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Query: UMLS:C0003128 (anovulation)
 1,718 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperprolactinemia is a common endocrine cause of infertility in women. The pathophysiology of hyperprolactinemia in infertility is understood incompletely; however, the adverse effects of high circulating levels of prolactin on the hypothalamic-pituitary-ovarian axis cause chronic anovulation and other defects of ovarian function. Mechanisms for prolactin-induced anovulation have been postulated, and there are several contemporary approaches to the diagnosis and treatment of prolactin-secreting pituitary adenomas.
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PMID:Hyperprolactinemia and female infertility. 264 73

To determine the prevalence of hormonal abnormalities in infertile African women, serum levels of luteinizing hormone, follicle stimulating hormone, prolactin, and progesterone were estimated using radioimmunoassay techniques during the midluteal phase in 2,047 female partners of infertile relationships. Of the patients investigated, 1,085 (53%) had abnormal serum levels of one or more of the hormones studied. Hyperprolactinemia, found in 537 (26.2%) of the patients, was the commonest hormonal abnormality. Serum progesterone level of 3 ng/mL or below which is indicative of anovulation was found in 235 (11.5%) patients, while the value of 5 ng/mL or below, suggestive of inadequate luteal functions, was found in another 121 (5.9%) patients. Since hyperprolactinemia, anovulation, and defective luteal function are treatable endocrine disorders, routine endocrine evaluation of infertile females in African societies is suggested.
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PMID:Serum levels of gonadotropins, prolactin, and progesterone in infertile female Africans. 288 88

Reproductive change during conditioning exercise (physical training provides a model of hypothalamic adaptation to alterations in the external and internal environment. Parallels exist between the reproductive changes with exercise and those occurring with physical illness, undernutrition and psychological trauma. Although menstrual cyclicity may be disrupted in younger women, luteal phase shortening, anovulation and decreased premenstrual symptoms within normal ovulatory cycles are the most frequent observations noted. Baseline LH, prolactin and oestradiol tend to be lower, and other hormones unchanged, in trained women. Testosterone may be decreased within the normal range in men. Recent evidence shows that LH pulse frequency, amplitude and area under the LH curve are decreased in both female and male runners. Interrelationships between increases in central dopamine, endorphin and probably some hypothalamic message(s) relating to nutritional state appear to modulate these reproductive changes. The clinical and therapeutic response to reproductive alterations in the context of exercise differs when these are seen as adaptive and not as disease processes (Prior and Vigna, 1985b).
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PMID:Physical exercise and the neuroendocrine control of reproduction. 289 27

The literature concerning endogenous hormonal profiles in women with breast cancer and breast-cancer risk has been critically reviewed. The many published reports have been divided into 11 groups, with each group centered on a particular hypothesis that has been either explicitly formulated by the authors of the reports or perceived by other workers as a unifying hypothesis in certain studies. The hypotheses reviewed are: the adrenal androgen insufficiency hypothesis, the anovulation/luteal inadequacy hypothesis, the estriol hypothesis, the ovarian androgen excess hypothesis, the thyroid dysfunction hypothesis, the prolactin hypothesis, the estrone hypothesis, the estrogen-window hypothesis, the estrogen-excess hypothesis, the melatonin hypothesis, and the estrogen hydroxylation hypothesis. It is concluded that there remain, at present, only four viable hypotheses: the hypotheses of increased risk with adrenal androgen deficiency, ovarian dysfunction (luteal inadequacy and excessive ovarian androgen secretion), increased 16 alpha-hydroxylation of estradiol, and the hypothesis of decreased risk with pregnancy-induced lowering of prolactin levels. Adrenal androgen deficiency seems to be pertinent only in premenopausal cancer patients, and may be a genetic defect. Ovarian dysfunction seems to be pertinent to both premenopausal and post-menopausal patients and may also have a strong genetic component. Increased estradiol hydroxylation likewise seems to have a genetic component. The prolactin effect differs from the others, in that it is clearly environmental, rather than genetic, and may represent a permissive effect rather than a true risk-promoting effect.
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PMID:Hormonal profiles in women with breast cancer (review). 305 48

In order to investigate the postulated relationship between hyperprolactinaemia and polycystic ovary syndrome (PCOS) we have studied 62 patients with PCOS. Only two patients had persistent prolactin (PRL) concentrations greater than the normal range on both random sampling and after blood sampling from intravenous cannula over 2 hours. Twenty-eight of the remaining patients had basal PRL secretion studied in more detail. Samples were collected at 15 min intervals during a 6 h period in all 28 patients and hourly samples were collected overnight from four patients. Results failed to demonstrate differences from control subjects in mean basal PRL concentrations, in spontaneous fluctuations or in increments related to stress, food or sleep. Lactotroph response to thyrotrophin releasing hormone, luteinising hormone releasing hormone and insulin stress testing in PCOS were determined. Results confirm a previous observation that normal PRL increments occur after ovulation and a blunted response follows a period of anovulation. This study has failed to find a consistent abnormality of lactotroph function in patients with PCOS other than that associated with anovulation.
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PMID:Studies of prolactin secretion in polycystic ovary syndrome. 308 93

It has been noticed that hyperprolactinemia can cause luteal insufficiency as well as anovulation in women. In order to explore the mechanism underlying this disorder, hyperprolactinemia was induced in baboons (Papio cynocephalus) by daily administration of sulpiride during follicular and early luteal phases. In hyperprolactinemic baboons, the plasma progesterone level was suppressed without notable changes in plasma estradiol, LH and FSH levels. When corpora lutea from these baboons were examined in vitro to investigate their ability to convert 14C-pregnenolone into various steroids, there was progressive inhibition of steroid metabolism related to the plasma levels of prolactin. These findings strongly suggest, although do not actually prove, that an elevated level of prolactin could directly impair luteal function by adversely affecting 3 beta-hydroxysteroid dehydrogenase activity.
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PMID:Impaired steroidogenic function of corpora lutea from hyperprolactinemic baboons induced by sulpiride. 309 3

Infertile women with normal serum prolactin (PRL) levels have been known to establish a pregnancy after the use of bromocriptine, a dopamine agonist. These data imply that there may be a group of women with a slight but significant increase in PRL secretion that may have resulted in their infertility. This study evaluates the thyrotropin-releasing hormone (TRH)-induced PRL and thyroid-stimulating hormone (TSH) response in normal women (NL, n = 6), women with anovulation and/or inphase endometrial biopsies (AN/IN, n = 12), and women with histologic evidence of luteal phase deficiency (LPD, n = 12). Most of these women were found to have elevated serum PRL values on random testing. There was a statistically significant increase in PRL response at all time intervals after TRH between the NL and AN/IN groups compared with the group with LPD on the basis of repeated measures analysis (P = 0.0013). There was no statistical difference in the TSH response between these three groups. Although the PRL response was statistically different, individual PRL response patterns were not diagnostic. It appears from these data that there is an increased PRL secretion in infertile women who have histological evidence of a LPD.
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PMID:Prolactin response to thyrotropin-releasing hormone in women with infertility and/or randomly elevated serum prolactin levels. 310 94

The authors compared 12 hyperprolactinemic patients with polycystic ovary (PCO) syndrome to 12 patients with galactorrhea-amenorrhea (GA) syndrome. Luteinizing hormone-releasing hormone (LH-RH) and thyreotropin-releasing hormone (TRH) tests were performed at the same time in every case to determine the reactivity of the pituitary gland. The distinctive features of the PCO syndrome were beyond the clinical symptoms the characteristic ovarian structure verified by ultrasound examination, as well as the elevated serum LH, testosterone levels and the estradiol concentration at the normal upper limit. The basal prolactin value was higher at the GA patients than at the PCO ones. The patients with PCO syndrome demonstrated significantly greater LH and prolactin elevation to the combined LH-RH + TRH test than the patients with GA syndrome. On the basis of basal prolactin, estradiol and stimulated prolactin values it is likely, that the hyperprolactinemia in the two groups developed through different pathomechanisms. The persistent anovulation and the abnormal hormonal milieu in PCO syndrome cause the increased secretion of the pituitary lactotrophs supported by the TRH test, whereas the central dopamine decrease is the most likely explanation in the non-tumourous GA cases.
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PMID:[Relation between hyperprolactinemia and polycystic ovary syndrome]. 311 Nov 26

To evaluate the prevalence of hyperprolactinemia in patients with polycystic ovarian syndrome (PCO), 72 patients with oligo- or anovulation were studied. All of the patients had persisting elevated LH (greater than 25 mIU/ml), normal FSH, high LH/FSH ratio (greater than 2.5), and exaggerated LH responses to LHRH. Mean testosterone and androstenedione concentrations were appreciably increased in these patients. Out of 171 samples for prolactin (PRL) determination from these 72 patients, only 5 patients had a PRL value above 30 ng/ml during the first sampling. The next sampling from these same 5 women disclosed that they were transiently hyperprolactinemic because the next samples showed a normal PRL value. To further investigate the PRL secretory capacity 500 micrograms of TRH and 10 mg of metoclopramide (MCP) were administered to these 72 and 44 patients, respectively. The PRL response to MCP was significantly blunted in these patients compared to normal women while the PRL response to TRH in these patients was not indistinguishable from that in normal women. These results indicate that the true prevalence rate of hyperprolactinemia in PCO may be low rather than high and the association of hyperprolactinemia with PCO may be coincidental rather than a pathogenically related phenomenon.
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PMID:Prolactin release in polycystic ovarian syndrome. 314 87

A TRH-test was performed in 305 normoprolactinemic patients with gynecological disorders in order to appreciate the possible relationship between luteal defect, anovulation, galactorrhea and prolactin. The basal prolactin mean values of each group (normal cycle, pure luteal defect, luteal defect with persistent estrogenic influence, anovulation: with or without galactorrhea) were not different. However, some patients with luteal defect with persistent estrogenic influence and galactorrhea had an exaggerated response to TRH, and women with oligomenorrhea or amenorrhea had a low one. Unapparent hyperprolactinemia appears infrequent in normoprolactinemic patients.
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PMID:[Does prolactin have a role in the physiopathology of luteal insufficiency?]. 315 46


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