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)

In order to determine the role of thyroid hormone in prolactin (PRL) secretion in patients with amenorrhea-galactorrhae, PRL response to 500 mug of iv thyrotropin-releasing hormone (TRH) was studied before and after the administration of triiodothyronine (T3) in 10 patients with amenorrhea-galactorrhea. Seven of these patients were euthyroid and the other 3 had hypothyroidism. The patients in the euthyroid group received 50 mug of T3 daily for 7 days and 75 mug q.d. for the ensuing 14 days. The hypothyroid patients received T3 at progressively increasing doses from 10 mug q.d. to 75 mug q.d. during 34 to 68 days. In the initial test, the elevated basal levels of PRL, 61.9 +/- 9.8 ng/ml (Mean +/- SE) exhibited a slight but insignificant net increase (7.7 +/- 2.1 ng/ml) after TRH injection in the euthyroid group. However, a marked response to TRH with a net increase of 147.2 +/- 26.3 ng/ml from the basal level of 47.3 +/- 11.2 ng/ml was observed in the hypothyroid patients. After treatment with T3, both the basal level (56.9 +/- 8.3 ng/ml) and the net increase (9.9 +/- 3.6 ng/ml) of PRL following TRH stimulation remained virtually unchanged in the euthyroid group. The hypothyroid group, in contrast, displayed a significant depression of both the basal level (26.1 +/- 13.0 ng/ml) and the net increase (33.8 +/- 6.5 ng/ml) of PRL to TRH stimulation. The diminution of the basal levels and responses of thyroid-stimulating hormone (TSH) to TRH stimulation was observed in all cases of both groups. These results suggest that the level of thyroid hormone has little pathogenic role in PRL secretion in euthyroid patients with amenorrhea-galactorrhea, in contrast to its marked effect in hypothyroid patients with amenorrhea-galactorrhea.
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PMID:Effect of triiodothyronine treatment on prolactin secretion in patients with amenorrhea-galactorrhea. 40 25

Four women, aged 17 to 23, were evaluated for secondary amenorrhea of 12 to 36 months' duration. All were considered to have hypothalamic hypothyroidism on the basis of low thyroxine (T4) concentrations, inappropriately low thyrotropin (TSH) levels, with a normal TSH response to thyrotropin-releasing hormone (TRH, 500 microgram intravenously) in three, and absence of a pituitary lesion. Nevertheless, menses did not resume after adequate replacement with thyroid hormone. Investigation of the pituitary-gonadal axis revealed a normal increase in both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) following the intravenous administration of gonadotropin-releasing hormone (GnRH). Three subjects received clomiphene citrate, 100 mg/day for five days, but a normal menstrual cycle was not induced. It is concluded that the amenorrhea was not due to thyroid hormone deficiency but, like the hypothyroidism, to a hypothalamic abnormality involving secretion of the appropriate releasing hormone.
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PMID:Hypothyroidism and amenorrhea due to hypothalamic insufficiency. A study in four young women. 40 87

A 22-year-old woman with recurrent goiter, hyperthyroidism, galactorrhea, and amenorrhea due to a pituitary tumor is described. She had been treated surgically twice for recurrent goiter with tracheal compression. Despite clinical signs of hyperthyroidism and slightly elevated plasma thyroid hormone levels (T4: 11 mug/dl; T3: 189 ng/dl), without thyroid hormone replacement therapy the basal TSH level was elevated up to 23 muU/ml and could not be suppressed by exogenous thyroid hormones: even when the serum thyroid hormone levels were raised into the thyrotoxic range (T4: 16.2 mug/dl T3: 392 ng/dl), the basal TSH fluctuated between 12 and 29 muU/ml. The basal PRL level was elevated up to 6000 muU/ml. The administration of TRH (200 mug iv) led only to small increments of TSH and PRL levels. Bromocriptin (5 mg p.o.) or l-dopa (0.5 g p.o.) suppressed TSH and PRL values significantly. After transsphenoidal hypophysectomy, TSH and PRL were below normal and the patient development panhypopituitarism. The adenoma showed two cell types which could be identified as lactotrophs and thyrotrophs by electronmicroscopy and immunofluorescence. From these data we conclude that the patient had a pituitary tumor with an overproduction of thyrotropin and prolactin.
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PMID:Recurrent goiter, hyperthyroidism, galactorrhea and amenorrhea due to a thyrotropin and prolactin-producing pituitary tumor. 98 24

Drugs that are known to affect breast morphology or breast secretion may be classified into 2 major groups: 1) drugs having a central action on the pituitary or hypothalamus and 2) steroids and several other compounds that act peripherally. Drugs in the 1st group affect lactation through stimulation or suppression of the lactogenic pituitary hormone prolactin. Their action may be directly on the pituitary or indirectly on the hypothalamus where the secretion of hypothalamic prolactin-inhibiting factor is affected. Drugs in the 2nd group act peripherally by exerting their action mainly at the level of breast tubules and acini. The most frequently used are estrogens which stimulate growth of the breast and suppress lactation, and suppress breast cancer in some women. Centrally acting drugs which cause galactorrhea also cause an increase in prolactin secretion, but the presence of estrogen-primed breast tissue is needed. A list of such drugs (including rauwolfia and phenothiazine derivatives, and opiates) is given. The most common mechanism of action by which psychotropic drugs increase prolactin secretion is by interfering with formation or release of dopamine from hypothalamus neurons and its subsequent action via an alpha-adrenergic receptor on hypothalamic cells that secrete prolactin-inhibiting factor. Reserpine and other rauwolfia drugs deplete hypothalamic neurons of catecholamines and prevent their reuptake by nerve endings. Phenothiazines interfere with the action of catecholamines at the alpha-adrenergic receptor sites. Prolonged use of drugs that stimulate pituitary activity may lead to formation of microadenomas of the pituitary. Continuation of galactorrhea for more than 2 weeks after stopping therapy suggest this result. L-dopa suppresses abnormal lactation by reduction in serum prolactin levels. Br-ergocryptine, an ergot derivative, has galactorrhea-blocking and prolactin-suppressing activity but is devoid of alpha-adrenergic activity. Barbiturates and pyridoxine may cause decrease in milk flow of nursing mothers. Peripherally acting drugs consist of estrogen, progesterone, and androgen as well as hypoglycemic-producing agents, thyroid hormone, corticosteroids, and spironolactone. Estrogen is the only steroid effective in suppression of puerperal lactation. There are several steroids effective in causing remission of breast cancer. The presence of an intact pituitary is apparently necessary if estrogens are to be effective in breast cancer. Corticosteroids may be effective in patients insenstive to sex hormones. Cytotoxic agents may be more effective when used in combination with corticosteroids. Galactorrhea occurring in a nulliparous woman taking oral contraceptives is always abnormal and suggests the possibility of a pitutitary tumor. Women with postpill galactorrhea-amenorrhea may also have such tumors. All cases of galactorrhea when sex hormones have been used should be studied for pituitary tumor.
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PMID:Drugs that affect the breast and lactation. 109 75

A case of postpartum amenorrhea and galactorrhea is reported, with several additional features leading to the diagnosis of primary hypothyroidism. Resolution of the amenorrhea and galactorrhea was noted coincident with adequate thyroid hormone therapy. The interrelationships of the many organ systems involved are discussed, and speculations advanced regarding the mechanisms operating in such cases. The diagnosis of the limited thyroid-reserve syndrome is elucidated.
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PMID:Postpartum galactorrhea-amenorrhea syndrome due to the limited thyroid reserve syndrome. 114 50

We have previously demonstrated that thyroid hormone synergizes with follicle-stimulating hormone (FSH) to exert stimulatory effects on granulosa cell differentiation and function, suggesting that it plays a physiological role in amplifying FSH-mediated differentiation of granulosa cells. The adequate differentiation of these cells, followed by normal follicle development, is indispensable for ovulation and subsequent corpus luteum formation. Thus, in the present studies, the clinical implications of thyroid hormone in the induction of ovulation and corpus luteum function were investigated. Serum levels of total 3,5,3'-triiodothyronine (T3) and total thyroxine (T4) as well as free T3 and T4 were significantly lower in patients with weight loss amenorrhea compared to normal cycling women. Although no ovulation was induced by clomiphene therapy when the serum T3 levels were less than 80 ng/dl, the rate of ovulation induced by clomiphene increased in parallel with the augmentation of serum T3 levels. This suggests that an adequate circulating level of thyroid hormone is one of the factors responsible for successful induction of ovulation by clomiphene citrate. Furthermore, the short luteal phase and insufficient progesterone secretion observed in patients with subclinical hypothyroxinemia were not improved by clomiphene therapy alone, but were improved markedly by combined treatment with thyroid hormone replacement and clomiphene citrate. These data imply that concomitant clomiphene treatment with thyroid hormone replacement therapy is of a great value not only for ovulation induction, but also for the treatment of luteal-phase defect in patients with subclinical hypothyroxinemia.
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PMID:A role for thyroid hormone in the induction of ovulation and corpus luteum function. 142 22

We report a girl with juvenile primary hypothyroidism revealed by growth retardation and a syndrome of primary amenorrhea-galactorrhea with hyperprolactinemia and suprasellar pituitary enlargement. Resolution of the pituitary enlargement and the amenorrhea-galactorrhea syndrome occurred after thyroid hormone replacement. No similar observation has been reported earlier in juvenile hypothyroidism.
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PMID:Primary amenorrhea-galactorrhea with hyperprolactinemia and huge pituitary enlargement in juvenile primary hypothyroidism. 145 96

Bone density of lumbar vertebrae (L2 to L4) and the whole body in 29 patients with anorexia nervosa were measured by dual photon absorptiometry, and the results were compared with those of 10 age-matched normal controls. The patients had significantly lower bone mineral density (BMD) in L3 and L2-4 than controls. However, there was no difference in whole-body BMD. L3 and L2-4 BMD was positively correlated with body weight and was negatively correlated with duration of illness and amenorrhea. Patients who had been more active 6 months before the time of the study had significantly higher L3 BMD than the less active patients. Most patients had an abnormally low serum estrogen level, whereas the mean serum levels of thyroid hormone (T3, T4), cortisol, calcitonin, parathyroid hormone and vitamin D were within the normal range. No correlation was found between L3 or L2-4 BMD and the levels of these hormones. These results suggest that severe weight loss, low physical activity, longer duration of amenorrhea and deficiency of estrogen contribute to bone loss in patients with anorexia nervosa, whereas calcium-regulating hormones such as parathyroid hormone, calcitonin and vitamin D are unlikely to be a primary contributor to bone loss.
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PMID:Reduced bone density and major hormones regulating calcium metabolism in anorexia nervosa. 148 25

The impact of chronic high volume athletic training on thyroid hormone economy has not been defined. We investigated the status of the hypothalamic-pituitary-thyroid axis (H-P-T) in women athletes with regular menstrual cycles (CA) and with amenorrhea (AA). Their data were compared with each other and with those derived from cyclic sedentary women (CS) matched for a variety of confounding factors including the intensity of exercise, caloric intake, and body weight. Alterations of the H-P-T axis were observed in women athletes compared to CS. While serum levels of T4, T3, free T4, free T3 and rT3 were substantially reduced (P less than 0.01) in AA, only serum T4 levels were significantly decreased in CA. Further, remarkable differences were found between CA and AA in that serum levels of free T4 (P less than 0.01), free T3 (P less than 0.01), and rT3 (P less than 0.05) were significantly lower in AA than in CA. Thyroid binding globulin and sex-hormone binding globulin concentrations were within their normal ranges for all groups of subjects. Both 24-h mean TSH levels and the circadian rhythm of TSH secretion were also comparable. However, the TSH response to TRH stimulation was blunted (P less than 0.01) in AA when compared to CA, but not to CS. Whereas the underlying mechanism(s) to account for the "global" reduction of circulating thyroid hormone in the face of normal TSH levels in AA is presently unknown, these observations provide information of clinical significance: 1) chronic high volume athletic training in women athletes with menstrual cyclicity is accompanied by an isolated T4 reduction; 2) an impaired H-P-T axis occurs selectively in athletic women in whom chronic high volume athletic training is associated with compromised hypothalamic-pituitary-ovarian function and amenorrhea.
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PMID:Hypothalamic-pituitary-thyroidal function in eumenorrheic and amenorrheic athletes. 163 53

A 37-year old housewife was admitted to our department because of long-standing amenorrhoea and galactorrhoea. After several hormonal examinations, she was proved to be suffered from primary hypothyroidism with hyperprolactinemia. In addition, brain computed tomography (CT) showed the finding of enhanced pituitary enlargement, suggesting pituitary hypertrophy or pituitary adenoma. Based on some therapeutic experiences in similar cases in several reports, we have performed only thyroid hormone replacement and followed up the patient. Plasma thyroid stimulating hormone (TSH) and prolactin concentrations returned to normal range in a few months after starting thyroid hormone replacement. Furthermore, the finding of pituitary enlargement has completely disappeared on brain CT and come to pregnancy during the course. Thus, it seems that the finding of pituitary enlargement might be due to pituitary hypertrophy. Therefore, we think that thyroid hormone replacement should be a first choice therapy preceding the pituitary surgery or bromocriptine therapy in such a case.
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PMID:[A case report of idiopathic myxedema with secondary amenorrhoea and hyperprolactinemia: effect of thyroid hormone replacement on reduction of pituitary enlargement and restoration of fertility]. 193 45


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