Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002453 (amenorrhea)
 6,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen women complaining of infertility (one with primary amenorrhoea, 14 with secondary amenorrhoea, and two with oligomenorrhoea) all had hyperprolactinaemia and were treated with clomiphene citrate and human chorionic gonadotrophin (HCG), and plasma oestradiol, FSH and LH levels were measured. Although adequate pre-ovulatory oestradiol levels were present, the surge of LH was absent until the injection of HCG after which all patients ovulated. There were 12 pregnancies in 9 patients resulting in 10 full-term livebirths, one premature livebirth and one continuing pregnancy. The relevance of these findings to the possible role of prolactin in amenorrhoea is discussed.
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PMID:Induction of ovulation with clomiphene and human chorionic gonadotrophin in women with hyperprolactinaemic amenorrhoea. 69 52

In adolescent girls, secondary amenorrhea can result from a variety of physiologic and psychologic disturbances. Previous reports associating amenorrhea and primary hypothyroidism have not distinguished between the alternative etiologic roles of thyroxine deficiency and hyperprolactinemia. We have evaluated two girls with secondary amenorrhea who had clinical and chemical evidence of hypothyroidism. Both had low basal T4 values (0.8 and 3.2 microgram/dl), calculated free T4 (0.1 and 0.7 ng/dl), and T3 (51 and 81 ng/dl). Both had undetectable basal TSH with normal TSH response to TRH. Basal FSH and LH values were normal, as was the response to LHRH. Basal prolactin levels were 6 and 14 ng/ml, respectively, and both girls had growth hormone responses of greater than or equal to 15 ng/ml in response to insulin-induced hypoglycemia. Pituitary-adrenal function and reserve were also normal. In neither patient was there any historical, physical, or laboratory features compatible with anorexia nervosa. After treatment with 1-thyroxine, both girls had a resumption in menses. These two adolescent girls thus appear to have isolated hypothalamic hypothyroidism. The associated secondary amenorrhea demonstrates that thyroid deficiency alone, without hyperprolactinemia, can interfere with normal hypothalamic-pituitary-ovarian function.
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PMID:Adolescent secondary amenorrhea: association with hypothalamic hypothyroidism. 76 30

The functional status of the hypothalamo-pituitary-gonadal axis was investigated in 127 women with anovulatory disease. Radioimmunoassayable circulating LH, FSH, and prolactin concentrations were measured. An attempt was made to localize the functional lesion by utilizing the following criteria: 1. Hypothalamic function: a) clomiphene test based upon hormonal parameters; b) recording of the pulsatile LH fluctuation (spiking) and of basal FSH. 2. Pituitary function: determination of the gonadotropin reserve by means of a standardized LRH test. 3. Ovarian function: a) measurement of plasma E2 and progesterone levels by RIA; b) gestagen bleeding test. All patients had amenorrhea of up to 14 years duration. A total of 17 hyperprolactinemic patients (13.4%) was found. Eight of these patients never experienced galatorrhea, in 7 only transient galactorrhea was reported, and in 2 cases galactorrhea persisted. All hyperprolactinemic patients were found to be clomiphene non-responders as well as nonspikers. The pituitary LH reserve varied from practically none to normal. Baseline LH was low whereas that of FSH was normal. In accordance with this observation E2 levels, with two exceptions, were found to be in the lower range of normal female concentrations. Thus, all but two patients exhibited gestagen withdrawal bleeding. In conclusion, the hyperprolactinemic anvoluatory syndrome is not necessarily associated with galactorrhea. In all cases of amenorrhea syndromes with or without galactorrhea, hyperprolactinemia should be excluded as it is very often associated with anovulation. The hyperprolactinemic anovulatory syndrome includes the following features: 1. gestagen withdrawal bleeding. 2. subnormal to normal E2 levels. 3. clomiphene nonresponsiveness. 4. LH-hypogonadotropism. 5. lack of LH secretory episodes. 6. FSH-normogonadotropism.
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PMID:Hyperprolactinemic anovulatory syndrome. 76 52

The results of the ultra low doses of synthetic LH-RH, 1.56, 3.125 and 6.25 mug, are presented in 8 normal women during the first week of the menstrual cycle and 14 patients with secondary amenorrhoea. Seven of these patients had "stress" amenorrhoea, and 7 had preceeding oligomenorrhoea. There was no significant difference between the mean basal gonadotrophin levels in the normal volunteers and those patients with secondary amenorrhoea. There was no significant difference in basal gonadotrophin levels or the response to LH-RH, between the two groups of amenorrhoea, stress and previous oligomenorrhoea. Basal FSH and oestradiol levels do not appear to influence the response to LH-RH. However, those patients with secondary amenorrhoea and a low basal LH (5 patients) had a significantly higher response to LH-RH at 1.56 and 3.125 mug than the amenorrhoeic patients with normal basal LH levels. Two patients with stress amenorrhoea and weight loss had an exaggerated response to LH-RH. The significance of this is discussed.
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PMID:Changes in pituitary and ovarian hormones following injection of ultra low dose LH-RH in normal and amenorrhoeic women. 76 51

An analysis of the gonadotrophin response to an intravenous injection of LH-RH (50 mug) has been undertaken in 41 patients with secondary amenorrhoea. Thirty-five of the patients were free of any recognizable pathology to account for their amenorrhoea and apparently had a dysfunction of the hypothalamic-pituitary axis. In these patients, the gonadotrophin response to LH-RH was highly variable. There was in general a correlation between baseline plasma LH or FSH levels and their respective increments. There was no correlation, however, between basal oestrogen levels and gonadotrophin increments except in the case of those patients whose basal levels of plasma FSH were higher than those of LH and in those patients whose body weight was less than the ideal for the population. It appears that the gonadotrophin response to a single injection of LH-RH in the majority of patients with secondary amenorrhoea of unknown origin is too variable to be of use either as a diagnostic or prognostic tool.
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PMID:An evaluation of the luteinizing hormone releasing hormone (LH-RH) test in patients with secondary amenorrhoea. 77 18

A case of diabetes insipidus is presented which appeared in a 13 year old girl associated with hormone-resistant amenorrhea; she went through two normal pregnancies and partutition at 22 and 25, indicating a fertile amenorrhea. During a total of 17 years of observation the amenorrhea persisted, with the exception of a few normal menstruation periods at the beginning of the disease. She remained permanently under treatment with pitressin tannate. Repeated administrations of estrogens, gestagens and chorionic gonadotrophin, had no effect. An endometrial biopsy revealed a presecretory phase. Acidophilic index in vaginal smears as well as serial determinations of urinary pregnanodiol indicated cyclic changes. Daily determinations of urinary pregnanodiol indicated cyclic changes. Daily determinations of plasma gonadotrophins during 28 days revealed normal levels, with normal FSH pulse and ovulatory type peak of LH. An LH-RH test gave marked and characteristic increase of both hormones. The data indicate the integrity of the hypothalamo-hypophyso-ovaric system, with cyclic changes and formation of corpus luteum, vaginal trophism and endometrial changes, concordant with the two normal pregnancies. In this case, the amenorrhea can only be explained by alteration of the usual endometrial vascular changes. The coexistence of diabetes insipidus and fertile amenorrhea is discused in relation with the possible participation of vasopressin in the mechanism of menstruation.
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PMID:[Fertile amenorrhea associated to diabetes insipidus]. 77 72

Normal women in the early follicular phase and in the luteal phase of the cycle, and patients with secondary amenorrhea received on consecutive days a rapid intravenous injection (50 mug) and a two or four-hour infusion (25 mug/h) of synthetic LH-FSH/RH. The responses of LH and FSH were evaluated by the measured plasma concentrations, as well as by the calculated pituitary secretion rates and by the amounts of hormone released. To estimate these pituitary secretion rates of LH and FSH, a simplified mathematical model is proposed. During an infusion of LH-FSH/RH the secretion rates of both LH and FSH increased in the three groups of women in a biphasic way with a dip after 1 to 2h of infusion, suggesting that besides the pool mobilized by a rapid intravenous injection of LH-FSH/RH there is a second pool of (stored) gonadotropins. For LH the increase above baseline concentrations was higher in group II (luteal phase) than in group I (follicular phase) or in group III (amenorrhea) and this both after a bolus injection and during infusion of LH-FSH/RH. For FSH a similar pattern of response prevailed during an infusion of LH-FSH/RH. After a bolus administration, however, the FSH release was relatively higher in group III (amenorrhea) than in both groups of normal women in which the increases were about the same. The latter finding suggests that the first pool of FSH is released by a different mechanism than the second pool.
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PMID:Secretion rates of LH and FSH during infusion of LH-FSH/RH in normal women and in patients with secondary amenorrhea: suggestive evidence for two pools of LH and FSH. 78 Mar 63

A study of the secretion of prolactin and plasma gonadotrophins was carried out comparatively in 3 groups of patients: histologically confirmed prolactin adenoma (group 1), idiopathic or iatrogenic amenorrhoea/galactorrhoea syndrome (group 2), empty sella turcica syndrome (group 3). The last group differs fundamentally from the two previous by the presence of a normal basal LH and FSH levels and normal LH-RH stimulation. Prolactin is not increased. It may be suppressed by L-dopa and stimulated by TRH. There exist no differences, apart from neuroradiological criteria, between the other two groups. The level of LH is slightly decreased but the response to LRH is positive, this effect often being more clear on FSH. Prolactin levels are raised, this no doubt explaining the negative response to TRH and chlorpromazine stimulation. Suppression by L-dopa is positiive, reflecting the absence of autonomy of prolactin adenomata. The water load test is unsatisfactory. There exists at the present time no method sufficiently discriminating to exclude the presence of a tumour at the origin of an amenorrhoea-galactorrhoea syndrome.
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PMID:[ Study of prolactin and blood gonadotropins in amenorrheas-galactorrhea. Dynamic exploation in 13 cases]. 80 17

The pituitary release of gonadotropins, prolactin, and TSH after the simultaneous intravenous administration of 50 mug LH-RH was 400 mug TRH was evaluated in 7 amenorrheic women with sellar enlargement and hyperprolactinemia. It was found that only minimal amounts of LH and FSH were released by LH-RH. All patients had elevated serum prolactin levels but TRH administration elicited negligible release of prolactin. This was in contrast to the normal TSH response to TRH in most of these women. It is concluded that intrasellar masses may be associated with hyperprolactinemia which does not necessarily cause galactorrhea and that impaired gonadotropin reserve correlates with the presence of amenorrhea.
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PMID:Pituitary hormonal reserve in patients presenting hyperprolactinemia, intrasellar masses, and amenorrhea without galactorrhea. 80 93

The clinical, radiological and endocrine findings in thirty-five women with hyperprolactinaemia and amenorrhoea are described. Twelve patients had radiological evidence of a pituitary tumour and six were tested after pituitary ablation. Seventeen patients with hyperprolactinaemia and normal pituitary X-rays were also studied. None was on any drug known to increase prolactin secretion and all patients were euthyroid when tested. Basal serum prolactin concentrations were high in the group with untreated pituitary tumours and in those with normal X-rays. The levels were variable in the post-ablation cases. The increase of prolactin after TRH was subnormal in all of the groups. Serum oestradiol concentrations were low in most patients and nineteen of twenty-one patients tested had no withdrawal bleeding after treatment with a progestogen. Mean serum gonadotrophin concentrations (basal and after LHRH) were normal in twenty-nine patients but subnormal in four post-ablative cases. Anovulatory responses to clomiphene were obtained in nineteen of twenty patients tested. Fifteen patients were treated with bromocriptine; twelve ovulated and eight became pregnant; two not responding had impaired LH and FSH production. Hyperprolactinaemic amenorrhoea is a common disorder with characteristic endocrine features. Galactorrhoea is unusual (30%). Treatment with bromocriptine lowers prolactin concentrations and rapidly repairs the reproductive defect.
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PMID:Clinical and endocrine features of hyperprolactinaemic amenorrhoea. 82 29


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