Mean Basal Luteinizing Hormone Research Articles

Clomiphene Citrate in the Treatment of Idiopathic or Functional Hypogonadotropic Hypogonadism In Men: A Case Series and Review of the Literature

Late-onset hypogonadotropic hypogonadism (LOH) is a complex, heterogeneous entity. Whenever treatment is indicated, the endocrine literature has recommend testosterone replacement. We present our experience with clomiphene citrate treatment in patients with LOH and a review of the literature. This retrospective case series included 18 male patients with hypogonadotropic hypogonadism, roughly according to the European Male Aging Study criteria for LOH, attended at an academic hospital outpatient clinic. Data were retrieved from the patients' electronic medical records. The patients' mean age (±SD) was 44.3 ± 6.3 years (range 21-67 years) referred for evaluation of low testosterone together with decreased libido, erectile dysfunction, fatigue or tiredness, anxiety, and osteoporosis. Clomiphene was initially prescribed at doses between 25 mg 3 times a week and 50 mg/day. At 6 to 8 weeks following initiation of treatment, mean basal total-testosterone increased from 7.6 ± 2.6 to 19.3 ± 5.2 nmol/L (P<.0001). Mean basal luteinizing hormone (LH) increased from 2.7 ± 2.1 to 8.3 ± 3.5 nmol/L (P<.0001). Mean basal follicle-stimulating hormone (FSH) increased from 4.2 ± 3.6 to 8.6 ± 6.2 nmol/L (P = .007). Testosterone and LH responses were invariably observed, including 2 patients with history of nonpituitary cranial pathologies, 2 with somewhat elevated FSH, and 1 with an eating disorder. Twelve (67%) patients reported improvement in symptoms. Side effects included transient nipple tenderness in 1 patient. Available data suggest that clomiphene is an efficient and convenient alternative to testosterone replacement therapy in a substantial subset of patients with LOH. Additional long-term controlled studies should further establish the role of clomiphene in LOH. FSH = follicle-stimulating hormone LH = luteinizing hormone LOH = late-onset hypogonadotropic hypogonadism.

Acquired Hypogonadotropic Hypogonadism (AHH) in Thalassaemia Major Patients: An Underdiagnosed Condition?

IntroductionIn males, acquired hypogonadotropic hypogonadism (AHH) includes all disorders that damage or alter the function of gonadotropin-releasing hormone (GnRH) neurons and/or pituitary gonadotroph cells. The clinical characteristics of AHH are androgen deficiency and lack, delay or halt of pubertal sexual maturation. AHH lead to decreased libido, impaired erectile function, and strength, a worsened sense of well-being and degraded quality of life (QOL).Patients and methodsWe studied 11 adult men with thalassemia major (TM) aged between 26 to 54 years (mean ± SD: 34.3 ± 8.8 years) with AHH. Twelve age- and sex-matched TM patients with normal pubertal development were used as a control group. All patients were on regular transfusions and iron chelation therapy. Fasting venous blood samples were collected two weeks after transfusion to measure serum concentrations of IGF-1, free thyroxine (FT4), thyrotropin (TSH), cortisol, luteinizing hormone (LH), follicle stimulating hormone (FSH), total testosterone (TT), prolactin and estradiol (E2), glucose, urea, creatinine and electrolytes (including calcium and phosphate). Liver functions and screening for hepatitis C virus seropositivity (HCVab and HCV-RNA) were performed. Iron status was assessed by measuring serum ferritin levels, and evaluation of iron concentrations in the liver (LIC) and heart using MRI- T2*. Bone mineral density was measured at the lumbar spine (L1–L4) for all patients with AHH by dual energy X-ray absorptiometry (DXA) using Hologic QDR 4000 machine.ResultsThe mean basal serum LH and FSH concentrations in AHH patients were 2.4 ± 2.2 IU/L and 1.2 ± 0.9 IU/L respectively; these, values were significantly lower compared to the control group. Semen analysis in 5 patients with AHH showed azoospermia in 3 and oligoasthenozoospermia in 2. The percentage of patients with serum ferritin level >2000 ng/ml (severe iron load) was significantly higher in AHH patients compared to controls, 5/11 (45.4 %) versus1/12 (8.3%), p=0.043. Heart iron concentrations (T2* values) were significantly lower in AHH patients compared to controls (p=0.004). Magnetic resonance imaging in the 3 azoospermic patients revealed volume loss and reduction of pituitary signal intensity. Heart T2* values were significantly reduced in the AHH group vs. the controls (p=0.004). On the other hand, liver iron concentration (mg/g dry weight) was not different between the two groups of TM patients. Using DXA, 63.6 % (7/11) of patients with AHH were osteoporotic, and 36.3 % (4/11) were osteopenic.ConclusionsIn this cohort of thalassemic patients iron overload and chronic liver disease appear to play a role in the development of AHH. Treatment of AHH in TM patients is a vital and dynamic field for improving their health and QOL. Early identification and management of AHH are very crucial to avoid long-term morbidity, including sexual dysfunction and infertility. Therapy aims to restore serum testosterone levels to the mid–normal range. Many exciting opportunities remain for further research and therapeutic development.

Hypogonadism in leprosy males

Context and objective: Leprosy is a chronic systemic infectious disease caused by Mycobacterium leprae (Hansen’s bacillus). It is a problem of public health concern mainly because of its social stigma and discrimination. Hypogonadism in male with Leprosy can occur due the involvement testicular of lepromatous disease. The aim this study here was to evaluate the gonadal function in male with chronic leprosy. Study design: Cross-sectional study in a leprosy outpatient clinic. Subjects and methods: Only the functional status of sexual hormones and male with more of 1 year of Leprosy were evaluated. Clinical data were not evaluated. Measurements were made of their serum levels of free testosterone (FT), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in 21 patients male with chronic lepromatous disease. The patients were subdivided two groups: up to 60 years (G1) and over 60 years old (G2), due to physiological decline of serum testosterone production in men over 60 years of age. Results: The mean age was 48.43 ± 18.65 years. Serum FT revealed low values in 37.5 % patients. Serum LH, and FSH revealed high values in 18.8 and 6.3% respectively. The mean basal LH and FSH levels were significantly elevated and the level of FT significantly reduced when compared the groups G1 and G2. Furthermore, the G1significantly correlated with low FT levels (P = 0.002). Conclusion: This study showed a high frequency of hypogonadism among male leprosy patients. The assessment of gonadal function to detect hypogonadism should be recommended routinely screening these individuals. Normal 0 21 false false false PT-BR X-NONE X-NONE MicrosoftInternetExplorer4

Testicular function and prolactin responsiveness to TRH and cimetidine after renal transplantation.

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 micrograms i.v. gonadotropin-releasing hormone (GnRH) were not dissimilar from controls. Both basal and GnRH-stimulated follicle-stimulating hormone (FSH) levels were elevated (p less than 0.02-0.05) and also positively correlated with the time spent on hemodialysis (p less than 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.

Effects of dispersal status on pituitary and gonadal function in the male spotted hyena

Male spotted hyenas ( Crocuta crocuta) reach puberty at 24 months of age and then usually emigrate from their natal clans one to 52 months later. Recent work has shown that reproductive success is very low among adult males still residing in their natal groups, and it is similarly low among recent or “short-term” immigrants. Long-term immigrants father the vast majority of cubs born. Here we inquired whether these differences in reproductive success might be associated with variation among males in pituitary or gonadal function. In one free-living hyena population in Kenya, we compared baseline levels of plasma luteinizing hormone (LH) and testosterone (T) among adult natal males, short-term immigrants, and long-term immigrants, and we also compared their pituitary and gonadal responses to GnRH challenge. Mean basal plasma LH values did not differ among groups, but mean basal T concentrations in long-term immigrants were higher than those in either natal males or short-term immigrants. Similarly, pituitary response to GnRH challenge did not vary significantly among groups, but testicular response to challenge was greater in long-term immigrants than in natal males or short-term immigrants. Thus adult natal and immigrant males exhibited similar pituitary function but testicular function was attenuated among adult males that had not yet left their natal groups and also among males attempting to become established in new social groups. This suggests that, like the act of emigration itself, the process of social integration during immigration may have important physiological consequences for male mammals transferring between groups.

Reproductive suppression and pituitary sensitivity to exogenous GnRH in the highveld mole‐rat (Cryptomys hottentotus pretoriae)

AbstractThe highveld mole‐rat Cryptomys hottentotus pretoriae exhibits an extreme reproductive division of labour. Reproduction in this seasonally breeding social mole‐rat is restricted to a breeding pair. The non‐reproductive females seem to be physiologically suppressed from reproducing, whereas the non‐reproductive males are restricted from sexual activity through incest avoidance. Circulating basal concentrations of luteinizing hormone (LH) between reproductive and non‐reproductive females were not significantly different, yet the response to an exogenous gonadotrophin‐releasing hormone (GnRH) challenge was significantly lower in non‐reproductive females when compared to reproductive females. The mean basal LH concentration in non‐reproductive females was not significantly different in and out of the breeding season. However, the magnitude of the LH response in non‐reproductive females out of the breeding season was greater than in the breeding season. The ovaries of reproductive females showed little change with respect to season. However, reproductive females had enhanced follicular activity in comparison to their non‐reproductive counterparts. This suggests that non‐reproductive females are under stricter control from the reproductive female when she is pregnant. The tropical African mole‐rats exhibit a continuum of socially induced infertility with differing social species inhabiting regions of varying degrees of aridity. In this spectrum, a predominantly behavioural repression is found amongst non‐reproductive females in social mesic‐adapted species, whereas a strictly physiological suppression is operative amongst non‐reproductive females in arid‐adapted social species. Here we show that the mesic‐adapted highveld mole‐rat does not fit this trend in that the non‐reproductive females seem to be physiologically suppressed. We discuss this in light of the seasonality of breeding and the ecological constraints that may operate during times of drought.

Hypothalamic-pituitary-testicular axis and seminal parameters in hyperthyroid males.

Information on the effect of abnormal thyroid function on male reproduction is less available than that for the female. To assess the effects of hyperthyroidism on hypothalamic-pituitary-testicular axis and on spermogram parameters, 25 male patients (19-47 years old) suffering from active Graves' disease were studied. Serum luteinizing hormone (LH), follicle stimulating hormone (FSH), and prolactin (PRL) were measured before and after administration of 100 microg GnRH plus 200 microg thyrotropin-releasing hormone (TRH). Testosterone (T), estradiol (E2), and 17-hydroxyprogesterone (17-OHP) were determined before and after 5000 IU human chorionic gonadotropin (HCG) administration. Serum sex hormone-binding globulin (SHBG), cortisol-binding globulin (CBG), androstenedione and bioavailable testosterone (bioT), and bioavailable estradiol (bioE2) were also measured. Spermograms according to World Health Organization (WHO) criteria were determined in 21 patients. Hormonal and seminal studies were repeated in six patients after 7 to 19 months of euthyroidism achieved after treatment for hyperthyroidism. As a control group, 10 normal men were evaluated. Impaired sexual function, gynecomastia, and low testicular volume were found in 12, 6, and 3 hyperthyroid patients. Mean basal LH was significantly higher than the control group (7.8 +/- 4.7 vs. 5.0 +/- 1.9 mIU/mL, respectively, p < 0.02), with hyperresponse to GnRH. The response of PRL to TRH was lower in patients versus control group (30 minutes: 3.9 +/- 3.4 and 12.0 +/- 2.8 ng/mL, p < 0.01). Basal levels of steroids and SHBG were significantly higher in patients than in normal men (T: 9.3 +/- 3.3 vs. 5.4 +/- 1.6 ng/mL, p < 0.005; E2: 62.2 +/- 25.2 vs. 32.1 +/- 11.0 pg/mL, p < 0.005; 17-OHP: 2.4 +/- 0.9 vs. 1.1 +/- 0.5 ng/mL, p < 0.001; SHBG: 102.3 +/- 37.3 vs. 19.0 +/- 5.0 nmol/L, p < 0.01). The maximal increment of T and 17-OHP after HCG was lower in hyperthyroid patients than in normal men (p < 0.019 and p < 0.001, respectively). Basal bioT was lower in patients than controls (1.7 +/- 0.8 and 3.1 +/- 1.9 ng/mL, p < 0.02). The following incidence of abnormal semen parameters was found: asthenospermia 85.7%, hypospermia 61.9%, oligospermia 42.9%, necrospermia 42.9% and teratospermia 19.0%. In euthyroidism, a normalization of 85% of seminal alterations was observed in the limited number of patients evaluated. Our results confirm that hyperthyroidism causes marked alterations of the gonadotropic and PRL axis and dramatically affects spermatic function. BioT measurement was useful to identify hypoandrogenism in these patients in spite of the high concentration of total testosterone. The restoration of most semen parameters when euthyroidism was achieved suggests that the alterations were induced by the Graves' disease.

Androgenic status in patients with lepromatous leprosy.

To assess the incidence of testicular atrophy by evaluation of hormonal status, testicular histology and sperm production in chronic lepromatous patients. Forty-one male patients with a mean age of 39.5 years (range 16-57) were studied at the Leprosy Hospital, Istanbul, Turkey, and were compared with 15 age-matched controls with proven fertility. Reduced testicular size was observed in 51% and gynaecomastia in 27%. Of the 31 patients who were married, 15 were primarily or secondarily infertile. Twelve of 16 patients had oligospermia or azoospermia. The mean basal luteinizing hormone (LH), follicle stimulating hormone (FSH) and oestradiol levels were significantly elevated and the level of testosterone significantly reduced when compared with the control group. Whenever leprosy is diagnosed patients should be informed of the need for treatment of an acute attack and the need for routine assessment of FSH, LH, testosterone and oestradiol levels to detect hypogonadism and potential infertility.

Impaired Response of Free Alpha-Subunits after Luteinizing Hormone-Releasing Hormone and Thyrotropin-Releasing Hormone Stimulations in Beta-Thalassemia Major

In order to clarify whether the damage in gonadotropin secretion due to iron overload in patients with beta-thalassemia is of pituitary or hypothalamic origin, 14 euthyroid patients (8 females and 6 males, age 15-24 years) affected by beta-thalassemia major with hypogonadotropic hypogonadism were studied. Luteinizing-hormone (LH), follicle-stimulating hormone (FSH) and free alpha-subunit (FAS) were measured during LH-releasing hormone (LH-RH) stimulation test, and thyroid-stimulating hormone (TSH), prolactin (PRL) and FAS during thyrotropin-releasing hormone (TRH) stimulation test. During LH-RH stimulation, the mean basal LH, FSH and FAS levels were similar to those found in normal prepubertal children, but the peak values were lower than those found in such children. Also during TRH stimulation, the mean peak values of FAS were lower than those of normal prepubertal children, but the TSH response was normal. The lack of response of gonadotropins and FAS to LH-RH cannot exclude hypothalamic failure; however, the normal response of TSH to TRH, in spite of the poor response of FAS, indicates that the origin of hypogonadotropic hypogonadism is the pituitary damage concerning not only the gonadotroph but also the thyrotroph cells.

Two-year results of treatment with depot leuprolide acetate for central precocious puberty

We report results from 2 years of therapy with the long-acting form of the gonadotropin-releasing hormone (GnRH) analog leuprolide acetate, which was previously reported in short-term trials to be efficacious in the treatment of central precocious puberty. Thirteen girls and two boys, aged 1.9 to 9.7 years, who satisfied clinical criteria including GnRH-stimulated luteinizing hormone (LH) greater than 10 IU/L (mean radioimmunoassay LH, 29.1 +/- 5.54 IU/L), received depot leuprolide, 6 to 15 mg intramuscularly every 4 weeks. Estradiol (or testosterone), insulin-like growth factor I, and GnRH-stimulated gonadotropins were obtained at baseline, at 2 months, and at 6-month intervals with bone age determinations. Pubertal progression ceased in all patients, and menses did not occur. Mean increase in height during therapy was 5.77 +/- 2.0 cm/yr. Predicted adult height increased over baseline by 5.52 +/- 1.16 cm at 18 months. Mean estradiol values in the girls declined from 3.3 +/- 0.6 to 0.60 +/- 0.03 ng/dl, with no overlap of baseline and treatment values. The mean basal LH value was unchanged by therapy; mean basal and peak LH values for all follow-up GnRH stimulation tests were 4.05 +/- 0.57 and 4.95 +/- 0.70 IU/L, respectively. Basal and peak follicle-stimulating hormone (FSH) values were suppressed from 4.10 +/- 0.62 and 10.06 +/- 1.34 IU/L, respectively, to generally undetectable levels (< 1). Comparison with untreated control patients suggested that basal LH did not completely return to prepubertal levels, whereas FSH levels were suppressed below prepubertal levels. Estradiol, FSH, and LH levels reached their nadir by 2 months; in contrast, mean serum levels of insulin-like growth factor I progressively declined from +0.57 +/- 0.19 SD score to -0.06 +/- 0.22 SD score at 24 months. Two girls were withdrawn from the study because of reactions at injection sites, with apparent sterile abscess formation in one patient. This study provides evidence that (1) long-term treatment with depot leuprolide is characterized by immediate and sustained laboratory and clinical suppression, (2) GnRH-stimulated LH and random FSH and estradiol concentrations are useful laboratory measures of efficacy, and (3) the progressive increase in predicted adult height is temporally associated with decreased serum levels of insulin-like growth factor I and striking deceleration of bone age advancement.

Value of suppression with a gonadotropin-releasing hormone agonist prior to gonadotropin stimulation for in vitro fertilization

This study examined the use of gonadotropin-releasing hormone agonist (GnRHa) suppression before gonadotropin stimulation in 26 patients with failed prior in vitro fertilization (IVF) attempts and variable basal serum gonadotropin levels. Leuprolide, 1 mg subcutaneously per day, was administered from the midluteal phase of the cycle before IVF treatment. Concomitantly, stimulation was initiated on cycle day 3 with human menopausal gonadotropin (hMG) and follicle stimulating hormone (FSH). Based on their prior IVF attempts and serum gonadotropin levels on cycle day 3, 9 patients were high responders with elevated mean basal luteinizing hormone (LH)/FSH, 8 were low responders with elevated mean basal FSH/LH, 7 were intermediate responders with normal mean basal FSH/LH and a history of premature LH surge, and 2 had elevated (perimenopausal) mean FSH and LH. Leuprolide was discontinued on the day of human chorionic gonadotropin (hCG) administration. Prior IVF attempts in the same patients with the same protocol, but without GnRHa suppression, were used as controls. The mean number of ampules of hMG and FSH was significantly higher in leuprolide cycles than in controls. The mean day of hCG administration was also higher for leuprolide cycles than for controls. The mean LH and progesterone levels on the day of hCG were significantly lower in leuprolide cycles. The mean number of preovulatory oocytes aspirated and transferred was higher in leuprolide cycles. Cancellation and pregnancy rates were improved in leuprolide cycles. It is concluded that prior GnRHa suppression is beneficial for follicular recruitment for IVF. More patients with variable basal serum gonadotropin levels need to be studied before definite recommendations are made.

Postpartum interval in beef cows shortened by enclomiphene.

This study was designed to determine whether an anti-estrogen can block the negative effect of estrogens on luteinizing hormone (LH) release and therefore decrease the postpartum interval in suckled beef cows. In Exp. I, eight suckled postpartum beef cows were randomly assigned to treatment and control groups. Treatment cows received 1 g/d clomiphene citrate (im) from d 21 to 28 postpartum, while control cows were injected with saline. On d 28 postpartum, there was no difference (P greater than .05) in mean total and basal LH concentrations or LH pulse frequency between treatment and control cows. All control cows exhibited estrus on d 52 +/- 3; treatment cows exhibited estrus on d 134 +/- 12 (P less than .05). In Exp. II, 17 suckled cows were randomly assigned to three treatment groups: 1) control group (n = 6) receiving one empty implant, 2) 10-cm enclomiphene implant group (n = 5) and 3) 30-cm enclomiphene implant group (n = 6). The silastic implants were placed sc on d 20 and removed on d 29 postpartum. Mean total LH concentrations during d 24 to 29 postpartum in the 30-cm enclomiphene implant group were higher than the 10-cm implant (P less than .05) and control group (P less than .05). The postpartum period in the 30-cm enclomiphene group (45 +/- 6 d) was shorter than the 10-cm implant (94 +/- 24 d) and control (96 +/- 20 d) groups (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Serum Luteinizing Hormone in Prepuberal Gilts After Ovariectomy or Adrenalectomy1

Serum luteinizing hormone (LH) concentrations after ovariectomy (OVX) and adrenalectomy (ADX) were studied in the prepuberal gilt. In Exp.I, gilts, 170 to 175 d of age and 80 to 85 kg body weight, were OVX (n = 5) or sham-OVX (n = 5). Blood samples were collected via jugular vein cannulae every 30 min for 8 h on d 1, 3, 5, 7 and 21 after surgery. In Exp. II, blood samples were collected via jugular vein cannulae every 30 min for 12 h on d 3, 5, 7 and 14 after surgery from five ADX, five sham-ADX and five nonsurgical control gilts of similar ages and weights as in Exp. I. In Exp. I, basal serum LH concentrations (means +/- SE, ng/ml) over all days were greater (P less than .05) in OVX (2.9 +/- .1) than in sham-OVX (1.1 +/- .2) gilts. Average basal serum LH concentrations were greater (P less than .05) on d 1 for both treatments than all other days sampled. The frequency of LH peaks (means +/- SE/8 h) was also greater (P less than .01) for OVX (3.5 +/- .3) than sham-OVX gilts (1.7 +/- .2). Similarly, the mean concentration of the LH peaks was greater (P less than .01) for OVX (4.1 +/- .2 ng/ml) than sham-OVX gilts (2.1 +/- .2 ng/ml). In Exp. II, mean basal serum LH concentrations, frequency of LH peaks and mean concentration of the LH peaks were similar for all treatments on each day sampled. The frequency of LH peaks (means +/- SE/12 h) was greater (P less than .05) on d 3 (3.4 +/- .3) than on d 5 (2.3 +/- .3) and d 7 (2.1 +/- .4), but similar to d 14 (2.8 +/- .5) in all treatments. In prepuberal gilts, ADX failed to influence serum LH concentration, whereas OVX caused a significant increase in serum LH concentration. We suggest that the ovary is the major steroid-secreting gland having a negative feedback on pituitary gonadotropin production in the prepuberal gilt.

Correlation between integrated LH and FSH levels and the response to luteinizing hormone relasing factor (LRF).

Integrated blood plasma levels of LH and FSH and their response to the iv administration of 100 mug synthetic LRF were studied in 29 normal subjects, 12 women with Stein-Leventhal syndrome, 8 subjects with primary gonadal failure, 7 women with Sheehan's syndrome, 20 subjects with pituitary tumors, 10 subjects with idiopathic gonadotropin deficiency and 5 subjects with hypothalamic tumors. Within each group there was considerable variation in the response of LH and FSH levels to LRF. In each group there was a statistically significant positive correlation between basal integrated gonadotropin levels and the response of the levels to LRF. Both within groups and between groups, the best indicator of the response to LRF was the basal levels of FSH and LH. In subjects with hypogonadotropic hypogonadism there was no significant difference in mean basal LH levels and mean response to LRF between patients with primarily pituitary disease (pituitary tumors or Sheehan's syndrome) and conditions which might represent hypothalamic disease (hypothalamic tumors or idiopathic gonadotropin deficiency). The response to an acute, single, injection of LRF appears to more directly reflect basal gonadotropin levels rather than disease category.

Luteinizing hormone and follicle stimulating hormone and the response to luteinizing hormone releasing hormone in relation to sex and age.

Serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) before and after intravenous injection of luteinizing hormone releasing hormone (LHRH) were studied in 71 male and female subjects of various ages. Mean basal FSH and LH levels were not significantly different in the male groups, except that FSH was significantly higher in the very old subjects. Postmenopausal female subjects had much higher concentrations of both hormones than had premenopausal women. LH was higher in female subjects shortly after the menopause than in very old female subjects. The serum concentrations of both FSH and LH 30 min. after intravenous injection of 200 mug LHRH were not different from the 60 min. values. There was no significant difference in the response of LH in the male groups. The peak FSH concentration was higher in the very old male subjects. Postmenopausal women had a much higher peak concentration of both FSH and LH than had younger subjects. The increment of LH, but not of FSH, was larger in female subjects shortly after the menopause than in very old female subjects. In both sexes there was a significant correlation between the basal FSH/LH ratio and age. In younger male subjects there was a close positive correlation between basal LH and serum testosterone, in older male subjects this correlation was negative and significant.

Pituitary-gonadal function in men with alcoholic cirrhosis of the liver.

Fourteen adult males with alcoholic cirrhosis were studied. Gonadotrophin responses to luteinizing hormone-releasing hormone (LRH) and testosterone (T) responses to human chorionic gonadotrophin (HCG) were determined and basal 17 beta oestradiol (E2) levels were measured in each case. The mean basal luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels, and the mean LH and FSH responses to LRH were not significantly different from a group of age-matched male controls. However, the five men with testicular atrophy all had an elevated basal FSH level and an exaggerated FSH response to LRH. The mean serum T of the cirrhotic men was significantly lower than that of the controls (P less than 0.05), while the mean E2 level was not significantly different. However, the mean E2 level in the eight patients with gynaecomastia was significantly higher than in those without gynaecomastic (P less than 0.05). All patients had a T response to HCG, including those 5 with low basal T levels. A significant negative correlation was found between the maximum rise in T after HCG (delta T) and the maximum LH response to LRH (delta LH), suggesting a mediating effect of T reserve on the LH response to LRH. These findings tend to exclude a suppressive effect of alcohol on the pituitary gland as a cause for the hypogonadism found in men with alcoholic cirrhosis. Furthermore, the evidence of some testicular T reserve despite low basal T levels, and the presence of normal basal LH levels, suggests that the low T production is not primarily due to leydig cell dysfunction.

The ovarian cycle of the bitch: plasma estrogen, LH and progesterone.

Plasma levels of luteinizing hormone (LH) progesterone and estrogen were determined in pregnant and nonpregnant cycles of female beagle dogs. Mean basal LH levels during estrus and proestrus were 1.4 + or -.1 ng/ml and peaked at 7.5 + or -.8 ng/ml on the 1st day of estru s. Preovulatory increases in progesterone and LH appeared to be temporally correlated and were significantly elevated by the 2nd day of estrus (p less than .001). Progesterone levels reached their maximum on the 25th day of estrus (22.9 + or -2.7). Estrogen levles increased from 26 + or -4 on Day 10 prior to the LH peak to 62 + or -4 pg/ml 1 day before the LH peak. Once the LH peak was established estrogen levels fell rapidly. In the luteal phases of 12 pregnant and 10 nonpregnant cycles there were no marked differences in mean maximum progesterone levels the ranges of individual maximum levels or the time of their occurrence. After Day 30 progesterone levels declined gradually and were significantly (p less than .001) variable in nonpregnant cycles compared with pregnant cycles once progesterone levels dropped below 1 ng/ml. Progesterone levels showed significant (p less than .05) daily changes during the 2 days prior to parturition. Plasma Estrogen levels were constant in nonpregnant cycles but significantly (p less than .01) increased during the 3 weeks prior to parturition. The results suggest that plasma estrogen initiates or potentiates the preovulatory release of LH that the early preovulatory release of progesterone may encourage the LH peak surge and the onset of behavioral estrus and that mechanisms exist that maintain elevated levels of plasma progesterone throughout pregnancy.

Amenorrhoea in anorexia nervosa: assessment and treatment with clomiphene citrate.

Seven patients with anorexia nervosa were studied, three during the acute stages of the illness, and four in whom weight gain had been achieved, but who suffered from persistent amenorrhoea of 18 to 79 months' duration.In the acute stage all patients had low serum luteinizing hormone (LH) levels which were unresponsive to clomiphene citrate. In those who had regained weight the mean basal LH levels were normal, and they responded to clomiphene with an initial doubling of serum LH during administration of the drug, followed by a second peak of serum LH four to seven days after the drug was stopped. Menstruation occurred in these patients 13 to 19 days after the clomiphene was discontinued, and in two patients regular spontaneous menstruation was initiated.The low LH levels unresponsive to clomiphene in the acute stage provide evidence for a hypothalamic abnormality in anorexia nervosa. After regain of body weight the drug seems to be effective in treating the amenorrhoea which may be persistent.