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)

Two patients are described who were suffering from primary hypothyroidism and who developed a pituitary microadenoma and macroadenoma with suprasellar extension, respectively, diagnosed by CT scan of the pituitary. Both patients originally presented with amenorrhea and galactorrhea. In addition to low serum T4 and T3 levels and an elevated TSH level, they also had hyperprolactinemia. The TRH test performed in one of the patients showed an exaggerated response of both TSH and PRL to TRH. Correction of hypothyroidism by prolonged (months) treatment with levothyroxine resulted in normalization of thyroid function tests as well as hyperprolactinemia and in regression of the pituitary tumor. It was concluded that primary hypothyroidism was the cause of the pituitary adenoma and the amenorrhea/galactorrhea syndrome. It is recommended that routine thyroid function tests be obtained for patients with hyperprolactinemia. Demonstrable primary hypothyroidism should be corrected for prolonged periods of time by levothyroxine therapy, and CT scanning of the pituitary should be repeated before any other treatment such as bromocriptine or surgery is attempted.
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PMID:Regression of a pituitary adenoma following levothyroxine therapy of primary hypothyroidism. 641 99

To investigate the role of catecholamines in the control of gonadotropin and prolactin release, we examined the effects of a catecholamine synthesis inhibitor (alpha-methyl-p-tyrosine, AMPT) administration and those of dopamine (DA) or epinephrine (EPI) infusion after endogenous catecholamine synthesis inhibition, on FSH, LH and PRL serum levels, in regularly cycling women and in patients with hyperprolactinemic amenorrhea. AMPT administration was followed by a prompt increase in serum PRL in regularly cycling women, but not in women with hyperprolactinemia either due to a PRL-secreting pituitary microadenoma or 'idiopathic'. Gonadotropin serum levels did not show any significant variation after AMPT in both normal and hyperprolactinemic women. DA infusion after endogenous catecholamine synthesis inhibition by AMPT, induced an appreciable decline in PRL levels in both normal and hyperprolactinemic subjects. Although the net decrements were higher in the hyperprolactinemic group, the PRL fall was similar in the two groups when expressed as a percentage of preinfusion PRL concentrations. LH serum levels similarly fell during DA infusion in normal women and in hyperprolactinemic patients, while FSH concentrations did not show any significant change. EPI infusion after analogous AMPT pretreatment was followed by an evident decrease in serum PRL in both normal and hyperprolactinemic subjects. No significant changes in FSH and LH serum concentrations were observed during EPI administration. These data, while confirming the existence of a functional derangement in the neural inhibitory control of PRL secretion in hyperprolactinemia either due to a PRL-secreting pituitary microadenoma or so-called 'idiopathic', do not agree with the hypothesis that tubero-infundibular DA hyperactivity inhibits gonadotropin secretion in hyperprolactinemic patients. The inhibitory action of exogenously administered DA might represent rather a pharmacological effect than express a physiological inhibitory role of hypothalamic DA pathway on gonadotropin secretion in humans.
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PMID:Catecholamines and pituitary function. I. Effects of catecholamine synthesis inhibition and subsequent catecholamine infusion on gonadotropin and prolactin serum levels in normal cycling women and in women with hyperprolactinemic amenorrhea. 642 87

10 examine the relationship between obesity and chronic anovulation, we compared basal serum LH, FSH, and PRL levels, determined at 20-min intervals, and basal C21 [progesterone, 17- hydroxyprogesterone , pregnenolone, 17-hydroxypregnenolone ( 17Pe ), and cortisol], C19 [testosterone (T), delta 4-androstenedione (A), and dehydroepiandrosterone] and C18 (estrone and estradiol) steroid hormone concentrations measured at 1- to 2-h intervals for a 24-h period in five normal weight cycling women (NC) and in two groups of weight-matched obese women. Five of the obese women were regularly cycling (OC), and six were amenorrheic (OA). Sex hormone-binding globulin (SHBG) and non-SHBG-bound T and estradiol concentrations were also measured in each woman. Compared to NC women, OC women had normal basal protein and steroid hormone concentrations, except for reduced 17Pe levels (P less than 0.05). Mean SHBG concentrations were reduced by approximately 30%, and non-SHBG-bound T was increased by 70%, although the differences were not significant. In addition, when six precursors of testosterone (pregnenolone, 17Pe , dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and A) were considered together as a group and the data analyzed by the kappa 2 test, a reduction in basal levels of these precursors was found in OC women relative to those in NC women (P less than 0.005). In OA women, mean concentrations of SHBG were markedly reduced and those of total T, A, estrone, and non-SHBG-bound T were significantly increased compared to those in both NC and OC women. Mean 24-h concentrations of LH tended to be greatest and FSH lowest in this group, but were not significantly different from those in the other groups. The mean LH pulse frequency was significantly greater in OA than in OC women (P less than 0.05). Mean 24-h PRL and cortisol levels were also reduced in OA women relative to those in NC women. These data suggest the possibility of a compensatory decline in total T production in OC women in an attempt to maintain normal hormonal homeostasis; as a consequence, ovulation continues in a cyclic fashion. In OA women, such compensatory mechanisms are no longer operative. Instead, a central and/or peripheral defect, resulting in overproduction of androgen, may also exist and lead to anovulation in OA women. In conclusion, our data imply that obesity is not a primary factor causing chronic anovulation. However, obesity may aggravate an already existing subtle defect in some women and result in amenorrhea.
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PMID:Endocrine comparison of obese menstruating and amenorrheic women. 642 58

Urinary excretion of estrogens and plasma concentrations of estrone, estradiol, LH, FSH, PRL, progesterone, testosterone, and sex hormone binding globulin were measured in nine chronic alcoholic women with cirrhosis or alcoholic fatty liver. They were aged 24-40 yr and all had secondary amenorrhea which had lasted for at least 3 months. The response of pituitary gonadotropin secretion to administration of LHRH and estradiol benzoate and of PRL secretion to TRH were also investigated. Urinary excretion of estrogens in the alcoholic women with liver disease was similar to that in normal postmenopausal women and less than half that in normal women of the same age in the midfollicular phase of the menstrual cycle. Plasma estradiol levels in the alcoholic women were lower than in the menstruating women but higher than in the postmenopausal women, whereas their plasma estrone levels were higher than in the menstruating women. Plasma concentrations of progesterone and testosterone in the alcoholic women did not differ from those in the postmenopausal women but were lower than in the menstruating women. In spite of the relative estrogen deficiency plasma LH and FSH levels were not elevated in the alcoholic women. The responses of LH and FSH to LHRH were similar in the patients and in the menstruating women. Intramuscular administration of estradiol benzoate did not increase plasma LH and FSH concentrations in the alcoholic women. Hyperprolactinemia was not found and there were no differences in the PRL responses to TRH between the patients and the control groups. In conclusion, disturbed regulation of gonadotropin secretion is an important factor in the genesis of estrogen deficiency and amenorrhea in alcoholic women with liver disease, although ovarian function may also be directly impaired.
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PMID:Sex hormones in amenorrheic women with alcoholic liver disease. 642 68

Pulsatile gonadotropin secretion was examined in seven women with hyperprolactinemia and amenorrhea by obtaining blood samples every 20 min for 24 h. When plasma PRL had returned to normal and menses had resumed during bromocriptine treatment, five women were restudied in an identical manner during the early to midfollicular stage of their cycles. Gonadotropin responses to a small dose of synthetic GnRH (25 ng/kg, iv) were measured after the initial 24-h study in each patient. In addition, low dose pulses of GnRH (25 ng/kg) were administered iv every 2 h for 88 h to three hyperprolactinemic women, and LH and FSH responses were determined. Before treatment with bromocriptine, mean +/- SE plasma gonadotropin concentrations (LH, 5.8 +/- 0.2 mIU/ml; FSH, 4.4 +/- 0.1 mIU/ml) were comparable to values during the follicular phase of normal menstrual cycles. LH pulse frequency during the pretreatment study in the hyperprolactinemic women (mean +/- SE, 7.6 +/- 1.2 pulses/24 h) was significantly less than that found during the early follicular stage of normal cycles (days 3-5; mean, 15.4 +/- 1.1 pulses/24 h). Mean +/- SE LH pulse amplitude before bromocriptine was 5.2 +/- 0.6 mIU/ml. The pattern of pulsatile LH secretion was highly variable before treatment and was characterized by prolonged periods (6-11 h) of low plasma LH concentrations. LH responses to GnRH were normal or increased (mean maximum increment in LH, 38.5 +/- 15.9; range, 4.3-125.2 mIU/ml), and no evidence of intermittent pituitary refractoriness was found during prolonged (88-h) administration of GnRH pulses. Treatment with bromocriptine was associated with the resumption of menses, and no significant change in mean gonadotropin concentrations. LH pulse frequency was increased (mean +/- SE = 10.2 +/- 1.0 pulses/24 h) and LH pulse amplitude was decreased (mean, 3.9 +/- 0.2 mIU/ml) in four of five patients receiving bromocriptine. Moreover, the pattern of pulsatile LH secretion was more uniform during treatment. We conclude that pituitary responsiveness to GnRH is not impaired in women with hyperprolactinemia and amenorrhea, and that periods of low LH secretion in these women are due to intermittent reductions in GnRH secretion. These observations suggest that the abnormal patterns of pulsatile gonadotropin secretion, and by inference GnRH secretion, are important factors in the etiology of amenorrhea associated with hyperprolactinemia.
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PMID:Abnormal patterns of pulsatile luteinizing hormone secretion in women with hyperprolactinemia and amenorrhea: responses to bromocriptine. 643 88

The role of stress in exercise-associated amenorrhea was investigated. Sex hormones [FSH, LH, androstenedione (A), testosterone, estrone, and 17 beta-estradiol (E2)], stress hormones [dehydroepiandrosterone, cortisol (F), PRL, norepinephrine, and epinephrine] and psychological status (Profile of Mood States and State-Trait Anxiety Inventory) were measured at rest and in response to a 40-min 80% of maximal aerobic power (VO2max) run in highly trained eumenorrheic (n = 8) and amenorrheic (n = 7) women runners matched for fatness [eumenorrheic, 16.5 +/- 2.3% (+/- SD); amenorrheic, 14.9 +/- 4.8] and maximal aerobic power (eumenorrheic, 58.9 +/- 5.7 ml/kg X min; amenorrheic, 59.8 +/- 4.6). Eumenorrheic runners were tested between days 3 and 8 of the follicular phase. At rest, decreased plasma FSH, LH, and E2 concentrations were found in amenorrheic women [eumenorrheic FSH, 10.5 +/- 4.1 mIU/ml; amenorrheic FSH, 4.9 +/- 1.6 (P less than 0.01); eumenorrheic LH, 14.1 +/- 6.1 mIU/ml; amenorrheic LH, 5.1 +/- 1.7 (P less than 0.01); eumenorrheic E2, 20 +/- 9 pg/ml; amenorrheic E2, 7 +/- 6 (P less than 0.05)]. Other sex and stress hormones and psychological measurements were similar in the two groups and were within the normal range. Ventilatory, cardiovascular, thermoregulatory, and psychological responses to the submaximal run were identical. Among eumenorrheic women, all stress hormones and A increased after exercise, but PRL, F, and A were unchanged among amenorrheic women. Estrone, E2, and testosterone did not change in either group. These observations are inconsistent with a general stress hypothesis of exercise-associated amenorrhea as well as with more specific hyperprolactinemic and hyperandrogenic hypotheses. In amenorrheic women, failure of PRL to increase in response to exercise may be due to their lack of E2, while failure of F and A to increase may indicate reduced adrenal 3 beta-hydroxysteroid dehydrogenase/isomerase activity.
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PMID:Exercise-induced stress responses of amenorrheic and eumenorrheic runners. 643 86

The clinical characteristics of women with galactorrhea and amenorrhea induced by drugs were studied. In addition, hyperprolactinemia was, experimentally, induced by sulpiride in women, and their endocrinological backgrounds were studied. The findings suggested that the mechanism of amenorrhea due to hyperprolactinemia was primarily the reduction of steroidogenesis in the ovary, and also the disturbance of positive feedback to the hypothalamus. Hyperprolactinemia was induced in rats by sulpiride, and the effect on pituitary lactotrophs was studied. In the hyperprolactinemic state caused by PIF inhibition by sulpiride it was indicated that there was a limit to prolactin secretion and release by the pituitary gland. It was also confirmed that a large amount of estradiol exerted a stimulating action directly on the PRL-producing cells of the pituitary gland.
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PMID:[A clinical study on the characteristics of galactorrhea-amenorrhea (especially of drug-induced galactorrhea-amenorrhea]. 643 54

A 43-yr-old woman, who had previously had a subtotal thyroidectomy, presented with hyperthyroidism and amenorrhea-galactorrhea due to a pituitary adenoma secreting TSH, TSH-alpha, and PRL. Her serum T4 concentration was 14 micrograms/dl; T3, 5.7 ng/ml, and TSH, 19-33 microU/ml. Serum TSH was not altered by TRH stimulation or T3 suppression. Basal plasma PRL levels were 19-27 ng/ml and plasma PRL doubled after TRH stimulation. A 900-mg pituitary tumor, removed by transphenoidal surgery, was studied in cell culture. After dispersion, tumor cells were maintained on an extracellular matrix produced by bovine corneal endothelial cells in a defined serum-free medium. The hormones released in the culture medium were analyzed by high pressure gel chromatography. Three fractions of tumor TSH were found, with respective apparent mol wts of 45,000 (11%), 28,000 (70%), and 20,000 (19%). Tumoral PRL eluted as a single peak of apparent mol wt of 24,000. Pharmacological studies of TSH, TSH-alpha, and PRL release using thyroid hormones (T3), dopamine agonist (bromocriptine), TRH, and cholera toxin yielded the following results: 1) T3 after 3 days of incubation produced a dose-dependent inhibition of TSH, TSH-alpha, and PRL release. Maximal inhibition (81%) was obtained at 10(-9) M and half-maximal inhibition at 4-6 X 10(-11) M. 2) Bromocriptine produced rapid and partial inhibition of hormone release. Maximal inhibition (51%) was obtained at 10(-8) M and half-maximal inhibition at 5 X 10(-10) M. 3) TRH at 10(-8) M concentration significantly stimulated PRL release but it had no effect on TSH release. 4) Adenylate cyclase activation by 10(-11) M cholera toxin increased TSH (152%), TSH-alpha (150%), and PRL (220%). Immunohistochemical analysis of serial 2 micron sections of the tumor showed that: 1) TSH-alpha immunoreactive cells were the most numerous, 2) TSH-beta positive cells were always positive for TSH-alpha, 3) PRL immunoreactivity was found either uniquely in some cells and colocalized with TSH-alpha immunoreactivity in other cells. However, by electron microscopy, the tumor cells were thyrotrophs. These data indicate that in this patient's tumor: 1) cells secreting TSH were responsive in vitro to near physiological concentrations of thyroid hormones. 2) The colocalization of PRL and TSH-alpha immunoreactivities in some cells raises the possibility either of fusion of differentiated pituitary cells synthesizing distinct hormones or of transformation of less differentiated multipotential pituitary cells.
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PMID:A human pituitary adenoma secreting thyrotropin and prolactin: immunohistochemical, biochemical, and cell culture studies. 648 Aug 9

To determine whether a significant energy drain during adolescence had a significant effect on puberty and normal reproductive function, 15 ballet dancers, aged 13--15 yr, who maintained a high level of physical activity from early adolescence were followed for 4.0 yr. Menarche was remarkably delayed in this group, occurring at a mean of 15.4 yr, significantly different (P < 0.01) from normal controls (12.5 yr) and normal music students (12.6 yr). In 2 dancers aged 18 yr, primary amenorrhea has persisted. While premenarchial, all of the dancers had varying breast development (Tanner stages 2--4) and low to low normal gonadotropin levels, normal PRL and T4 levels, and normal skull x-rays. The dancers' mean body weight and calculated body fat were significantly less than in controls (P < 0.05). The progression of sexual development and the onset of menarche correlated in 10 or 15 subjects with a decrease in exercise and/or injury causing forced rest of at least 2-month duration. During this interval, weight gain was minimal or absent, with no significant change in body composition. A significant dichotomy in the order of pubertal development was also noted; while breast development and menarche were delayed, pubic hair development was not affected. Reversion to the amenorrheic state occurred in 11 of 13 patients with a return to exercise without a change in weight. In conclusion, energy drain may have an important modulatory effect on the hypothalamic pituitary set point at puberty and, in combination with low body weight, may prolong the prepubertal state and induce amenorrhea.
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PMID:The effects of exercise on pubertal progression and reproductive function in girls. 677

TRH, metoclopramide (MCP), chlorpromazine (CPZ), and insulin (ITT) stimulation tests of PRL secretion were carried out in age-matched controls and before and after successful removal of pituitary prolactinomas in women with the galactorrhea-amenorrhea syndrome. In preoperative patients there was a blunted or absent PRL response to TRH in 87%, to MCP in 100%, to CPZ in 100%, and to ITT in 93%. Two to 6 months after successful tumor removal, serum PRL rose 2-fold (the usual criterion for a normal response) in 73% after TRH, in 100% after MCP, but in only 13% after CPZ and in only 14% on ITT. However, the PRL increment with all four tests was significantly lower than that in normal controls. One to 8 yr after successful surgery, the PRL increments after TRH and MCP were returning to normal, but the PRL responses to CPZ and ITT remained blunted. GH, ACTH, and TSH reserves were intact in all patients. The diminished PRL response to all stimulation tests observed up to 6 months postoperatively might be explained by the persistence of a negative feedback effect from high PRL levels associated with the tumor. The more persistent impairment of the PRL response to CPZ and ITT is unexplained but suggests a hypothalamic defect.
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PMID:Persistent defect in regulation of prolactin secretion after successful pituitary tumor removal in women with the galactorrhea-amenorrhea syndrome. 677 3


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