incidence of sexual dysfunction and the role of hyperprolactinemia in this respect were similar to those which are found among male patients on hemodialysis.

Primary hypogonadism has been commonly reported among uremic men on hemodialysis, characterized by low testosterone levels, increased luteinizing hormone and sometimes follicle-stimulating hormone levels. Little is known about the influence of hyperprolactinemia and age on this hypogonadism. In 149 hemodialysis patients and in 60 healthy subjects the serum levels of testosterone (T), gonadotropins (LH and FSH) and prolactin (PRL) were assessed through radioimmunoassay. Mean +/- SD hormone levels were: T 274 +/- 125 ng/100 ml, lower than controls; LH 44.7 +/- 46.1 mlU/ml and FSH 17.6 +/- 18.4 mIU/ml, both higher than controls. PRL 31.3 +/- 49.4 ng/ml, higher than controls. A positive correlation between LH and FSH, a negative correlation between PRL and both T and LH was found. Moreover T and FSH were correlated with age only in the normoprolactinemic patients. These data suggest: a common damaging mechanism by uremia on both interstitial and tubular structures of the testis; a central antigonadal influence of hyperprolactinemia even if a direct action on the testis cannot be excluded; a worsening action of age on the gonadal function of these patients.

Primary hypogonadism occurring among uremic men on hemodialysis has been widely investigated, yet few data are available concerning the general pattern of steroidogenesis. In 161 hemodialysis patients and in 83 healthy subjects, serum levels of gonadotropins (LH and FSH), prolactin (PRL), testosterone (T), androstenedione (A), estrone (E1), estradiol (E2), and dehydroepiandrosterone-sulphate (DHEA-S) were assessed through RIA methods. Mean +/- SD hormone levels were: LH 45.6 +/- 41.1 mIU/ml, FSH 16.3 +/- 16 mIU/ml, PRL 42.4 +/- 69.1 ng/ml, A 0.83 +/- 0.27 ng/ml, E1 64.3 +/- 31.7 pg/ml, all higher than controls; T 289 +/- 125 ng/100 ml, E2 11.8 +/- 3 pg/ml, and DHEA-S 1.4 +/- 1.4 micrograms/ml, all lower than controls. The A/T and E1/E2 ratios were also higher than controls and showed a good positive linear correlation (r = 0.40; p less than 0.001) between each other. The uremic damage acts at the testis level, impairing the activity of the enzyme 17-beta-hydroxysteroid-dehydrogenase (17-OHSD), even if a derangement of the peripheral interconversion between steroids cannot be excluded.

The present study was designed to test the effect of acute administration of dexamethasone on the postcastration and gonadotrophin-releasing hormone (GnRH)-induced rise of LH, and to examine whether the inhibitory action of glucocorticoids on LH secretion was mediated by the opioid system. Rats were castrated and injected 10-10.5 h later in a first set of experiments with saline, dexamethasone (250 micrograms/rat), nalmefene (2 mg/kg body weight) or nalmefene plus dexamethasone. The response to GnRH was tested 11 h after castration (time 0) in all groups. Dexamethasone caused a significant (P less than 0.005) decrease in basal serum concentrations of LH, while saline and nalmefene did not induce any change. The administration of dexamethasone preceded by nalmefene increased basal concentrations of LH (1.6 times), with an effect significantly greater than that of dexamethasone (P less than 0.001), nalmefene (P less than 0.05) or saline (P less than 0.005) alone. GnRH induced a significant (P less than 0.001) increase in serum concentrations of LH in all groups. In a second set of experiments, administration of naloxone (2 mg/kg body weight) increased LH levels (P less than 0.05) and similarly reversed the inhibitory effect of dexamethasone on LH.(ABSTRACT TRUNCATED AT 250 WORDS)

Forty-five uremic men, aged 20 to 68 years, undergoing periodic hemodialysis were investigated regarding their plasma testosterone ('I') and human prolactin (hPRL); in 25 of those. plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), estrone ( E l ) and 17-p estradiol (EJ were also measured by radioirnmunoassay (RIA). Means -+ standard deviations were: T = 379 k 157 ng/dl; hPRL = 24 2 30 ng/ml; LH = 49 c 48 rnlU/ml; FSH = 10 ? 8 mlU1 ml; E l = 108 2 35 pg/ml; and E, = 10 t 6 pg/ml. Twenty percent had hyperprolactinemia, and 24% had hypotestosteronemia. LH was elevated in 95% of men, while FSH was higher than normal in only three cases (12%). E, was tentatively low in ME6, while El was elevated in 76% of men. Hyperprolactinemia could be due to hemodilution, reduced renal excretion. stress, or hypothalamic-pituitary disregulation; it cannot be accounted for by E, induction, since E2 was low in 6 4 % of patients. Low T can be explained by a local toxic effect of uremia on the testis. and high LH would be the result of decreased negative feed-back. FSH is normal indicating that inhibin production by the testis was unaltered. Low EZ can be explained by testicular damage and/or reduced T. The increase in El. mainly of adrenocortical origin, may be due to increased adrenocorticotropic hormone (ACTH) as a result of stress conditions imposed by chronic renal failure and periodic hemodialysis.

The hypothalamic-pituitary-testicular axis and the regulation of prolactin secretion were investigated in eleven male renal transplant recipients.Mean serum levels of testosterone and estrone were normal, whereas those of androstenedione and estradiol were low. Mean basal luteinizing hormone (LH) levels were slightly elevated, but the peak responses to 50 pg i.v. gonadotropin-releasing hormone (GnRH) were not dissimilar from controls. Both basal and GnRH-stimulated follicle-stimulating hormone (FSH) levels were elevated (p < 0.02-0.05) and also positively correlated with the time spent on hemodialysis (p < 0.005-0.002).Basal prolactin (PRL) levels were normal, in all subjects. Nine out of 11 patients had a normal PRL response to Thyrotropin-releasing Hormone (TRH). However only six out of 11 had a normal response to 200 mg i.v. Cimetidine (Cim). Three subjects normally responding to TRH failed to respond to Cim.Uremic primary hypogonadism is not fully reversed by renal transplantation: a slight defect in the pituitary LH release may persist and the impairment of the tubular testicular function is left unchanged. While uremic hyperprolactinemia is corrected, the responsiveness to PRL-stimulating agents, particularly Cim, is not restored to normal, reflecting a derangement at the pituitary as well as the hypothalamic level. Hodenfunktion und Reaktion des Prolaktinspiegels auf T R H und Cimetidin nach einer NierentransplantationZusammenfassung: Bei 1 1 mannlichen Nierentransplantations-Patienten wurde die Hypothalamus-Hypophysen-Hodenachse und der Regelkreis der Prolaktinsekretion untersucht.Die Grundwerte von LH waren nur leicht erhoht, aber die Maximalantwort auf 50 pg GnRH i.v. unterschied sich nicht von den Kontrollwerten. Die basalen und GnRH-stimulierten Werte von FSH stiegen signifiiant an (p < 0,05-0,Ol) und zeigten eine positive Korrelation mit der Dauer der Hamodialyse (p < 0,005-0,002). Die Grundwerte von Prolaktin (PRL) waren normal bei allen Patienten. Neun von 11 Patienten zeigten eine normale Reaktion auf TRH. Jedoch zeigten nut sechs der 11 Patienten eine normale Reaktion auf Cimetidin (Cim). Drei von den Patienten, die normal auf TRH antworteten, reagierten nicht auf Cim.Uramisch bedingter primslrer Hypogonadismus kann nicht vollstiindig durch Transplantation riickgiingig gemacht werden. Eine geringe Storung der Hypophysenausschuttung von LH bleibt erhalten, warend die tubulare Hodenfunktion unveriindert ist. Die uramisch bedingte Hyperprolaktiniimie kann korrigiert werden, aber die Reaktion auf PRL-stimulierende Mittel, besonders Cim wird nicht normalisiert. Das kann sowohl eine Storung in der Hypophyse als auch im Hypothalamus bedeuten.