Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

2-n-Butyl-3-(4'-diethylaminoethoxy-3',5'-diiodobenzoyl)-benzofurane (amiodarone), a drug used in arrythmias and angina pectoris, contains 75 mg of organic iodine/200 mg active substance. Four studies were performed to test its effect on thyroid hormone metabolism: (a) nine male subjects were treated with 400 mg of amiodarone for 28 days; (b) five male subjects received, for the same period of time, 150 mg of iodine in the form of Lugol's solution; (c) five subjects received 300 mug L-thyroxine (T4) for 16 days; from the 10th to the 16th day, 400 mg of amiodarone was added; and (d) five euthyroid subjects received 300 mug L-T4 for 16 days. The changes in serum thyroid-stimulating hormone (TSH), serum total T4, 3,5,3'-triiodothyronine (T3), free T3, and 3,5',3'-triiodothyronine (reverse T3, rT3) were measured, and the pituitary reserve in TSH was evaluated by a thyrotropin-releasing hormone (TRH) test. The results show that amiodarone induced a decrease in serum T3 (28+/-5.1 ng/100 ml, mean+/-SEM, P less than 0.0S and 82.7+/-9.3 ng rT3/100 ml, P less than 0.01). The control study with an equal amount of inorganic iodine did not induce these opposite changes but slightly lowered serum rT3, T3, and T4. In the third study, serum rT3 increased as under amiodarone treatment, thereby proving that these changes were peripheral. It is suggested that amiodarone changes thyroid hormone metabolism, possibly by reducing deiodination of T4 to T3 and inducing a preferential production of rT3. Amiodarone also increased the response of TSH to TRH. The maximal increment of serum TSH above base line was 32+/-4.5 muU/ml under treatment and 20+/-3 muU/ml before treatment (P less than 0.01). During this test, the serum T3 increase was more pronounced than during the control period (83+/-13 and 47+/-7.4 ng/100 ml, P less than 0.05).
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PMID:Effect of amiodarone on serum triiodothyronine, reverse triiodothyronine, thyroxin, and thyrotropin. A drug influencing peripheral metabolism of thyroid hormones. 78 94

Levels of thyrotropin-releasing hormone (TRH) were quantitated in human lumbar spinal fluid (CSF) utilizing a sensitive and specific TRH radioimmunoassay. Endogenous TRH was sufficiently stable in CSF to permit 85% recovery of intact TRH after 48 h storage at 4 C. TRH levels in AM or PM samples obtained from 15 women and 12 men were easily detected in all CSF specimens. No significant difference between the TRH concentration in CSF of men and women was observed (44.2+/-6.8 and 38.1+/-6.5 pg/ml (mean+/-SE) respectively). TRH concentrations were 40.2+/-6.9 pg/ml (mean+/-SEM) in AM and 41.4+/-8.0 pg/ml in PM samples. By contrast, CSF cortisol levels obtained concurrently were twofold higher in AM than PM (0.68+/-0.08 vs 0.38+/-0.02 mug/100 ml (mean+/-SEM) respectively, P less than 0.001). These data are consistent with the possibility that a portion of the TRH in CSF can be derived from the central nervous system (CNS) and unrelated to the hypo-physiotropic control of thyrotropin (TSH) synthesis and secretion.
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PMID:Thyrotropin-releasing hormone (TRH): Measurements in human spinal fluid. 80 91

Plasma human prolactin levels were measured by homologous radioimmunoassay in patients with primary breast cancer and in normal women of similar age. In normal controls mean (+/- SEM) basal plasma prolactin levels were 11.9 +/- 1.5 ng/ml and intravenous injection of synthetic thyrotropin-releasing hormone (TRH), 500 mug, caused a significant rise in plasma prolactin in all subjects examined with a maximum response of 52.6 +/- 3.3 ng/ml (mean +/- SEM). Markedly high plasma prolactin levels and exaggerated plasma prolactin responses to TRH were demonstrated in some patients with breast cancer. However, mean basal plasma prolactin levels and mean plasma prolactin increments following TRH in patients with breast cancer did not differ significantly from those in normal subjects. Plasma prolactin responses to TRH were slightly blunted during the administration of androgen in patients with breast cancer. These results suggest that some of the patients with primary breast cancer have abnormal prolactin secretion.
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PMID:Plasma prolactin responses to thyrotropin-releasing hormone in patients with breast cancer. 81 51

The pathophysiological role of the central dopaminergic mechanism in human essential hypertension (EHT) is still unknown, so we investigated a possible relationship between the central dopaminergic activity and salt sensitivity to blood pressure in patients with EHT. We divided 22 inpatients with EHT into salt-sensitive (SS, n = 11) and non-salt-sensitive (NSS, n = 11) groups according to an 8% increase of mean blood pressure (MBP) when dietary salt intake was increased from 2 g/day to 20 g/day for two periods of 7 days each. The change of central dopaminergic activity by salt load was evaluated as the percentage change of plasma prolactin (PRL) response to a small dose (25 micrograms) of thyrotropin-releasing hormone (TRH) administered intravenously. The mean percentage change of PRL response by salt load in the SS group was -9.4 +/- 8.5% (mean +/- SEM), which was remarkably lower than the 26.8 +/- 5.5% in the NSS group (P less than .01). There was a significant negative correlation between the percentage change of PRL response and that of MBP by salt load (r = -0.456, P less than .05). These results suggest that a lack of activation of the central dopaminergic system by salt load may contribute in part to a rise in blood pressure in SS patients with EHT.
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PMID:Salt sensitivity and central dopaminergic activity in patients with essential hypertension. 168 22

We randomly administered thyrotropin-releasing hormone (200 micrograms, as an i.v. bolus) or control saline (in isovolumic amount) to 30 male diabetic subjects (23 IDDM, 7 NIDDM) in fair metabolic control (HbA1 9.7 +/- 0.3%, means +/- SEM) and to 12 healthy male controls on two different mornings. While GH in the basal state was similar in IDDM, NIDDM and normal subjects, TRH administration evoked a significant GH release only in a single IDDM individual. The only GH-responder to TRH was a newly-diagnosed (two weeks) IDDM patient, still with a high glycated hemoglobin level (HbA1 11.1%), despite normal plasma glucose levels. Saline infusion did not affect GH concentrations either in normals or in diabetics. Exaggerated GH responses to TRH are uncommon in diabetic patients in good metabolic conditions.
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PMID:Inappropriate growth-hormone (GH) response to thyrotropin-releasing hormone (TRH) occurs infrequently in well-regulated diabetes mellitus. 211 57

The aim of this study was to test the hypothesis that low serum T3 concentrations may promote an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in patients with anorexia nervosa. Eight anorexic women and two anorexic men, ages 15-25 years, with low free T3 circulating levels (mean +/- SEM = 2.8 +/- 0.3 pmol/l) were studied. A TRH test (200 micrograms IV) was carried out under basal conditions and repeated following treatment with oral T3 (1.5 micrograms/kg BW/day) for eight days. Following T3 administration, GH levels dropped significantly from a baseline of 7.1 +/- 1.3 micrograms/l to 3.1 +/- 0.7 micrograms/l (p less than 0.02), as did GH peak responses to TRH (9.0 +/- 1.0 micrograms/l vs 4.4 +/- 0.8 micrograms/l, p less than 0.01). ANOVA and analysis of area under the curve (AUC) confirmed that after T3 treatment there was a significant reduction in TRH-induced GH release in these patients (GH AUC: 902 +/- 132 micrograms/l vs. 456 +/- 91 micrograms/l, p less than 0.02). TSH responses to TRH, which were normal prior to T3 treatment, completely disappeared following it, and PRL responses to TRH also were diminished. Although our experimental approach does not permit a conclusion that low T3 levels were the primary reason for these changes, the data support the theory that low T3 circulating levels may facilitate abnormal GH secretion and the GH-releasing activity of intravenous TRH.
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PMID:Triiodothyronine administration reduces serum growth hormone levels and growth hormone responses to thyrotropin-releasing hormone in patients with anorexia nervosa. 212 17

The mechanisms whereby growth hormone (GH) secretion is decreased in human obesity remain obscure. We studied the response of plasma GH and prolactin (PRL) to an I.V. dose of 0.5 mcg/kg of growth hormone releasing factor (GRF) in three groups of children: lean (N = 12), obese (N = 15) and GRF-deficient, i.e. children with complete GH deficiency on the basis of conventional provocative testing and evidence of hypothalamic dysfunction on the basis of thyrotropin-releasing hormone testing (N = 7). Mean (+/- SEM) peak plasma GH after GRF was blunted to the same extent in obese and in GRF deficient children (11.1 +/- 2.2 and 8.3 +/- 2.8 ng/ml) as compared to lean control children (34.7 +/- 4.7 ng/ml). The pattern of PRL response to GRF was however different in GRF deficient children, whose high basal PRL levels increased further after GRF injection, and in obese and lean children, who had n alpha acute change in PRL levels after GRF. Baseline plasma somatomedin C concentrations were low for age in GRF deficient children and tended to be high for age in obese children. On the basis of these discrepant patterns of response of PRL to GRF and plasma somatomedin C concentrations, we conclude that GRF deficiency does not account for the decreased GH secretion observed in obese children.
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PMID:Evidence against growth hormone-releasing factor deficiency in children with idiopathic obesity. 309 43

Although prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) have been described by many investigators, PRL secretion after insulin stimulation has rarely been documented in patients with anorexia nervosa (AN). We investigated PRL responses to TRH (500 micrograms) and insulin (0.1 U/kg) in 19 women with AN and 10 normal women. Levels of PRL stimulation at 60 min and later following insulin administration were significantly lower in AN than in normal women. PRL increased by at least 10 micrograms/ml after insulin in 42% of women with AN and in 70% of normal women. The maximum PRL increase (max delta PRL) did not differ after the two stimulations in the normal women. However, in AN, the max delta PRL after insulin stimulation (17.2 +/- 4.0 micrograms/l, mean +/- SEM) was significantly lower than that after TRH (49.1 +/- 6.4 micrograms/l). These findings suggest that anorectic women may have a disturbance in hypothalamic functions. Insulin-induced hypoglycemia is useful to determine the integrity of the hypothalamic-pituitary axis for PRL secretion, in combination with TRH stimulation.
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PMID:Prolactin responses to hypoglycemia and thyrotropin-releasing hormone in anorexia nervosa. 314 79

Studies in vitro and in vivo have shown that thyrotropin-releasing hormone (TRH)-induced calcium ion changes in the adenohypophysial cells play an important role in release of hormones by the anterior pituitary. To determine the effect of the calcium blocker nifedipine on TRH-induced thyroid-stimulating hormone (TSH) and prolactin (PRL) release, TRH stimulation tests were performed before and after 74 hours of nifedipine therapy in ten patients. Although the magnitude of the TSH and PRL mean peak increase above baseline was slightly lower during calcium blocker administration (TSH 14.1 +/- 4.8 SEM v 16.4 +/- 4.5 SEM; PRL 37.7 +/- 4.5 SEM v 41.7 +/- 5.4 SEM), this was not statistically significant. Use of nifedipine in clinically effective doses does not appear to significantly interfere with TRH-stimulated release of TSH or PRL, in vivo.
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PMID:Effect of nifedipine on TRH stimulation of TSH and PRL release by the pituitary gland. 391 37

Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. Ten patients (group 1) had retinopathy corresponding to stage III-V (Scott's classification), and the remaining seven patients (group 2) had no retinopathy despite longer duration of diabetes in comparison with the patients in group 1. There were no differences in age, percent of ideal body weight, and serum HbA1 levels between the two groups. Basal serum GH levels were 1.9 +/- 0.4 ng/ml (mean +/- SEM) in group 1, and not different from the values in group 2 (1.6 +/- 0.7 ng/ml). However, GH responses to synthetic human GRH-44 (1 micrograms/kg body wt, i.v. bolus) were significantly greater in group 1, as judged by the maximal response or integrated GH secretion after the administration of GRH. There were no differences in serum insulin-like growth factor I (IGF-I) levels between group 1 (262 +/- 35 ng/ml) and group 2 (232 +/- 30 ng/ml), and no significant correlation was found between serum IGF-I levels and GH responses to GRH in either of the two groups. Paradoxical GH responses to TRH (500 micrograms, i.v. bolus) were found in only one patient in each group. We have thus demonstrated that GH responses to GRH are more pronounced in diabetic patients with retinopathy than in patients without this complication, although it remains to be determined whether or not greater GH responses to GRH are causally related to the development of diabetic retinopathy.
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PMID:Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. 392 95


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