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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of serum triiodothyronine (T(3)) and thyroxine (T(4)) concentrations on the release of prolactin in man was studied by determining the prolactin response to synthetic thyrotropin-releasing hormone (TRH) in hypothyroid and hyperthyroid patients before and after correction of their serum thyroid hormone abnormalities. The maximum increment in serum prolactin above the basal level (maximum Delta prolactin) was used as the index of response to TRH. In 12 patients with primary hypothyroidism, the maximum Delta prolactin in response to TRH fell from 100.5+/-29.1 ng/ml (mean +/-SEM) before treatment to 36.1+/-6.0 ng/ml (P < 0.01) during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily. The mean serum T(3) level increased from 57+/-8 to 138+/-10 ng/100 ml, and the mean serum T(4) level increased from 3.0+/-0.4 to 7.2+/-0.4 mug/100 ml during this treatment. In eight normal subjects the maximum Deltaprolactin in response to TRH was not significantly different during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily from the response before treatment. In 10 patients with hyperthyroidism, the maximum Deltaprolactin in response to TRH increased from 14.2+/-2.9 ng/ml before treatment to 46.9+/-6.7 ng/ml (P < 0.001) during antithyroid treatment. The mean serum T(3) level fell from 313+/-47 to 90+/-8 ng/100 ml, and the mean serum T(4) level fell from 20.8+/-2.5 to 6.8+/-0.6 mug/100 ml during this treatment. These results show that changes from normal serum levels of T(3) and T(4) are associated with changes in prolactin responses to TRH; subnormal serum levels of T(3) and T(4) increase TRH-induced prolactin release, whereas substantially higher than normal serum levels of T(3) and T(4) inhibit this release.
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PMID:Thyroid hormone inhibition of the prolactin response to thyrotropin-releasing hormone. 419 18

We have treated 68 thyrotoxic patients with Graves' disease with a single daily dose of 30 mg methimazole until they were clinically euthyroid and their plasma thyroid hormone concentrations were within normal limits. Sixteen of 56 patients (29%) treated 4.8 +/- 0.2 months (mean +/- SEM; range, 1.5-8.5 for their initial attack of thyrotoxicosis have remained in remission for 54.4 +/- 7.7 months (range, 12-105). Twenty-seven of the patients who relapsed were treated with a subsequent 1-yr course of methimazole. Five of these patients (19%) have maintained a remission for 29.6 +/- 10.8 months (range, 3-66); the remainder relapsed after 7.1 +/- 2.3 months (range, 1-50). If the patients lost to follow-up while known to still be in remission are excluded, the sustained remission rate is 12 of 52 (23%) for initial short term therapy and 3 of 25 (12%) for the subsequent 1-yr of antithyroid treatment. The results of short term antithyroid drug treatment in 12 patients previously treated with long term antithyroid drugs or thyroidectomy were similar, but the follow-up period was not as long. Short term antithyroid drug therapy is a potentially long lasting, innocuous, and relatively inexpensive program for the treatment of Graves' disease, especially for patients with small goiters.
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PMID:Follow-up comparison of short-term versus 1-year antithyroid drug therapy for the thyrotoxicosis of Graves' disease. 618 55

Plasma cAMP was determined using the method of Tovey et al. in normal pregnant women with a mean concentration of 18.9 +/- 0.8 pmol/ml (x- +/- SEM). Between weeks 9-12 and 33-36 of gestation, there were two peaks, with a mean cAMP of 22.5 +/- 2.4 which were significantly increased in comparison to the other weeks of pregnancy. Significantly decreased values were found in patients with threatened abortion (weeks 12-28) which terminated in abortion (11.6 +/- 2.4; p < 0.01). In premature labor no differences were found. During therapy with fenoterol there were highly significantly increased plasma cAMP levels (48.2 +/- 2.8; p < 0.0005). During thyroid hormone therapy in euthyroid goiter, cAMP was significantly decreased (14.0 +/- 1.4; p < 0.05). 1 week after cessation of therapy a highly significant increase of cAMP was observed (38.2 +/- 6.9; p < 0.0005). There was a negative linear regression between T3 and cAMP (2p < 0.01). In pregnancy with hypertension cAMP was significantly elevated (30.5 +/- 3.8 p < 0.0005), but nearly normal under antihypertensive therapy. In pregnancy with edema only, no difference was found. Induction of labor with PGE2 alpha was followed by a decrease of plasma cAMP.
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PMID:Plasma cAMP in normal and abnormal human pregnancy. 625 65

Thyroid hormones have been implicated in the prenatal lung development of several species. To investigate the possibility that thyroid hormones could play a role in human lung development, we examined nuclei from fetal human lung for the presence of high affinity T3-binding sites. A single class of high affinity (Kd = 35 +/- 3 pM) binding sites for L-T3 was identified in nuclei from fetuses between 12-19 weeks of gestation. The T3-binding capacity increased 65% between 12-13 weeks (binding capacity, 0.227 and 0.282 fmol/micrograms DNA in two experiments) and 16-19 weeks of gestation [binding capacity, 0.420 +/- 0.014 (SEM) fmol/micrograms DNA; n = 8]. Maximal binding was achieved after 4 h of incubation at 20 C. The half-times for dissociation of the T3-receptor complex were 36 h, 10.5 h, 3 h, and 23 min at 2, 20, 25, and 37 C, respectively. The relative order of potency of thyroid hormone analogs in displacing L-T3 from the receptor was: T3-proprionate greater than 3.3'-5-triiodothyroacetic acid greater than L-T3 greater than D-T3 greater than L-T4 greater than 3,5-diethyl-3'-isopropyl-D,L-thyronine greater rT3 greater than 3,5-dimethyl-3'-isopropyl-L-thyronine. Some receptors were released from the nuclei into the supernatant during incubation (7.8 +/- 0.3% after 4 h at 20 C). This release increased with incubation time and temperature, but was independent of T3 concentration, Ca2+, and gestational age. Incubation at 37 C also inactivated some of the receptors, but T3 provided dose-dependent protection from this loss of binding activity. Our results are consistent with the proposal that nuclear receptors mediate a direct effect of thyroid hormones on developing human lung as early as the second trimester of gestation.
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PMID:Identification and characterization of nuclear 3,5,3'-triiodothyronine-binding sites in fetal human lung. 626 37

Lymphocyte Na-K ATPase was evaluated as an index of thyroid status in man. Lymphocytes from 24 untreated hypothyroid patients and 11 hyperthyroid subjects were sampled in parallel with normal lymphocytes, and Na-K ATPase activity was assessed by measurements of ouabain binding to a plasma membrane fraction or to whole cells. In both systems, ouabain bound saturably and specifically, resulting in linear Scatchard plots. Normal lymphocyte plasma membranes bound 2.30 +/- 0.16 pmol ouabain/mg protein (mean +/- SEM; n = 11), with a Kd of 68 +/- 12 nM. Intact normal lymphocytes bound 3.24 +/- 0.30 pmol ouabain/10(7) cells (n = 14), representing 189,000 sites/cell. In hypothyroidism, ouabain binding, when compared with normal cells sampled on the same day, was reduced by 22.0 +/- 5.3% (n = 11; P less than 0.001) in plasma membranes and by 29.1 +/- 3.5% (n = 14) in whole lymphocytes (P less than 0.001), but there was no significant change in the Kd in the membrane fraction. In 6 subjects, the decrease in ouabain binding to lymphocytes was reversed by thyroid hormone replacement. Red cells from hypothyroid subjects showed normal ouabain binding. Ouabain binding to hyperthyroid plasma membranes (2.42 +/- 0.18 pmol/mg protein) was not significantly different from normal. The results in hypothyroid subjects are consistent with the hypothesis that lymphocyte Na-K ATPase is regulated by thyroid hormones. However, lymphocyte Na-K ATPase does not increase in parallel with elevated thyroid hormone levels in hyperthyroidism. The mechanisms underlying these observations remain to be clarified.
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PMID:Effect of thyroid status on ouabain binding to the human lymphocyte. 628 Dec 92

The concentration of thyroid hormone nuclear receptors varies from one tissue to another, the anterior pituitary (AP) gland possessing the highest. Since 3,5,3',1-triiodothyronine (T3) controls within a narrow range the secretion of TSH from the pituitary gland, this study was carried out to establish whether T3 modulates its own pituitary nuclear receptors and if so, whether this modulation is correlated with the thyroidal status and TSH secretion. Salt-solubilized T3 nuclear receptors were measured in the AP gland of thyroidectomized and intact adult male rats as well as in thyroidectomized rats treated with T3. In intact male rats the maximum binding capacity of pituitary T3 nuclear receptors (MBC-T3nR), determined by Scatchard analysis, was 578 +/- 45 fmoles T3/mg protein or 27 +/- 3 fmoles T3/AP (mean +/- SEM, n = 19). 2 weeks after thyroidectomy there was a marked decrease in serum T3 and T4 concentrations as well as in the MBC-T3nR (231 +/- 26 fmoles T3/mg protein or 9.3 +/- 1.2 fmoles T3/AP, n = 7) which was still observed 8 and 16 weeks after thyroidectomy. The affinity constant (Ka) of T3 for its pituitary nuclear receptors was significantly greater in thyroidectomized rats than in intact rats (3.61 +/- 0.70 vs. 1.09 +/- 0.15 X 10(10) M-1, P less than 0.001). To test whether treatment with T3 would restore a normal MBC-T3nR, 2-week thyroidectomized rats were injected with T3(0.5 micrograms/100 g b.w.) and killed 10 min, 1, 3, 15 or 24 h after T3 injection. 10 min after T3 injection MBC-T3nR was not altered but it returned to normal values 1 h after injection (441 +/- 97 fmoles T3/mg protein) and was maintained so for at least 3 h. 15 h after T3 injection MBC-T3nR was again decreased in spite of serum T3 levels that were twice as high as in normal rats. In contrast, when T3 was injected at the dose of 1.0 micrograms/100 g b.w. the MBC-T3nR was maintained within the normal range as long as 24 h after the injection (428 +/- 125 fmoles T3/mg protein) with serum T3 concentrations that were twice the normal levels (1.27 +/- 0.06 vs. 0.67 +/- 0.01 ng/ml). These results support the hypothesis that T3 modulates the concentration of its own nuclear receptors in the rat pituitary gland. The absence of any effect of T3 10 min after injection is suggestive of an effect of T3 on the synthesis of its receptors rather than on an alteration of unoccupied receptors that would require T3 for adequate configuration and detection. This modulation of pituitary T3 receptors by T3 may provide an additional mechanism of regulation of TSH secretion in thyroid insufficiency.
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PMID:Modulation of thyroid hormone nuclear receptor levels by L-triiodothyronine (T3) in the rat pituitary. 631 85

To gain insight in the influence of the pituitary gland on the renin-angiotensin system plasma renin substrate (PRS) and the response of PRA to stimulation were studied in a homogeneous group of 20 female patients with the same etiology and degree of pituitary failure, before treatment (group P), after hydrocortisone substitution (group F), and after hydrocortisone and thyroid hormone treatment (group F + T). All patients were studied before and after each treatment by response to two stimulatory tests, acting through two different pathways; orthostasis test (O-T) and the furosemide test (Furo-T). Results were compared between groups, each patient serving as her own control, and with those obtained in a 12 healthy women control group (group C). The diet contained about 85 meq Na/day. Compared to group C (O-T response, 5.97 +/- 0.54 ng ml-1 h-1; Furo-T response, 6.71 +/- 0.82 ng ml-1 h-1; mean +/- SEM), PRA response to both tests was blunted in group P (O-T: 2.48 +/- 0.46, P less than 0.001; Furo-T: 3.02 +/- 0.53, P less than 0.001) and remained so in F (O-T: 2.18 +/- 0.40, P less than 0.001; Furo-T: 2.52 +/- 0.28, P less than 0.001), In group F + T, the response to both tests was greater than in P and F (O-T, 6.61 +/- 1.19; Furo-T, 4.36 +/- 0.44; 0.001 less than P less than 0.05). However, whereas the response to orthostasis is entirely normalized, the response to a diuretic remained significantly smaller than in group C (P less than 0.01). These improvements were observed without significant change in PRS concentration which remained low. We conclude that panhypopituitarism is accompanied by an altered renin angiotensin system. Basal levels of PRS and PRA are low and unresponsive to adequate stimulation. Whereas glucocorticoid therapy alone is without effect on this hyporeninism, addition of thyroid hormones completely normalized the response to orthostasis and significantly improved furosemide response.
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PMID:The renin-angiotensin system in panhypopituitarism: dynamic studies and therapeutic effects in Sheehan's syndrome. 633 39

In vitro release of thyroid hormone was investigated under basal and TSH-stimulated conditions in the solitary autonomously functioning thyroid nodules (AFTN). A small portion (0.5 g of wet weight) of the nodules and adjacent thyroid tissues removed surgically from five patients with solitary AFTN were prepared for the dispersed cell culture. In the experiment on non TSH-stimulated (basal) conditions, those culture media which were totally replaced on the 5th day after primary culture were utilized for the determination of thyroxine (T4) and triiodothyronine (T3) by radioimmunoassay. T4 and T3 levels in culture media of the functioning nodules were 1.15 +/- 0.33 microgram/dl (mean +/- SEM) and 2.72 +/- 0.68 ng/ml, contrasted with levels of 0.67 +/- 0.09 microgram/dl and 1.24 +/- 0.22 ng/ml in the paranodular tissues. The mean ratios of T3/T4 of the nodules and paranodular tissues were 0.25 +/- 0.02 and 0.19 +/- 0.02, respectively (p less than 0.05). Meanwhile, in another experiment under TSH stimulatory conditions employing 40 and 80 microU/ml of human TSH, there were no significant differences in T4 and T3 releases when the two groups were compared.
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PMID:In vitro study on release of thyroid hormone in solitary autonomously functioning thyroid nodules using cell culture method. 639 19

Although protein-calorie malnutrition (PCM) is known to result in various abnormalities of thyroid function, the exact relationship between the two is not clearly understood. Therefore, the thyroid function of 10 men, 13-55 yr of age, with severe PCM was studied in a clinical research ward before and 3-4 months after protein-calorie repletion. Before repletion, all subjects had low serum T4 (mean +/- SEM, 5.1 +/- 0.5 micrograms/dl) and T3 (74 +/- 6 ng/dl) concentrations. Eight subjects were chemically euthyroid, and their free T4 (1.5 +/- 0.1 ng/dl) and serum TSH (2.9 +/- 1.4 microU/ml) values were normal. Two subjects were chemically hypothyroid, with low free T4 values and high serum TSH values. After repletion, the 8 euthyroid subjects had significant increases in serum T4 (P less than 0.01) and T3 (P less than 0.005), but TSH did not change. Serum T4 and T3 were still lower (P less than 0.05-0.001) and TSH higher (P less than 0.01) than in 28 normal men of comparable age coming from the same area. After repletion, values remained unchanged in the 2 hypothyroid subjects, except for moderate increases in serum T3 and slight decreases in TSH. In all PCM subjects, values of thyroidal exchangeable iodine (23.1 +/- 7 vs. 42.9 +/- 8 mg; P less than 0.02), estimated thyroidal I per g wet wt (1.05 +/- 0.3 vs. 1.99 +/- 0.36 mg; P less than 0.02), and thyroidal iodide clearance (13.8 +/- 1.6 vs. 19.4 +/- 1.3 ml/min; P less than 0.002) were lower before repletion than after; the protein-bound 131I level (72 h; 0.27% vs. 0.08 dose/liter; P less than 0.05) was higher, but thyroid hormone secretion rates (200 +/- 49 vs. 153 +/- 25 micrograms/day) were not significantly different. Thyroid iodide clearance was lower even though plasma inorganic iodine (6.3 +/- vs. 12.5 +/- 3 micrograms/liter; P less than 0.05) and daily urinary iodine excretion (158 +/- 43 vs. 395 +/- 62 micrograms; P less than 0.01) were lower before than after repletion. In 2 PCM euthyroid subjects, baseline thyroid 131I uptake was lower before than after repletion, and the magnitude of the increase after TSH (10 U, im) stimulation was greater when the malnourished state improved. TSH increased concentrations of serum T4 and T3 both before and after protein repletion. After repletion, one hypothyroid patient failed to respond to TSH; the other had a small increase in 131I uptake but not in serum T4 or T3. The results indicate defective thyroid iodine concentration in human PCM, but adequate hormone secretion. This situation leads to depletion of thyroid iodine stores. This alteration, if extreme, might result in hypothyroidism. Adequate protein-calorie intake tends to reverse these abnormalities.
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PMID:Defective thyroidal iodine concentration in protein-calorie malnutrition. 640 12

Urine samples from 8 healthy subjects, from 16 patients with primary hypothyroidism and 8 patients with Graves' hyperthyroidism were pre-purified in SP-Sephadex-C-25 cation-exchange-chromatography, subjected to reverse phase high-pressure liquid chromatography (HPLC) with 0.01 M ammonium acetate pH 4 as a polar and propanol as a non-polar solvent with a 1%/min gradient and assayed in our TRH radioimmunoassay. Urine TRH-immunoreactivity levels were measured before and after 3 months of treatment with thyroxine or methimazole. The urine TRH-levels in healthy subjects were 5.5 +/- 1.4 ng/1 (mean +/- SEM, n = 8). In the hypothyroid patients, the urine TRH levels were 50.6 +/- 40 ng/1 before and 71.7 +/- 45.3 ng/1 after 3 months of treatment with thyroxine. These values did not significantly differ from those in healthy subjects. The large variations were due to highly elevated values in 3 patients. In 2 hypothyroid patients with initially high urine TRH values, 67 and 657 ng/1, urine TRH was measured 5 and 18 months later and was found to have decreased to 5 and 11 ng/1. In the hyperthyroid patients, urine TRH levels were 10.3 +/- 3.9 ng/1 before and 8.9 +/- 3.3 ng/1 after the treatment with methimazole and did not differ significantly from the levels in healthy subjects. After 3 months of treatment, the hyper- and the hypothyroid patients were euthyroid. Our results show, that, except in 2 hypothyroid patients, there does not appear to be any relationship between urine TRH levels and serum TSH or thyroid hormone levels in hypothyroid and hyperthyroid patients.
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PMID:Urine TRH immunoreactivity in hypothyroid and hyperthyroid patients. 642 29


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