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Typical for critical illnesses are substantial alterations within the hypothalamic-anterior pituitary-peripheral hormonal axes that are proportionate to the risk of poor outcome. These neuroendocrine responses to critical illness follow a biphasic pattern. The acute phase (first hours to days) is characterized by an increased release of anterior pituitary hormones, whereas altered target-organ sensitivity and hormone metabolism result in low levels of the anabolic peripheral effector hormones and contribute to the substantially elevated levels of the catabolic hormone cortisol. The prolonged phase of critical illness is hallmarked by a uniform suppression of the neuroendocrine axes, predominantly of central/hypothalamic origin, which contributes to the low (or insufficiently high in the case of cortisol) circulating levels of the target-organ hormones. Several of the acute-phase adaptations to critical illness are due to or accentuated by the concomitant fasting. Accepting the lack of macronutrients as well as the neuroendocrine responses to such fasting in the acute phase of critical illness has shown to beneficially affect outcome. In contrast, the neuroendocrine alterations that occur in the chronic phase of illness while patients are fully fed contribute to bone and skeletal muscle wasting and impose risk of adrenocortical atrophy. The combined administration of those hypothalamic releasing factors, which have been identified as suppressed or deficient during prolonged critical illness, may be a promising strategy to enhance recovery. The potential impact of treatment with such hypothalamic releasing factors on recovery from critical illness as well as on long-term rehabilitation should be investigated in future randomized controlled clinical trials.

Precocious puberty is an early sexual maturation before the age of 8 in case of girls and 9 in boys. There are two types: isosexual precocious puberty--characteristic are appropriate for the child's genetic and gonadal sex; and heterosexual precocious puberty--sexual characteristic are inappropriate for the genetic sex (feminizing syndrome in boys or virilizing syndrome in girls). Precocious puberty is an important problem in childhood gynecology pediatrics, endocrinology and psychology.

In 31 patients with multiple sclerosis (MS) the endocrine functions of the hypothalamus, the pituitary and several peripheral endocrine glands were assessed with a combined pituitary test; 3/31 patients had an endocrine disease: one primary hypothyroidism, one primary amenorrhea and one primary male hypogonadism. We found no patient with endocrine disease of the hypothalamus, the pituitary or the adrenals. However, the poststimulatory secretion of cortisol, growth hormone or thyroid-stimulating hormone was impaired in 7/31 patients, suggesting a possible preclinical endocrine insufficiency in these patients.

The patient with PCOD remains a challenge to the reproductive endocrinologist. Although successful induction of ovulation can often be achieved using standard therapeutic regimens of CC or hMG, too often this group of anovulatory patients fails to respond as expected. Over the past 10 to 15 years, alternate approaches to ovulation induction have been investigated with encouraging results. Whereas no one method is productive in all patients, these varied regimens offer us a number of options in dealing with this difficult clinical problem.

Prolonged pulsatile exogenous GnRH allows differentiation between hypothalamic and pituitary causes of hypogonadotrophic hypogonadism and is able to induce ovulation and pregnancy in most of women with hypothalamic amenorrhea (HA). When compared with human menopausal gonadotropin, GnRH appears to be a more efficient therapy of HA but yields inferior results in chronic anovulatory patients with persistent LH secretion. Pulsatile GnRH following a GnRH-analog suppression represents a new promising treatment of infertile women with polycystic ovarian syndrome. However such a combined therapy is time-consuming and only permits to attempt 3 to 4 stimulated cycles during a year. Therefore the successful preliminary reports need to be confirmed by a further randomized study.

Superagonistic analogues of Gn-RH given chronically produce a paradoxic inhibition of pituitary gonadotropin secretion and consequently decrease the peripheric hormones estradiol and progesterone to a postmenopausal level. For curative purposes buserelin (SuprefactR, Hoechst) treatment has been performed by the authors in two cases of breast cancer. The patients--one with NED (no evidence of disease) and the other with pulmonary and osseal metastases--in addition to low hormonal levels developed amenorrhoea. A group of climacteric complaints were observed without any toxic side effects, however. The treatment of premenopausal women suffering from breast cancer with chronic administration of Gn-RH analogues may constitute a valuable alternative to surgical oophorectomy.

Twenty-five GH-deficient children were treated with GHRH (1-44), once daily sc for 6-24 months. At the 6th month of therapy, 40% of our patients showed a catch-up growth (responders), while the remaining 60% did not (nonresponders). No differences in auxological and biological variables at inclusion were found between the two groups. However, integrated GH secretion elicited by iv GHRH at inclusion was significantly (p less than 0.025) higher in responders than in non responders. During GHRH therapy, no significant increase in IGF 1/SmC was found in both groups. In all patients treatment was discontinued after 6-24 months, when its effect on growth rate failed. After a wash-out period of at least 6 months, patients were submitted to biosynthetic GH therapy. After 6 months of GH treatment a significant catch-up growth was found in both responder and non-responder children. Although the majority of GH-deficient children have hypothalamic rather than pituitary dysfunction, GHRH therapy is found to be less effective than GH treatment. Other methods of GHRH administration are worth investigating.

The effects of the administration of gonadotropin-releasing hormone (GnRH) on the increase of testis and prostate volume was monitored by ultrasound in six patients affected by idiopathic hypogonadotropic hypogonadism. A significant increase of testis volume was observed after 90 and 180 days (6.65 versus 3.32 mL, 99.1% net increase and 8.47 mL, 176.8% increase, respectively) of pulsatile GnRH treatment. A similar increase of prostate volume was observed at day 90 (12.67 versus 7.78 mL, 70.3% net increase) and day 180 (14.70 mL, 97.7% increase). The ultrasound monitoring of the modifications of testis and prostate volume may represent a biological assay of the effects of GnRH treatment and offer additional data on the response of target organs to the hormonal treatment.

Human growth hormone releasing hormone (GHRH) fails to stimulate human growth hormone (GH) in hypercortisolism. In order to study whether the responsiveness to GHRH stimulation returns after cure of the hypercortisolism, the GH response to GHRH was examined in 8 patients at least 5 yr after they had undergone bilateral adrenalectomy as their sole treatment for Cushing's disease. None had current evidence of a pituitary macroadenoma. A group of 8 healthy subjects matched for age and sex formed the control group. All patients and subjects received an iv injection of GHRH 1 microgram/kg, after an overnight fast, blood samples were taken before and at 15, 30, 45, 60, 90 and 120 min. There was no statistical difference between the peak GH or area under curve (AUC) response (median, range) in the two groups studied (adrenalectomized peak GH 9.2 (4.6-32.0) vs 16.5 (7.5-63) mU/l, adrenalectomized AUC response 647.5 (344.2-1489.5) vs 1103.5 (339.7-5188.5) mU/l. Patients with Cushing's disease once cured of hypercortisolism, have a GH response to GHRH.

The necessity of luteal-phase supplementation in an IVF programme is of continuing interest. After ovarian stimulation with clomiphene and human menopausal gonadotrophin (HMG), the beneficial effect of supporting the luteal phase has never been scientifically demonstrated. After ovarian stimulation with GnRH agonist/HMG, the luteal phase seems to be inadequate, but in a previous study we did not find evidence to support the need for oral progesterone supplementation. To evaluate the beneficial effect of human chorionic gonadotrophin (HCG) supplementation, we performed a multicentre, double-blind, randomized study with HCG (193 transfers) against placebo (194 transfers). The ongoing pregnancy rate per transfer cycle was significantly better with HCG (18.7 versus 9.3). This is the first truly objective (randomized) study demonstrating the beneficial effect of supporting the luteal phase in an IVF programme.

Changes in circulating inhibin levels were related to changes in testosterone (T) and the gonadotrophins luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in a hypogonadotrophic hypogonadal man before and during pulsatile gonadotrophin-releasing hormone therapy which resulted in normal spermatogenesis. Before treatment, the plasma inhibin levels in the patient (210 +/- 50 U/l; mean +/- SD of four samples) were lower than in normal controls (552 +/- 150 U/l; p less than 0.01), as were T (1.1 nmol/l) and gonadotrophin (less than 1.0 IU/l) levels. Within 1 week of gonadotrophin-releasing hormone treatment, plasma LH (14.1 +/- 0.7 IU/l) and FSH (14.4 +/- 0.6 IU/l) reached supraphysiological levels. In response, T and inhibin concentrations increased progressively to reach high normal levels (27.7 +/- 1.6 nmol/l and 609 +/- 140 U/l) at 4 weeks, by which time the gonadotrophin levels stared to decline and gradually returned to the normal range between 12 and 24 weeks of treatment. There was a concomitant decrease in T and inhibin levels which remained within the normal range. The decline in the FSH level following the rise in testicular hormones was earlier and steeper than that of LH (37.5% decrease at 4 weeks vs. 30.4% at 12 weeks), suggesting that T and inhibin may act together to inhibit pituitary FSH secretion as opposed to LH secretion which is primarily controlled by T. It is concluded that, in man, during maturation of the pituitary-testicular axis, changes in circulating inhibin parallel those of T, and quantitatively normal inhibin secretion is dependent on gonadotrophin stimulation. FSH secretion may be regulated through negative feedback control, by both T and inhibin.

Pharmacoendocrinological studies have shown that psychotropic drugs with different actions have different effects on anterior pituitary hormone secretion in man. Substances with different effects on the central nervous system are characterized by a different pharmacoendocrinological profile. Studies with various receptor blockers have shown varying influences on the DMI-induced growth hormone, prolactin, and ACTH/cortisol secretion. Growth hormone stimulation was shown to be mediated by alpha 2-receptors and inhibited by beta-receptors. Investigations in male and female endogenous depressive patients demonstrated a significantly blunted growth hormone response to DMI compared with age- and sex-matched healthy subjects. A comparative study in male endogenous depressive patients showed a significantly diminished growth hormone stimulation both after DMI and after growth hormone-releasing hormone compared to healthy male subjects. In further tests a simultaneous application of four releasing hormones (GHRH, CRH, GnRH, TRH) was used. These investigations showed a significantly lower GH stimulation in endogenous depressive patients compared with age- and sex-matched healthy subjects, but not in neurotic depressive or schizophrenic patients. Cortisol stimulation was similar in all groups of patients and healthy subjects. TSH stimulation was significantly lower in endogenous depressive and schizophrenic patients than in healthy subjects. Somatomedin-C concentrations were significantly elevated in endogenous depressed patients compared with healthy subjects. The blunted growth hormone response in endogenous depression could be explained by inhibitory influences such as increased somatomedin-C concentrations or a hyperactivity of central beta-adrenergic-receptors.

Nine clomiphene citrate-resistant polycystic ovarian disease (PCOD) patients received intravenous gonadotropin-releasing hormone (GnRH) pulses before and immediately after 1 month of GnRH agonist (GnRH-a) therapy. Circulating gonadotropin and ovarian steroid levels, as well as follicular development, were measured throughout therapy. Results were compared with those obtained from five hypogonadotropic patients treated with GnRH pulses only who ovulated during six of seven treatment cycles. Only two PCOD patients ovulated normally with GnRH pulses before GnRH-a therapy. Aberrant gonadotropin and ovarian steroid secretory patterns were noted in the others. After GnRH-a, gonadotropin and ovarian steroid hormone levels were similar to those of the hypogonadotropic patients. Subsequent secretory responses to GnRH pulses were partially normalized. However, only two additional PCOD patients ovulated.

Gonadotropins are released in a pulsatile fashion at a frequency of between 1 and 2 hours in the follicular phase of the menstrual cycle. Human menopausal gonadotropins are usually administered intramuscularly. We evaluated the gonadal response to intravenous human menopausal gonadotropins administered in a pulsatile fashion over nine treatment cycles in three anovulatory infertile women. Human menopausal gonadotropin pulses in doses up to 12 IU follicle-stimulating hormone at frequencies between 2 to 3 hours over 3 to 17 days resulted in ovulation in five cycles with one pregnancy being conceived. In the ovulatory cycles (5,000 to 10,000 IU of human chorionic gonadotropin was used to induce ovulation), the 17 beta-plasma estradiol level was 961 +/- 128 versus 326 +/- 95 pg/ml (mean +/- SEM) in the anovulatory cycles (p = 0.015). The dose of human menopausal gonadotropins (in ampules of Pergonal, 75 IU of follicle-stimulating hormone and 75 IU of luteinizing hormone) in the intravenous cycles needed to induce ovulation was 12.3 +/- 1.4 versus 20.4 +/- 0.9 for intramuscular cycles (n = 80 in 23 women, p = 0.008). Treatment was well tolerated and without complications. We are continuing to explore the use of this apparently more efficient mode of administering human menopausal gonadotropins to anovulatory patients resistant to other techniques of ovulation induction therapy.

Sixteen women with primary and secondary amenorrhoea were treated with pulsatile GnRH administered subcutaneously. Ovulation was successfully induced in 6/8 women with hypogonadotrophic hypogonadism; and in 2/2 women with idiopathic hyperprolactinaemia; but in only 3/6 women with amenorrhoea associated with an elevated LH:FSH ratio. Using serial blood sampling, we were unable to demonstrate the establishment of a physiological pattern of gonadotrophin secretion in the presence of an apparently normal menstrual cycle. Nor did we observe a consistent relationship between injection of GnRH and the resultant gonadotrophin response. A reduction or total cessation of both pituitary and gonadal sensitivity to GnRH was observed in four women. Possible reasons for these findings are discussed.

Testosterone in plasma was measured by radioimmunoassay in cows with ovarian cysts and in cows during the estrous cycle. Concentrations of testosterone in plasma (60.8 +/- 2.7 pg/ml; mean +/- standard error) in cows with ovarian cysts were variable but within the range in cows during the estrous cycle. Mean concentrations of testosterone in plasma increased from 46.3 pg/ml at estrus to 85.1 pg/ml on day 13 of the estrous cycle. In cows with ovarian cysts, concentrations of testosterone in plasma declined within 24 h following prostaglandin F2 alpha and tended to increase by 9 days following gonadotropin releasing hormone. The role of testosterone in estrual behavior and inhibiting resumption of ovarian cycles is likely minimal.

Thirty-six postpartum Holstein cows consisting of eighteen cows that shed the placenta soon after calving (NRP) and eighteen cows that retained placenta greater than 24 h (RP) were used. There were four treatment groups. Group I consisted of 9 NRP cows which received intramuscular injection of sterile saline on day 15 postpartum. The second group consisted of 9 NRPN cows which received 100 micrograms of gonadotrophin releasing hormone on day 15 postpartum (NRPT). The third group consisted of 9 RP cows which received saline on day 15 postpartum (RPN) and the fourth group consisted of 9 RP cows which received 100 micrograms of gonadotrophin releasing hormone on day 15 postpartum (RPT). Blood samples were collected once daily during the first month and once every other day during the second month postpartum. In addition fourteen cows (RPT, n = 7; NRPT, n = 7), were used to study short-term changes in serum luteinizing hormone concentrations following gonadotrophin releasing hormone treatment on day 15 postpartum. Blood samples were obtained from these cows every 15 min during 1 h before and 6 h after gonadotrophin releasing hormone administration. Sera from all samples were assayed for progesterone and luteinizing hormone concentrations. Starting from four days after calving rectal palpations and ultrasound examinations of the ovaries were carried out once every four days until day 28 postpartum in order to monitor ovarian changes. All cows were inseminated on the first estrus after day 60 postpartum and examined for pregnancy between 35 and 42 days after insemination.(ABSTRACT TRUNCATED AT 250 WORDS)

Premenstrual syndrome (PMS) is a diagnostic enigma that causes significant morbidity in many woman. Numerous theories have been proposed in an attempt to explain the varied symptoms that occur cyclically in women with PMS. Suggested etiologic theories of PMS include psychological abnormalities, nutritional deficiencies, aberrations in the renin-angiotensin-aldosterone axis, altered prostaglandin activity, hormonal imbalances, and changes in endogenous opioid peptide activity. Because of the lack of standardized diagnostic criteria, clinical drug trials for PMS have been severely compromised. For every proposed cause of PMS, there exists a drug or drug class that has been investigated for treatment of the associated symptoms. Many clinical studies are uncontrolled, a significant deficiency in study design for a disorder that is associated with a high placebo response rate. At the present time, no definitive treatment for PMS exists and therapy must be individualized according to clinical response. This review article defines PMS, describes one of the current approaches to the diagnostic work-up, discusses the proposed etiologies of PMS, and reviews the various proposed treatment modalities.

The physiological and pathophysiological basis of hypothalamic amenorrhoea are reviewed as well as the clinical results of chronic intermittent (pulsatile) administration of Gn-RH in the treatment of infertility. Hypothalamic amenorrhoea is considered to be the result of a deficient hypothalamic secretion of Gn-RH. By pulsatile administration of Gn-RH, which is a pre-requisite of normal pituitary gonadotrophic function, deficient endogenous Gn-RH is replaced. If an adequate dose of Gn-RH is provided, which takes into account the degree of impairment of hypothalamic function in the individual case, follicular maturation, ovulation and corpus luteum formation are achieved in nearly every treatment cycle. Although dependent also on factors other than the treated dysfunction, a high conception rate is achieved.

The response to low-dose pulsatile gonadotropin-releasing hormone (GnRH) therapy was tested in three hypogonadotropic hypogonadal male patients and a boy with delayed puberty showing different luteinizing hormone responses (delta LH) to test doses of 25 micrograms GnRH intravenously before treatment. Four male patients, 16 to 20 years of age, three with Kallmann's syndrome and one with idiopathic delay of puberty, received 2 micrograms GnRH subcutaneously every 2 1/2 hours for 3 months by the use of the Zyklomat pump (Ferring GmbH, Kiel, FRG). In two patients with Kallmann's syndrome and decreased delta LH, serum testosterone did not increase during treatment, even after increasing the dosage and changing the route of administration (4 micrograms subcutaneously or 8 micrograms intravenously every 2 1/2 hours for 4 weeks with every dosage). The third patient with Kallmann's syndrome and the boy with delayed puberty, both with normal delta LH, presented normal serum testosterone after 3 months of subcutaneous low-dose treatment. The different responses to a GnRH test dose corresponding to the response to pulsatile GnRH therapy probably reflect different degrees of maturation of the pituitary gonadotrophs.

With the availability of synthetic analogues of the hypothalamic releasing hormones, analysis of their interactions with pituitary receptors has been achieved. The most studied is gonadotrophin-releasing hormone (GnRH). Pituitary receptors for this peptide show a positive correlation with gonadotrophin secretion and responsiveness to exogenous GnRH in experimental animals, an indication of their physiological importance. GnRH is also required for maintenance of a 'normal' complement of GnRH receptors and, when administered intermittently, can effect significant increases in unoccupied receptors. Conversely, the continuous administration of high GnRH or agonist analogue (GnRH-A) doses leads to pituitary desensitization through disruption of receptor-mediated events. Thus, for stimulation of fertility using GnRH, the peptide should be administered in small doses at physiological frequency (approximately once every two hours) to avoid pituitary desensitization. The desensitizing properties of long-acting GnRH-A are of potential value as contraceptives agents and where a medical castration is desirable. The physiological correlates of pituitary receptors for thyrotrophin-releasing hormone, somatostatin (GHRIH) and corticotrophin-releasing factor await elucidation.

Ovulatory dysfunction is a leading cause of female infertility in the United States. Fortunately, ovulatory dysfunction is often amenable to treatment. Thorough testing is necessary to identify the exact cause of anovulation before conventional ovulation-inducing therapy is started. Careful patient monitoring is essential to avoid risks such as the ovarian hyperstimulation syndrome. Several newer ovulation-inducing agents are available for use in special situations.

A patient with congenital adrenal hypoplasia (AH) and hypogonadotrophic hypogonadism was treated with pulsatile subcutaneous GnRH therapy for 16 weeks in an attempt to induce puberty. No rise in serum LH or FSH concentrations occurred despite increasing doses of GnRH (2.8 micrograms/pulse-22.4 micrograms/pulse). In contrast a similar programme of therapy successfully initiated the biochemical changes of puberty in a patient with Kallmann's syndrome. Both patients before therapy had low basal serum LH and FSH concentrations with blunted LH and FSH responses to GnRH stimulation. After 1 week, serum LH and FSH rose into the normal adult range in the patient with Kallmann's syndrome. This study fails to confirm a previous report which suggested that intermittent low dose GnRH therapy may be of value in inducing puberty in AH. The reasons for the difference of pituitary responsiveness to GnRH in AH and Kallmann's syndrome are unclear at present.

In a group of three patients affected by severe hypothalamic amenorrhea, gonadotropins behaviour before and during pulsatile GNRH therapy, was investigated with more accuracy for seven cycles. The treatment was administered intravenously with a dosage of 5 ug/90 min. The number of cycles for pregnancy was of 1.75 with a pregnancy rate of 57.1%. The gonadotropins response to an acute test with 100 ug of GNRH performed in the three patients at the 7th day of their first treatment cycle was compared with response to the same test done before the beginning of the pulsatile therapy. Some considerations about the results were suggested.

The early hormonal changes that lead to follicular maturation and/or hyperstimulation in women requiring ovulation induction with either human menopausal gonadotropin or gonadotropin-releasing hormone have not been elucidated. This study was undertaken to assess the relative contribution of follicle-stimulating hormone and luteinizing hormone to estradiol secretion and follicular maturation in patients receiving human menopausal gonadotropin or gonadotropin-releasing hormone. The study group consisted of 10 women (26 to 38 years of age) with secondary amenorrhea as a result of hypothalamic dysfunction who had failed to ovulate when given clomiphene citrate. The patients were randomly assigned to either human menopausal gonadotropin (n = 5) or gonadotropin-releasing hormone (n = 5) treatment. On day 5 after the onset of induced menses, all women had baseline blood samples obtained at 10-minute intervals for 4 hours. At this time either 150 U of human menopausal gonadotropin or 75 ng/kg of gonadotropin-releasing hormone administered hourly was given, and blood sampling every 10 minutes was continued for an additional 6 hours. Thereafter, patients were evaluated daily until ovulation. A significant and sustained increase in the mean plasma follicle-stimulating hormone level was first measured during the third hour after human menopausal gonadotropin administration (p less than 0.05. The area under the curve of the mean plasma follicle-stimulating hormone value after this initial increase was significantly greater than its baseline (2119 +/- 240 versus 1425 +/- 188 mlU/ml; p less than 0.01). This rise in mean follicle-stimulating hormone level was followed in less than 2 hours by a significant and uniform rise in mean plasma estradiol concentration (p less than 0.05). In contrast, no immediate change in the mean levels of luteinizing hormone, follicle-stimulating hormone, or estradiol occurred after gonadotropin-releasing hormone administration. The mean daily levels of luteinizing hormone were similar in both groups; however, mean daily follicle-stimulating hormone (20.0 +/- 1.1 versus 9.2 +/- 1.4 mlU/ml) and estradiol (1004 +/- 174 versus 495 +/- 83 pg/ml) levels were significantly higher in patients treated with human menopausal gonadotropin than in those treated with gonadotropin-releasing hormone (p less than 0.001 and p less than 0.05, respectively). In addition, only in patients receiving human menopausal gonadotropin was a positive correlation found between mean daily plasma estradiol and follicle-stimulating hormone (r = 0.685, p less than 0.05) levels and between mean daily plasma estradiol and prolactin (r = 0.94, p less than 0.001) levels.(ABSTRACT TRUNCATED AT 400 WORDS)

The effects of gonadotrophin releasing hormone (GnRH) on the reproductive performance of dairy cows with retained placenta were studied. Three hundred and seventy-eight cows diagnosed as having retained placenta received intramuscular injections of either 2 mL sterile water or 200 micrograms of GnRH in 2 mL sterile water between day 8 and day 14 postpartum. Rectal palpation was performed at the time of treatment and ten to 20 days after treatment in order to determine the rate of uterine involution. Thereafter, monthly rectal examinations were carried out until insemination. Pregnancy diagnosis was made by rectal palpation at 40 days or more after breeding. Using the entire experimental population, there were no significant differences between GnRH-treated and control cows for the rate of uterine involution, the occurrence of reproductive problems, the interval from parturition to first observed estrus, the interval from parturition to first insemination, the interval from parturition to conception, the number of services per conception, the total number of services per cow regardless of conception and the incidence of culling for infertility. When the data for herds in which breeding began earlier in the postpartum period (herds having a mean less than or equal to 80 days from parturition to first service for retained placenta cows) were considered, the GnRH treatment resulted in a significantly shorter (p less than or equal to 0.01) calving to conception interval as compared to control cows. Also, there was a significant reduction (p less than or equal to 0.05) in the total number of services per cow regardless of conception and a significant reduction in the interval from parturition to first service.(ABSTRACT TRUNCATED AT 250 WORDS)

Intensive research in field of gynecological endocrinology has led to various new results. For nonspecialists it seems to be difficult to draw conclusions from puzzling detail for the therapy of the patient. Today's conception of human cyclus-physiology is illustrated in this report. The various types of amenorrhoea are gathered into four functional groups. Therapy from the acting gynecologist's point of view is presented as well.

A GnRH superagonist, buserelin, was administered for 16 days to a postmenopausal woman with a testosterone-secreting ovarian tumor. Serum gonadotropin levels decreased by more than 70%, and serum testosterone fell by more than 50%. This short term study demonstrates that in these uncommon tumors androgen secretion is gonadotropin sensitive, and suggests that GnRH analogs may have therapeutic value in such patients.