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

The therapeutic efficacy of bromocriptine in the treatment of anovulation was assessed in 19 women who failed to return to fertility following discontinuation of oral contraceptive (OC) use. Plasma concentrations of prolactin were normal. Treatment with bromocriptine restored ovulation and menstruation in 9 of the 13 amenorrheic patients and in 5 of 6 oligomenorrheic women. Given the high success rate (74%), it is concluded that bromocriptine is an effective treatment for postpill anovulation in women with normal prolactin levels.
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PMID:Bromocriptine for induction of ovulation in normoprolactinaemic post-pill anovulation. 6 7

Serum gonadotropin levels were determined in 10 patients with the amenorrhea-galactorrhea syndrome before and following acute iv administration of synthetic LH-releasing hormone (LHRH) or conjugated estrogens, in order to clarify the hypothalamic derangements in the gonadotropin secretion in patients with hyperprolactinemia. The basal prolactin (PRL) levels were elevated in all the patients, and blunted responses to 500 mug of iv synthetic thyrotropin-releasing hormone (TRH) injection were found in 9 out of the 10 patients. The basal levels of LH and FSH were subnormal in 2 and 3 patients, respectively, while those in the remaining patients were normal or slightly elevated. Normal or excessive responses of gonadotropins to 100 mug of iv LHRH were observed in most patients, 9 for LH and 10 for FSH out of 10 patients. In 10 normal cyclic women at the mid-follicular phase (D7-9) and 10 hypothalamic amenorrhea patients without galactorrhea, LH release was found 48 to 72 h after the iv injection of 20 mg conjugated estrogens (Premarin). This LH release following Premarin injection was completely abolished in the patients with amenorrhea-galactorrhea. These data seem to indicate that in patients with hyperprolactinemia, tonic secretion of gonadotropin is maintained fairly well, while of the positive feedback effect of Premarin on the release of LH is impaired. It is suggested that impaired LH release may be partly responsible for anovulation and amenorrhea in patients with hyperprolactinemia.
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PMID:Impaired LH release following exogenous estrogen administration in patients with amenorrhea-galactorrhea syndrome. 17 47

After being suspected in the presence of galactorrhoea, it is now easy to prove hyperprolactinism thanks to radioimmunoassay of prolactin. The repercussions of hyperprolactinism on gonad function are now well known, especially in women where they lead to anovulation then amenorrhoea, whereas in man there occurs hypoandrogenism with loss of libido. Hyperprolactinemia may occur in numerous circumstances and may be deduced logically from the mechanism of secretory regulation of this hormone. Among the latter, one cause dominates the others by its therapeutic consequences, I.e. the presence of an adenoma or microadenoma secreting prolactin discovered thanks to tomography of the sella turcica. The treatment of hyperprolactinism has advanced in recent years with the introduction of dopamineric drugs such as bromcriptin which permits one to normalise prolactinemia and thus restore gonad function. It's use requires however certain precautions and neurological and ophthalmic supervision when htere is a microadenoma.
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PMID:[Hyperprolactinism and antiprolactin drugs]. 19 33

Gonadal function in both sexes is under the synergistic control of the pituitary gonadotrophins, follicle stimulating hormone (FSH) and luteinising hormone (LH) which are in turn influenced both by the hypothalamus (via the gonadotrophin releasing hormone) and by feedback signals from the gonads. There is good evidence that such feedback is mediated by steroid hormones and by a product of the germinal epithelium, termed inhibin. A logical approach to reproductive disorders involves the localization of the primary disturbance either to the hypothalamo-pituitary unit or to the gonad, on the basis of history, physical findings and the results of hormone assays. In men, the majority of disorders leading to infertility are of unknown aetiology and cannot, therefore, be treated specifically. In women, anovulation is usually readily treatable and recent studies have emphasised the usefulness of prolactin assays and of specific treatment for hyperprolactinaemia in restoring ferility. Increased understanding of the mechanisms leading to infertility may provide valuable new approaches to fertility control.
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PMID:Fertility and the physician. 26 95

In order to investigate the possible stimulating effect of danazol on fertility, a randomized clinical trial was performed on 40 women with unexplained infertility. Of these 40 women, 21 received 200 mg of danazol daily for 100 days and 19 received a placebo treatment during the same period. Serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, estrone, estradiol, progesterone, and testosterone were followed before, during, and after treatment. Danazol administration induced anovulation in all women, with prompt resumption of normal ovulatory function after discontinuation of the drug. No influence was seen on serum LH, FSH, and testosterone levels, but serum estrone, estradiol, and progesterone levels decreased significantly during treatment. Serum prolactin levels also decreased, but not significantly. No pregnancies occurred in the placebo group during a 6-month follow-up period. In the danazol group, five pregnancies occurred, of which two were ectopic and three went to term. The difference in pregnancy rate between both groups was statistically significant (P less than 0.05).
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PMID:The "treatment" of unexplained infertility with danazol. 37 55

The neuroendocrine status of Long-Evans female rats was evaluated at several key stages of reproductive senescence. Young (4-8 mo), middle-aged (10-14 mo) and old (24-30 mo) animals were studied according to reproductive state. The reproductive states studied were (1) regularly cycling, (2) constant estrus and (3) pseudopregnant, as determined by vaginal smear cytology. Neuroendocrine parameters at the levels of the hypothalamus, pituitary and steroid-producing organs were compared between each group. DA3, E and NE concentrations in the median eminence of the hypothalamus were determined by a highly sensitive radioenzymatic assay. LRF content in the median eminence was measured by radioimmunoassay. Circulating levels of LH, FSH, PRL and six steroids were determined. Changes in hormone and neurotransmitter concentrations were deomonstrated in association with the various stages of reproductive senescence and with age advancement. These changes involved the hypothalamic, pitiutary and steroid systems. NE content in the median eminence, FSH in serum and circulating androstenedione were all significantly increased in middle-aged, cyclic rats prior to the onset of senescent anovulation. DA concentration in 24 mo. old constant estrous rats (30.7 +/- 7.7 pg/microgram, N = 6) and in 30 mo. old pseudopregnant rats (27.5 +/- 7.1 pg/microgram, N = 6) was significantly reduced compared to young (6 mo. old), cyclic controls on proestrous (55.0 +/- 4.7 pg/microgram, N = 12). This DA reduction was associated with a 3-fold increase in circulating prolactin. The results are discussed in terms of a regulatory cascade model of female reproductive senescence (Finch, 1976).
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PMID:Hypothalamic-pituitary-ovarian interactions during reproductive senescence in the rat. 38 Feb 82

Twice daily oral thyrotropin-releasing hormone administered to female baboons throughout the menstrual cycle had no significant influence on cycle length or upon estrogen levels but produced blunted midcycle LH peaks and luteal phase progesterone levels in three fourths of the treatment cycles. Mean plasma prolactin levels were increased approximately 2.5-fold relative to untreated, ovulatory control cycles. CB-154 alone did not alter cycle length or endocrine parameters examined (mean prolactin levels were decreased but not significantly). Cycles during which CB-154 was administered concomitantly with TRH were characterized by normal ovulation as evidenced by luteal phase progesterone levels. Since the effect on LH secretion was reversed by concomitant CB-154 administration, TRH-induced anovulation in animals given long-term treatment appeared to be mediated through physiologic mechanisms sensitive to elevated circulating prolactin levels. However, this conclusion must be considered equivocal since prolactin levels were also elevated during ovulatory cycles following long-term TRH therapy. Finally, these data do no exclude the alternative possibility that anovulation in baboons given long-term TRH treatment was a reflection of thyroid disturbance and not directly attributable to elevated prolactin.
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PMID:Effect of synthetic thyrotropin-releasing hormone on ovulation in baboons. 40 81

Prolactin exists in man as a distinct and separate anterior pituitary hormone from growth hormone. It is important in lactation and the control of gonadal function, although it may have a much wider and basic metabolic role, similar to its role in lower forms. In clinical endocrinology it is important as an index of pituitary and hypothalamic diseases; thus prolactin levels are elevated in association with these conditions and this reflects the normal tonic inhibitory hypothalamic control of prolactin by PIF; DA is the most important PIF. Hyperprolactinaemia causes hypogonadism in both men and women; it may present in women with amenorrhoea, oligomenorrhoea, polymenorrhoea, regular cycles with anovulation or a defective luteal phase, and impotence in men. In either sex galactorrhoea is reported to occur in only 30 per cent of patients. Neurotransmitter therapy, with dopamine agonists which act as functional analogues of PIF, restores prolactin levels to normal and leads to a return of normal gonadal function. The mechanism of the hypogonadism is not clear and is discussed together with the problems associated with inducing pregnancy in these patients, who may harbour microadenomata of the pituitary.
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PMID:Prolactin. 40 65

The correlation between hyperprolactinaemia induced by the administration of neuroleptic drugs, disturbances of the vaginal cycle and mammary gland stimulation in rats was investigated as a test model simulating the clinical syndrome of hyperprolactinaemia and amenorrhoea with anovulation. In acute experiments in which clozapine, sulpiride and chlorpromazine were administered orally to rats of both sexes, there were rapid increases in the level of prolactin in the serum with peak values between 15 and 60 min. The responses of female rats to various doses of sulpiride were consistently higher than those of male rats. Hyperprolactinaemia induced by sulpiride in dioestrous rats failed to desensitize the ovaries to the ovulatory effect of exogenous luteinizing hormone releasing hormone. Studies of these substances and of metoclopramide, haloperidol and thioridazine were then carried out in females rats by daily oral administration over a period of 13 days. The increases in the level of prolactin in the serum were paralleled by disruption of the vaginal cycle up to and including constant dioestrus and by mammary gland stimulation which, like the preceding phenomena, showed dose-dependence. The potencies of these six neuroleptics, as estimated from their effects on the mammary gland, appeared to be haloperidol greater than sulpiride greater than or equal to metoclopramide = thioridazine greater than chlorpromazine greater than clozapine.
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PMID:Correlation between the effects of neuroleptics on prolactin release, mammary stimulation and the vaginal cycle in rats. 56 36

A case of hyperprolactinemic anovulation with amenorrhea and galactorrhea, due to Phenothizine derivative (Majeptil) is presented. Treatment with bromocriptine, 2.5 mg b.i.d., p.o., or L-Dopa, 500 mg, p.o., did not suppress serum prolactin and menstrual cycle was not resumed. Pituitary prolactin response to TRH and Pituitary LH and FSH response to LHRH were found to be normal. It seems that at the dose used, bromocriptine (a dopaminergic agonist) cannot counteract the phenothiazine induced hyperprolactinemia. Hence, it is not effective in induction of ovulation while the patient is under phenothiazine treatment.
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PMID:Failure of bromocriptine to suppress prolactin in majeptil-induced hyperprolactinemia. 57 42


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