THE THYROTROPHIN RESPONSE TO THYROTROPHIN RELEASING HORMONE DURING TREATMENT IN PATIENTS WITH GRAVES' DISEASE

1977 ◽  
Vol 85 (2) ◽  
pp. 335-344 ◽  
Author(s):  
E. Haug ◽  
H. M. M. Frey ◽  
T. Sand

ABSTRACT Thyrotrophin releasing hormone (TRH) tests were performed at 4 or 8 weeks intervals, after the initiation of anti-thyroid treatment in 15 patients with Graves' disease. All TRH tests were negative as long as the serum levels of thyroxine (T4) and triiodothyronine (T3) were elevated, and normalization of the serum levels of these hormones always occurred before the response to iv TRH was restored. In 13 patients the time from the patients for the first time were registered as biochemically euthyroid varied from 0–9 months (mean 3.1 months), before normal TRH response was restored. Two patients were still TRH non-responsive at the end of the study, even though they had been biochemically euthyroid for as long as 17 and 18.5 months. The TRH test, therefore, is not helpful in the evaluation of the effect of anti-thyroid treatment in patients with Graves' disease. There was an increase in the serum level of thyrotrophin (TSH) from 3.4 ± 0.3 (sem) to 4.3 ± 0.5 (sem) ng/ml (P <0.05), and a decrease in the serum level of total T4 from 19.4 ± 1.1 (sem) to 5.8 ± 0.8 (sem) μg/100 ml in 13 patients from the first examination until the last time they were examined before restored TRH response. This finding shows that the pituitary gland has retained its ability to synthesize and secrete TSH even though no TSH could be released by iv TRH. In 6 TRH non-responsive patients with Graves' disease, serum TSH levels were suppressed from 2.5 ±1.2 (sem) ng/ml before the administration of a single dose of 3 mg T4 orallly, to 0.9 ± 0.2 (sem) ng/ml, 7 days after the T4 administration. Thus, the negative feed-back effect on the pituitary gland of the thyroid hormones is operating in these patients. This finding indicates that the TRH non-responsiveness in euthyroid patients with Graves' disease is not due to pituitary depletion of TSH, since the negative feed-back effect of the thyroid hormones is operating normally.

1980 ◽  
Vol 86 (2) ◽  
pp. 357-362 ◽  
Author(s):  
TAKAMURA MURAKI ◽  
TERUO NAKADATE ◽  
YUKIKO TOKUNAGA ◽  
RYUICHI KATO

Morphine reduced the release of thyroid-stimulating hormone (TSH) which was stimulated by exposure to cold and by thyroidectomy as well as reducing the basal level of TSH in the serum of male rats. The inhibitory effect of morphine was antagonized by naloxone which did not enhance the basal or cold-induced TSH release. Pretreatment with morphine did not reduce the release of TSH induced by exogenous thyrotrophin-releasing hormone (TRH) but enhanced it. This effect of morphine was also antagonized by naloxone. The above results suggested that the effect of morphine in reducing levels of serum TSH was not mediated by blocking the effect of TRH on the anterior pituitary gland, but that it was probably mediated by the inhibition of the release of TRH.


1973 ◽  
Vol 73 (3) ◽  
pp. 455-464 ◽  
Author(s):  
P. A. Torjesen ◽  
E. Haug ◽  
T. Sand

ABSTRACT The rapid iv administration of 0.5 mg of synthetic thyrotrophin-releasing hormone (TRH) increased the serum thyroid-stimulating hormone (TSH) concentration in 20 normal subjects from baseline levels of 2.0 ± 0.5 ng/ml (sem) to peak values of 6.0 ± 0.7 ng/ml (sem) in women and 4.5 ± 0.5 ng/ml (sem) in men. The maximal increase occurred 30 min after TRH. The serum growth hormone (HGH) concentrations increased from baseline levels of 2.6± 1.0 ng/ml (sem) to peak values of 7.8± 1.3 ng/ml (sem) in women. In men there was no rise in the serum HGH concentrations. The serum levels of luteinizing hormone (LH) and folliclestimulating hormone (FSH) did not change significantly. In patients with hyperthyroidism the serum TSH concentrations did not change following TRH. Patients with primary hypothyroidism showed an exaggerated and prolonged increase in serum TSH concentrations after TRH administration. A routine TRH-stimulation test is proposed.


1977 ◽  
Vol 85 (3) ◽  
pp. 479-487 ◽  
Author(s):  
J. Lindholm ◽  
H. Dige-Petersen ◽  
L. Hummer ◽  
P. Rasmussen ◽  
O. Korsgaard

ABSTRACT The secretion and biological activity of thyroid stimulating hormone (TSH) were studied in 22 patients with a pituitary tumour (17 acromegalics and 5 patients with a chromophobe adenoma) and in 36 hypophysectomized patients (16 acromegalics and 20 with a chromophobe adenoma). Thyroid function was assessed by serum thyroxine (T4), serum triiodothyronine (T3), and thyroxine-binding globulin (TBG) concentration. Serum TSH was measured before and after injection of TSH releasing hormone (TRH), and in 19 hypophysectomized patients the T3 response after TRH was measured. In addition a TRH test was performed 1–2 weeks after surgery in 11 patients. The basal serum TSH did not differ from euthyroid control values in any of the groups and no late effect of hypophysectomy was observed. Subnormal peak TSH values were seen in 10 out of 37 euthyroid patients, whereas 9 out of 11 hypothyroid patients responded normally. Hypophysectomy caused an immediate but transient decrease in peak TSH in patients with a chromophobe adenoma only. The rise in serum T3 after TRH was significantly lower in hypophysectomized patients than in controls. An increase in TSH was followed by a T3 response in all patients except in 4 out of 8 euthyroid acromegalics. In patients operated on for a chromophobe adenoma the T3 response was correlated with serum T4, whereas this was not the case in acromegalics.


1983 ◽  
Vol 98 (1) ◽  
pp. 1-6 ◽  
Author(s):  
A. R. Sheth ◽  
P. R. Sheth ◽  
R. Roy

Inhibin administered to adult male rats delayed the in-vivo pituitary responsiveness to thyrotrophin releasing hormone (TRH) as observed in terms of prolactin release in the serum. It also decreased the sensitivity of the pituitary gland to TRH, in terms of TSH release. However, inhibin alone did not alter the serum levels of prolactin and TSH, although it significantly suppressed serum FSH levels. In addition, the inhibin effect on FSH release was blocked by TRH.


1975 ◽  
Vol 80 (2) ◽  
pp. 297-301 ◽  
Author(s):  
E. Hansen ◽  
C. Kirkegaard ◽  
Th. Friis ◽  
K. Siersbæk-Nielsen

ABSTRACT The response in serum thyrotrophin (TSH) to thyrotrophin releasing hormone (TRH) has been studied in 5 euthyroid patients with familial thyroxine-binding globulin (TBG) deficiency. Total serum thyroxine (T4), serum triiodothyronine (T3) and free T4 index and free T3 index were significantly and equally decreased, but in spite of these findings the serum TSH and the response to TRH was normal. The TRH test seems to be a better indicator of the euthyroid state in familial TBG deficiency than the measurement of free T4 and free T3 in serum.


1978 ◽  
Vol 87 (1) ◽  
pp. 80-87 ◽  
Author(s):  
K. Siersbæk-Nielsen ◽  
C. Kirkegaard ◽  
P. Rogowski ◽  
J. Faber ◽  
B. Lumholtz ◽  
...  

ABSTRACT A possible extrathyroidal effect of propylthiouracil (PTU) and carbimazole on serum levels of thyroxine (T4), triiodothyronine (T3), 3,3′,5′-triiodothyronine (reverse T3) and on thyrotrophin-releasing hormone (TRH) induced thyrotrophin (TSH) release was estimated in 19 patients with severe hypothyroidism treated with T4. During PTU medication a significant decrease in serum T3 from 90 ± 16 (sd) to 79 ± 23 ng/100 ml (P < 0.01) and a reciprocal increase in serum reverse T3 from 51 ± 14 (sd) to 58 ± 20 ng/100 ml (P < 0.025) were found. No significant changes in serum T4, basal serum TSH or response to TRH could be demonstrated. Carbimazole did not change any of the parameters studied.


1994 ◽  
Vol 141 (3) ◽  
pp. 527-533 ◽  
Author(s):  
J Timisjärvi ◽  
V Ojutkangas ◽  
E Eloranta ◽  
M Nieminen ◽  
J Leppäluoto ◽  
...  

Abstract The reindeer in its natural habitat is subject to great annual variations in ambient temperature, illumination and nutrition. To ascertain the effect of these environmental factors on thyroid function, serum thyroid-stimulating hormone (TSH), thyroxine (T4), tri-iodothyronine (T3) and reverse T3 (rT3) concentrations were measured four times a year (2 June, 8 October, 21 November, and 24 February) in 14 animals housed outdoors at latitude 69°10′N. They all showed statistically significant (P<0·05) seasonal changes. Serum TSH and T4 were highest in February (623 ± 30 ng/ml and 287 ± 19 nmol/l respectively). TSH was lowest in October (318 ± 47 ng/ml) and T4 in November (199 ± 19 nmol/l). The T3 concentration was highest in November (3·0 ± 0·3 nmol/l) and lowest in June (1·8 ± 0·2 nmol/l). In contrast, rT3 was highest in June (3·6 ± 1·2 nmol/l) and lowest in November (1·9 ± 0·6 nmol/l). Thus, there was an inverse relationship between T3 and rT3 (linear regression r= −0·406, P<0·01). TSH, T4, T3 and rT3 responses to exogenous thyrotrophin-releasing hormone (synthetic TRH; 500 μg i.m.) were determined in ten animals. The magnitude of their response to TRH was significantly (P<0·05) dependent on the time of year. When compared with the control level all the parameters rose significantly (P<0·05). The greatest rise in serum TSH occurred in October (219 ± 151% and the smallest in February (66 ± 53%). The corresponding figures for T4 were 56 ± 60% in June and 11 ± 18% in February, for T3 143 ± 45% in October and 73 ± 46% in June, and for rT3 25 ± 13% in October and 12 ± 10% in February. In conclusion, significant annual variations occur in the reindeer serum concentrations of TSH and thyroid hormones as well as in their responses to exogenous TRH. Environmental factors greatly affect the pituitary-thyroid axis in this mammalian species living far in the North. The observed variations probably reflect an adaptation of the species to the annual environmental cycle. Journal of Endocrinology (1994) 141, 527–533


1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.


1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.


1985 ◽  
Vol 69 (2) ◽  
pp. 113-121 ◽  
Author(s):  
C. A. Ollis ◽  
S. Tomlinson ◽  
D. S. Munro

Graves’ disease is the commonest form of hyperthyroidism in which excessive production of thyroid hormones by the hyperplastic overactive thyroid gland produces elevated serum levels of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). Many of the manifestations of Graves’ disease, increased basal metabolic rate, increased heart rate, heat intolerance, sweating and nervousness, can be attributed to the peripheral actions of the excess thyroid hormones. The pathogenesis of many of the other dramatic features of Graves’ disease, such as the eye involvement or localized skin changes, is not fully understood, but circulating immunoglobulins with thyroid stimulating activity are almost certainly linked to excess thyroid hormone production and thereby cause the hyperthyroidism.


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