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)

We tested the hypothesis that the neuroendocrine control of gonadotropin secretion is altered in certain women distance runners with secondary amenorrhea. To this end, we quantitated the frequency and amplitude of spontaneous pulsatile LH secretion during a 24-h interval in nine such women. The ability of the pituitary gland to release LH normally was assessed by administration of graded bolus doses of GnRH during the subsequent 8 h. Compared to normally menstruating women, six of nine amenorrheic distance runners had a distinct reduction in spontaneous LH pulse frequency, with one, three, six, five, four, or two pulses per 24 h (normal, 8-15 pulses/24 h). This reduction in LH pulse frequency occurred without any significant alterations in plasma concentrations of estradiol and free testosterone or 24-h integrated serum concentrations of LH, FSH, or PRL. Moreover, in long-distance runners, the capacity of the pituitary gland to release LH was normal or accentuated in response to exogenous pulses of GnRH. In the six women athletes with diminished spontaneous LH pulsatility, acute ovarian responsiveness also was normal, since serum estradiol concentrations increased normally in response to the GnRH-induced LH pulses. Although long-distance runners had significantly lower estimated percent body fat compared to control women, specific changes in pulsatile gonadotropin release did not correlate with degree of body leanness. In summary, certain long-distance runners with secondary amenorrhea or severe oligomenorrhea have unambiguously decreased spontaneous LH pulse frequency with intact pituitary responsiveness to GnRH. This neuroendocrine disturbance may be relevant to exercise-associated amenorrhea, since pulsatile LH release is a prerequisite for cyclic ovarian function. We speculate that such alterations in pulsatile LH release in exercising women reflect an adaptive response of the hypothalamic pulse generator controlling the intermittent GnRH signal to the pituitary gland. The basis for amenorrhea in the remaining runners who have normal pulsatile properties of LH release is not known.
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PMID:Altered neuroendocrine regulation of gonadotropin secretion in women distance runners. 392 10

Idiopathic hyperprolactinemia (IH) can be defined as the presence of elevated serum PRL levels in a patient in the absence of demonstrable pituitary or central nervous system disease and of any other recognized cause of increased PRL secretion. This study examined the long term clinical outcome of 41 patients (mean age, 26 yr) with IH followed for up to 11 yr (mean, 5.5 yr). Initial and final PRL levels were determined by RIA in the same laboratory. A correction factor was used to obviate periodic changes in the potency of the NIH standards used in the PRL assay, so that all results are expressed in terms of the original VLS no. 1 standard. The initial serum PRL levels ranged from 27.2-243 ng/ml, with a mean of 57 ng/ml. Only three patients had initial serum PRL levels greater than 100 ng/ml. All had a normal skull x-ray and/or brain computed tomographic scan during their initial visit. All 41 patients had galactorrhea and/or amenorrhea. Serum PRL levels remained the same, decreased, or returned to normal in 34 of 41 patients. The mean PRL level at the time of reevaluation was 35 ng/ml. Thirty-four percent of the patients had a normal serum PRL level. Only 17% of the patients had serum PRL levels that were significantly higher (greater than 50% of their original value). Six of 9 patients with an initial serum PRL level less than 40 ng/ml had normal levels. One patient developed a pituitary tumor (initial PRL, 150 ng/ml). All patients reevaluated with brain computed tomographic scans had normal pituitary size. No patient reported a worsening of signs or symptoms, and in many, improvement (n = 16) or complete resolution (n = 8) of the amenorrhea and/or galactorrhea occurred. Twenty-seven spontaneous or bromocriptine-induced normal pregnancies and deliveries occurred without development of a pituitary tumor. Therefore, our data clearly challenge the use of ablative pituitary therapy for IH and raises questions of the benefit of chronic medical therapy for this condition.
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PMID:The natural history of idiopathic hyperprolactinemia. 398 Jun 70

18 patients with "primary empty sella" were reviewed for this study. In 3 of them the sellar enlargement was discovered occasionally by performing skull radiographs for other reasons. The galattorrhea-dismenorrhea or amenorrhea syndrome and obesity were the most common clinical features. Endocrinological tests were normal in ten patients and abnormal in eight. Slight elevation of serum PRL was the most common record. 12 patients had enlarging of the sella turcica; in 4, only the floor was asymmetric and in 2 the sella was quite normal. In 5 patients C.T. without intra-thecal contrast was sufficient to discover the E.S. In 13 patients we performed C.T. cysternography by injecting in the lumbar subarachnoid space 8-10 ml of Iopamidolo 200. This is an excellent and safe technique to perform C.T. cysternography.
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PMID:[Primary empty sella. Clinico-radiologic considerations in 18 cases]. 403 90

In two of eight premenopausal women with somatotropic adenomas, galactorrhea was the earliest clinical feature, associated in one patient with amenorrhea. These two patients did not have clinically evident acromegaly. Mean basal serum GH levels were elevated and did not decrease after glucose ingestion. Both patients had modest hyperprolactinemia. Histological and immunocytological studies of the adenomas showed numerous adenomatous somatotropic cells and some alpha-subunit- and PRL-containing cells. In these patients, the origin of the hyperprolactinemia was not clear. In one patient, elevated GH secretion was probably responsible for the galactorrhea, since it disappeared after surgical treatment despite persistence of hyperprolactinemia. In conclusion, galactorrhea, isolated or associated with amenorrhea, can be the only clinical manifestation of a somatotropic adenoma.
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PMID:Somatotropic adenoma manifested by galactorrhea without acromegaly. 404 May 30

Three patients with hyperprolactinemia and large extrasellar pituitary macroadenomas were treated with bromocriptine, 10 mg daily, for 8 weeks. In spite of correction of their amenorrhea, galactorrhea, and hyperprolactinemia, radiologic evaluation by CT scan failed to show evidence of tumor shrinkage. After surgical resection, histologic examination revealed that PRL-secreting cells comprised only a small portion of the tumor cell population in two patients and in the third patient were completely absent. These cases illustrate that large nonfunctional pituitary tumors may mimic signs and symptoms of a prolactinoma and stress the importance of adequate radiologic evaluation during medical management.
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PMID:Lack of tumor reduction in hyperprolactinemic women with extrasellar macroadenomas treated with bromocriptine. 405 27

The aim of this study was to evaluate the role of endogenous opiates in the mechanism of decreased LH secretion in women with anorexia nervosa. For this purpose the effect of opiate receptor blockade with naloxone on LH, FSH, PRL, and beta-endorphins secretion was studied in 24 women with anorexia nervosa and 7 normal women. Serum LH, FSH, PRL, beta-endorphin-like substance, ACTH, and cortisol concentrations were measured before and after opiate receptor blockade after a single iv dose of 0.2 mg/kg naloxone or saline. Mean serum LH and FSH concentrations increased significantly after naloxone in the normal women. Eleven patients had a significant increase in serum LH concentrations in response to naloxone and 13 did not respond to naloxone with an increase in LH concentration. In the first group the basal LH values were higher than those in the second group. In the majority of patients in the first group amenorrhea preceded the wt loss, whereas in most patients in the second group amenorrhea appeared during the phase of wt loss. Naloxone did not alter pulsatile LH secretion in 6 women. No effect of naloxone on serum FSH and PRL concentrations was found. A significant increase in beta-endorphin-like substance levels after naloxone administration occurred in patients with anorexia nervosa. However, serum ACTH and cortisol concentrations were not altered in response to naloxone. In conclusion, the increase in LH release after opiate receptor blockade by naloxone suggests that endogenous opiates may play a role in the mechanism of inhibited LH secretion at least, in the majority of those women with anorexia nervosa in whom amenorrhea preceded wt loss. The results also point to a different mechanism of ACTH and beta-endorphin secretion in patients with anorexia nervosa.
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PMID:The role of endogenous opiates in the mechanism of inhibited luteinizing hormone (LH) secretion in women with anorexia nervosa: the effect of naloxone on LH, follicle-stimulating hormone, prolactin, and beta-endorphin secretion. 608 96

Combined therapy with thyroid hormone (desiccated thyroid) and bromocriptine (CB-154) was applied in a 29-year-old patient with amenorrhea-galactorrhea due to primary hypothyroidism. Two months after commencing administration of desiccated thyroid, the elevated serum level of TSH returned to the normal range while that of PRL remained within the supranormal range (from 134 ng/ml to 86.7 ng/ml). However, it fell to the normal range 2 weeks after administration of CB-154 with thyroid hormone. Subsequently, the galactorrhea completely ceased and ovulatory menstruation resumed with 3 months, and conception was achieved directly after that menstrual period. Only desiccated thyroid was administered during pregnancy and the patient delivered a male infant weighing 2,800 g without difficulty.
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PMID:Pregnancy following combined therapy with thyroid hormone and bromocriptine in a patient with amenorrhea-galactorrhea due to primary hypothyroidism. 612 25

A virilization syndrome in a normally menstruated 20--year-old woman, due to adrenocortical tumor, is reported. Preoperative basal hormonal study showed normal plasma gonadotropins, androstenedione (A) and cortisol, slightly elevated testosterone (T), markedly increased urinary 17 ketosteroids (17KS) excretion and plasma dehydroepiandrosterone-sulfate (DHEA-S) levels. Thus DHEA-S was the major constituent of the androgen excess. Urinary 17KS and plasma DHEA-S did not change after ACTH, whereas increased after dexamethasone (DXM)-hCG administration. PRL and LH responses to TRH and LHRH tests were exaggerated. Echotomography, pneumoperitoneum radiography and selective adrenal venous angiography showed a tumor in the left adrenal gland. After the tumor removal all abnormalities were corrected. Light and electron microscopy showed well differentiation of the tumoral cells with typical ultrastructural characteristics of androgen-secreting tissue. It is concluded that the absence of amenorrhea and of LH suppression does not exclude the possibility of an androgen-secreting tumor. Moreover, the unusual finding of slightly elevated T value may be reported to enzymatic defect at the neoplastic cellular level. Furthermore the paradoxical DXM-hCG androgen response may be due to spontaneous variations in hormone secretion by the tumor or to cell receptors alteration.
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PMID:Virilization syndrome in a young woman due to an androgen-secreting adenoma. 623 9

Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. Nine normal menstruating diabetic women, 12 normal women in the early follicular phase, and nine consecutive nondiabetic women with functional amenorrhea served as controls. No significant differences were found in relation to diabetes regulation within the two diabetic groups. Amenorrheic patients with diabetes mellitus had significantly lower basal PRL levels than normal women and estradiol levels compared to the other groups. Basal plasma LH concentrations were significantly lower in women with amenorrhea and diabetes mellitus than in nondiabetics with amenorrhea, whereas plasma FSH levels were similar in all groups. The LH response to GnRH was significantly lower in amenorrheic patients with diabetes mellitus than in normal women, and a significant correlation (r = 0.81, P less than 0.01) was found between the LH response to GnRH and the basal estradiol level in these women. The FSH response to GnRH and the PRL response to TRH were similar in all groups. Amenorrheic diabetics had significantly lower PRL responses to MTC compared to other groups, and nondiabetics with amenorrhea had significantly lower PRL response than normal women. It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. These hormonal changes may in part be caused by a raised central dopaminergic activity leading to a depression of pituitary ovulatory mechanisms.
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PMID:Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus. 640 66

To determine whether decreased bone density in patients with PRL-secreting pituitary tumors is specifically related to hyperprolactinemia or is a consequence of disordered pituitary-gonadal function common to all amenorrheic states, we measured the bone mineral content of the radius by photon absorptiometry in normal subjects, in women with amenorrhea and normal serum PRL levels, and in women with PRL-secreting pituitary tumors. The women did not differ significantly in mean age, height, weight, or serum calcium, phosphorous, gonadotropin, testosterone, vitamin D, or PTH concentrations, and all had normal renal and thyroid function. The bone mineral content in women with amenorrhea and normal serum PRL levels (0.91 +/- 0.02 g/cm) was not significantly different from that in control subjects (0.88 +/- 0.01 g/cm). Patients with PRL-secreting tumors studied 2-5 yr after transsphenoidal surgery had significantly diminished bone mineral content whether they were cured (0.82 +/- 0.02 g/cm) or had persistent amenorrhea and hyperprolactinemia (0.81 +/- 0.02 g/cm). Serum estradiol concentrations did not differ significantly in the four groups, and there was no correlation between estradiol concentration and bone mineral content or between PRL concentration and bone mineral content in the amenorrheic women. The presence of decreased bone mineral content in hyperprolactinemic patients suggests that PRL may have a direct effect on bone and may be another indication for early treatment of PRL-secreting pituitary tumors.
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PMID:Bone density in amenorrheic women with and without hyperprolactinemia. 640 18


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