Oral administration of TRH in puerperal women: effect on insufficient lactation, thyroid hormones and on the responses of TSH and prolactin to intravenous TRH

1980 ◽  
Vol 93 (4) ◽  
pp. 413-418 ◽  
Author(s):  
O. Ylikorkala ◽  
S. Kivinen ◽  
A. Kauppila
Keyword(s):  
Oral Administration ◽  
Thyroid Hormones ◽  
Plasma Samples ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Trh Stimulation ◽  
Stimulation Tests ◽  
Tsh Levels

Abstract. Thirteen puerperal women with insufficient lactation were treated with thyrotrophin releasing hormone (TRH) 20 mg twice daily for two weeks. Intravenous (iv) TRH stimulation tests were done before the TRH therapy and within 3–5 h after the last dose of oral TRH. Plasma samples were assayed for prolactin (Prl), thyrotrophin (TSH), triiodothyronine (T3) and thyroxine (T4) by radioimmunoassays, and the lactational response was objectively monitored in 11 women. Oral TRH treatment was associated with significantly (P < 0.05) depressed Prl levels (23.0 ± 7.9 μg/l vs. 61.4 ± 26.2, mean ± sem), no change in TSH levels (3.7 ± 0.4 IU/1 vs. 4.0±0.4) but significantly (P<0.01) elevated T3 (2.17±1.14 nmol/l vs. 1.83 ± 0.09) and T4 (131.6 ± 7.9 nmol/l vs. 96.6 ± 5.8) levels. Oral TRH entirely blocked the TSH response and significantly (P<0.01) blunted the Prl response to iv TRH stimulation. No improvement in lactation was observed.

DIFFERENT EFFECTS OF ORAL DOSES OF TRIIODOTHYRONINE OR THYROXINE ON THE INHIBITION OF THYROTROPHIN RELEASING HORMONE (TRH) MEDIATED THYROTROPHIN (TSH) RESPONSE IN MAN

1975 ◽  
Vol 80 (1) ◽  
pp. 42-48 ◽  
Author(s):  
K. W. Wenzel ◽  
H. Meinhold ◽  
H. Schleusener
Keyword(s):  
Oral Administration ◽  
Binding Sites ◽  
Direct Action ◽  
Normal Range ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Tsh Secretion ◽  
Inhibiting Protein ◽  
Oral Doses

ABSTRACT Since contradicting results about the existence of T3 or T3 and T4 receptors in pituitary tissue have been reported, the influence of L-triiodothyronine (L-T3) or L-thyroxine (L-T4) on TRH stimulated TSH release was investigated. Oral administration of 50 μg L-T3 caused an increasing inhibition of TSH response to 400 μg TRH from 64 % 2 h after L-T3 intake to 29% after 24 h, while serum T3 peaks up to 5.45 ng/ml occurred between 2 to 4 h after L-T3 ingestion and became normal after 8 to 10 h. This delay in the T3 action on TRH inhibition agrees with the postulate that T3 induces the synthesis of an inhibiting protein which is blocking TSH liberation. Oral administration of 1000 μg L-T4 induced increments of serum T4 up to 221 ng/ml between 6 to 24 h after intake; however, a TRH inhibition of 62 % did not become evident before 48 h. At this time T3 levels had risen to the upper normal range. These results support the theory that T3 is responsible for the regulation of TSH secretion. An intra-pituitary conversion from T4 to T3 seems more likely the cause of the TRH inhibition rather than the peripheral T4-T3 conversion or a direct action by T4 binding sites in the pituitary.

EFFECT OF THYROID STATUS ON THE THYROTROPHIN-RELEASING HORMONE-DEGRADING ACTIVITY OF RAT SERUM

1976 ◽  
Vol 71 (1) ◽  
pp. 13-19 ◽  
Author(s):  
N. WHITE ◽  
S. L. JEFFCOATE ◽  
E. C. GRIFFITHS ◽  
K. C. HOOPER
Keyword(s):  
Thyroid Hormone ◽  
Human Serum ◽  
Thyroid Function ◽  
Thyroid Status ◽  
Rat Serum ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Levels

SUMMARY The TRH-degrading activity of rat serum in vitro is five times more potent than that of human serum. In rats, it is significantly reduced in hypothyroidism (thiouracil-induced) and significantly increased in hyperthyroidism (T3 or T4-induced). This suggests a possible role in the regulation of adenohypophysial-thyroid function which is probably, in turn, dependent on thyroid hormone, rather than TSH, levels.

scholarly journals Low Growth Hormone Levels in Short-Stature Children with Pituitary Hyperplasia Secondary to Primary Hypothyroidism

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Minghua Liu ◽  
Yanyan Hu ◽  
Guimei Li ◽  
Wenwen Hu
Keyword(s):  
Thyroid Hormones ◽  
Short Stature ◽  
Primary Hypothyroidism ◽  
Thyroid Antibodies ◽  
Gh Secretion ◽  
Pituitary Hyperplasia ◽  
Stimulation Tests ◽  
The Mean ◽  
Tsh Levels

Objective. The follow-up of GH levels in short-stature children with pituitary hyperplasia secondary to primary hypothyroidism (PPH) is reported in a few cases. We aimed to observe changes in GH secretion in short-stature children with PPH. Methods. A total of 11 short-stature children with PPH accompanied by low GH levels were included. They received levothyroxine therapy after diagnosis. Their thyroid hormones, IGF-1, PRL, and pituitary height were measured at baseline and 3 months after therapy. GH stimulation tests were performed at baseline and after regression of thyroid hormones and pituitary. Results. At baseline, they had decreased GH peak and FT3 and FT4 levels and elevated TSH levels. Decreased IGF-1 levels were found in seven children. Elevated PRL levels and positive thyroid antibodies were found in 10 children. The mean pituitary height was 14.3±3.8 mm. After 3 months, FT3, FT4, and IGF-1 levels were significantly increased (all p<0.01), and values of TSH, PRL, and pituitary height were significantly decreased (all p<0.001). After 6 months, pituitary hyperplasia completely regressed. GH levels returned to normal in nine children and were still low in two children. Conclusion. GH secretion can be resolved in most short-stature children with PPH.

Luteinizing hormone responses to luteinizing hormone releasing hormone (LHRH) in acute mania and the effects of lithium on LHRH and thyrotrophin releasing hormone tests in volunteers

1989 ◽  
Vol 19 (1) ◽  
pp. 69-77 ◽  
Author(s):  
R. Hunter ◽  
J. E. Christie ◽  
L. J. Whalley ◽  
J. Bennie ◽  
S. Carroll ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Thyroid Stimulating Hormone ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Trh Stimulation ◽  
The Status ◽  
Hormone Responses ◽  
Independent Features ◽  
Stimulating Hormone

SynopsisThe endocrine responses to Luteinizing Hormone Releasing Hormone (LHRH) of eight drug-free males with mania were determined. Basal levels of Luteinizing Hormone (LH) and the plasma levels following injection of LHRH were elevated in patients compared with controls; Follicle Stimulating Hormone (FSH) and testosterone were not different. Elevated levels of LH have been described previously in recovered manic patients and have been suggested to be state-independent features of mania. In order to clarify the status of this finding, the effects of lithium administration upon hormone responses to LHRH in six male volunteers were also investigated, together with the effects upon Thyrotrophin Releasing Hormone (TRH) stimulation of Thyroid Stimulating Hormone (TSH) and prolactin release. Lithium increased the basal levels of LH and levels after injection of LHRH without effect upon FSH and testosterone. Lithium also increased basal and TRH stimulated release of TSH and basal prolactin levels. Lithium was without effect upon prolactin responses to TRH. The results are discussed in relation to current information on the mechanism of lithium's action. The implications for neuroendocrine work on recovered patients taking lithium are also explored.

Decreased prolactin responsiveness to thyrotrophin-releasing hormone and metoclopramide in hyperthyroidism

1985 ◽  
Vol 110 (2) ◽  
pp. 221-226 ◽  
Author(s):  
Sven Röjdmark ◽  
Anders Carlsson
Keyword(s):  
Oral Administration ◽  
Normal Subjects ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Normal Individuals ◽  
Cytoplasmic Membranes ◽  
Before And After ◽  
The One

Abstract. To investigate whether prolactin (Prl) responsiveness to thyrotrophin-releasing hormone (TRH) differs in thyrotoxic and normal individuals, serum Prl was determined before and after iv injection of 200 μg TRH in 10 patients with untreated thyrotoxicosis and also in 9 normal subjects. Both the maximal Prl increment after TRH and the total Prl response, represented by the Prl incremental area, were significantly larger in the normal subjects compared with the thyrotoxic (max Prl increment 56 ± 11 vs 15 ± 3 ng/ml, P< 0.001; Prl incremental area 3071 ± 522 vs 579 ± 171, P <0.001; mean ± sem). The maximal Prl increase after 15 mg oral metoclopramide (MET) was also significantly larger in the normal (125 ± 13 ng/ml) than in the thyrotoxic subjects (60 ± 13 ng/ml, P < 0.01). When 200 μg TRH was injected iv 90 min after oral administration of 15 mg MET, an additional Prl increase was observed in normal individuals (21 ±6 ng/ml, P < 0.01). In thyrotoxic patients, however, iv TRH failed to induce a significant increase in Prl after oral priming with MET (0 ± 3 ng/ml). When 7 thyrotoxic patients, made euthyroid by 125I-treatment, were investigated according to the same protocol as the one mentioned above, they displayed normal Prl responses to iv TRH and to oral MET. Furthermore, they showed a significant Prl response to iv TRH after oral priming with MET (20 ± 8 ng/ml, P < 0.05). These findings imply that pituitary lactotrophs of untreated thyrotoxic patients might have cytoplasmic membranes with decreased permeability to Prl and/or reduced stores of releasable Prl which return to normal after oral 125I-therapy.

Preferential release of tri-iodothyronine following stimulation by thyrotrophin or thyrotrophin-releasing hormone in sheep of different ages

1992 ◽  
Vol 132 (1) ◽  
pp. 93-100 ◽  
Author(s):  
R. Peeters ◽  
N. Buys ◽  
D. Vanmontfort ◽  
J. Van Isterdael ◽  
E. Decuypere ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Plasma Concentrations ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Neonatal Injection ◽  
Different Ages ◽  
Neonatal Lambs

ABSTRACT The influence of TRH and TSH injections on plasma concentrations of tri-iodothyronine (T3) and thyroxine (T4) was investigated in neonatal (injection within 0·5 h after delivery) and growing lambs and in normal, pregnant and lactating adult ewes (all 2 years old and originating from Suffolk, Milksheep and Texal cross-breeds). Neonatal lambs had higher levels of T3, T4 and GH compared with all other groups, whereas prolactin and TSH were higher in lactating ewes. In all animals, injections of TRH increased plasma concentrations of prolactin and TSH after 15 min but not of GH at any time. Small increases in T3 and T4 were observed in neonatal lambs, without any effect on the T3 and T4 ratio, after prolactin administration, whereas prolactin did not influence plasma concentrations of T3 or T4 in all other experimental groups. Similar results for thyroid hormones were obtained after TRH or TSH injections. It was therefore concluded that the effects observed after TRH challenge were mediated by the release of TSH. With the possible exception of neonatal lambs, plasma concentrations of T3 after administration of TRH or TSH were always increased before those of T4; the increase in T3 occurred within 0·5–1 h compared with 2–4 h for T4 in all experimental groups. This resulted in an increased ratio of plasma T3 to T4 up to 4 h after injection. It is concluded that, in sheep, TRH and TSH preferentially release T3 from the thyroid gland probably by a stimulatory effect of TSH on the intrathyroidal conversion of T3 to T4. Journal of Endocrinology (1992) 132, 93–100

Thyrotrophin -releasing hormone in diagnosis

1974 ◽  
Vol 12 (8) ◽  
pp. 31-32
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Diagnostic Tests ◽  
Anterior Pituitary ◽  
Pituitary Stalk ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Hormone Levels ◽  
Thyroid Hormone Levels ◽  
Hypothalamic Function

Thyrotrophin-releasing hormone (TRH - Roche) is a synthetic tripeptide, L-pyroglutamyl-L-histidyl-L-proline-amide, which is identical with the porcine, ovine and human hypothalamic hormone that promotes the secretion of thyrotrophin. Secreted in the hypothalamus, it passes down the capillaries of the pituitary stalk to the anterior pituitary and there causes release of thyrotrophin. Thyroid hormones (triiodo-thyronine (T3) and thyroxine (T4)) interfere with the thyrotrophin (TSH)-releasing action of TRH, so that excess thyroid hormones block TSH release in response to TRH; conversely when thyroid hormone levels are low, increased secretion of TSH occurs. The hypothalamic secretion of TRH is probably directly influenced by the concentration of thyroid hormones in the blood reaching it. In addition TRH promotes the secretion of prolactin from the pituitary. TRH-Roche is marketed in Britain for use in hospitals in diagnostic tests of thyroid and of pituitary-hypothalamic function.

INTRAVENOUS AND PERORAL TRH STIMULATION IN SPORADIC ATOXIC GOITRE

1977 ◽  
Vol 85 (3) ◽  
pp. 508-514 ◽  
Author(s):  
C. Kirkegaard ◽  
J. Faber ◽  
T. Friis ◽  
U. Birk Lauridsen ◽  
P. Rogowski ◽  
...  
Keyword(s):  
High Frequency ◽  
Diagnostic Value ◽  
Stimulation Test ◽  
Trh Test ◽  
Thyrotrophin Releasing Hormone ◽  
Normal Thyroid ◽  
Releasing Hormone ◽  
Trh Stimulation ◽  
Significant Difference ◽  
Bovine Tsh

ABSTRACT Thyrotrophin releasing hormone (TRH) stimulation test with 200 μg iv was performed in 35 patients with atoxic sporadic goitre. In 23 patients with diffuse goitre 7 showed a lack of increase in serum thyrotrophin (TSH) at a significantly increased frequency compared to controls (P = 0.0028). In 4 patients with solitary nodules 2 showed no significant response to TRH (negative), while 3 of the 8 patients with multinodular goitres had negative TRH test. Only 6 of the 12 TRH negative patients also had non-suppressible 131I uptake following T3. No significant difference in age and thyroid parameters was found between the TRH negative and TRH positive patients. In 7 TRH negative patients the test was repeated with 400 μg TRH but all remained negative. Five of these patients were given TRH perorally 80 mg daily for 2 weeks resulting in a significant increase in serum T4 and T3. No detectable increase in TSH was found. The response to iv bovine TSH in 4 TRH negative patients was found to be normal, suggesting that there was normal thyroid sensitivity to TSH. Our findings suggest that patients with TRH negative atoxic goitre can release biological active TSH following prolonged TRH stimulation. The high frequency of a negative standard TRH test in atoxic goitre seems to diminish the diagnostic value of the standard TRH test.

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