EXTRATHYROIDAL EFFECTS OF PROPYLTHIOURACIL AND CARBIMAZOLE ON SERUM T4, T3, REVERSE T3 AND TRH-INDUCED TSH-RELEASE IN MAN

1978 ◽  
Vol 87 (1) ◽  
pp. 80-87 ◽  
Author(s):  
K. Siersbæk-Nielsen ◽  
C. Kirkegaard ◽  
P. Rogowski ◽  
J. Faber ◽  
B. Lumholtz ◽  
...  
Keyword(s):  
Serum Levels ◽  
Reverse T3 ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Basal Serum ◽  
Serum T4 ◽  
Serum Tsh

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.

EFFECT OF THYROTROPHIN-RELEASING HORMONE ON SERUM LEVELS OF PITUITARY HORMONES IN MEN AND WOMEN

1973 ◽  
Vol 73 (3) ◽  
pp. 455-464 ◽  
Author(s):  
P. A. Torjesen ◽  
E. Haug ◽  
T. Sand
Keyword(s):  
Normal Subjects ◽  
Serum Levels ◽  
Thyroid Stimulating Hormone ◽  
Primary Hypothyroidism ◽  
Serum Growth Hormone ◽  
Maximal Increase ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Baseline Levels ◽  
Serum Tsh

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.

EFFECT OF THYROTROPHIN RELEASING HORMONE (TRH) IN PATIENTS WITH PITUITARY DISORDERS

1977 ◽  
Vol 85 (3) ◽  
pp. 479-487 ◽  
Author(s):  
J. Lindholm ◽  
H. Dige-Petersen ◽  
L. Hummer ◽  
P. Rasmussen ◽  
O. Korsgaard
Keyword(s):  
Pituitary Tumour ◽  
Thyroid Stimulating Hormone ◽  
Trh Test ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Basal Serum ◽  
Chromophobe Adenoma ◽  
Before And After ◽  
Hypothyroid Patients ◽  
Serum Tsh

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.

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
Keyword(s):  
Serum Level ◽  
Thyroid Hormones ◽  
Pituitary Gland ◽  
Serum Levels ◽  
Graves Disease ◽  
Trh Test ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
First Time ◽  
Serum Tsh

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.

SERUM THYROTROPHIN AND THE RESPONSE TO THYROTROPHIN RELEASING HORMONE IN SYMPTOMLESS AUTOIMMUNE THYROIDITIS AND IN BORDERLINE AND OVERT HYPOTHYROIDISM

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg
Keyword(s):  
Autoimmune Thyroiditis ◽  
Elevated Serum ◽  
Mean Value ◽  
Primary Hypothyroidism ◽  
Overt Hypothyroidism ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Mean ◽  
The Individual ◽  
Serum Tsh

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.

scholarly journals Inhibition of pituitary type 2 deiodinase by reverse triiodothyronine does not alter thyroxine-induced inhibition of thyrotropin secretion in hypothyroid rats

2005 ◽  
Vol 153 (3) ◽  
pp. 429-434 ◽  
Author(s):  
P Cettour-Rose ◽  
T J Visser ◽  
A G Burger ◽  
F Rohner-Jeanrenaud
Keyword(s):  
Specific Inhibitor ◽  
Adult Rats ◽  
Reverse T3 ◽  
Brown Adipose ◽  
Tsh Secretion ◽  
Serum T3 ◽  
Serum T4 ◽  
Serum Tsh ◽  
Tsh Levels

Objectives: Intrapituitary triiodothyronine (T3) production plays a pivotal role in the control of TSH secretion. Its production is increased in the presence of decreased serum thyroxine (T4) concentrations and the enzyme responsible, deiodinase type 2 (D2), is highest in hypothyroidism. In order to document the role of this enzyme in adult rats we developed an experimental model that inhibited this enzyme using the specific inhibitor, reverse T3 (rT3). Methods: Hypothyroidism was induced with propylthiouracil (PTU; 0.025 g/l in drinking water) which in addition blocked deiodinase type 1 (D1) activity, responsible for the rapid clearance of rT3 in vivo. During the last 7 days of the experiment, the hypothyroid rats were injected (s.c.) for 4 days with 0.4 or 0.8 nmol T4 per 100 g body weight (bw) per day. For the last 3 days, the same amount of T4 was infused via s.c. minipumps. In additional groups, 25 nmol rT3/100 g bw per day were added to the 3-day infusion of T4. Results: Infusion of 0.4 nmol T4/100 g bw per day did not affect the high serum TSH levels, 0.8 nmol T4/100 g bw per day decreased them to 57% of the hypothyroid values. The infusions of rT3 inhibited D2 activity in all organs where it was measured: the pituitary, brain cortex and brown adipose tissue (BAT). In the pituitary, the activity was 27%, to less than 15% of the activity in hypothyroidism. Despite that, serum TSH levels did not increase, serum T4 concentrations did not change and the changes in serum T3 were minimal. Conclusions: We conclude that in partly hypothyroid rats, a 3-day inhibition of D2 activity, without concomitant change in serum T4 and minimal changes in serum T3 levels, is not able to upregulate TSH secretion and we postulate that this may be a reflection of absent or only minimal changes in circulating T3 concentrations.

SERUM THYROTROPHIN, PROLACTIN AND GROWTH HORMONE, RESPONSE TO TRH DURING OESTROGEN TREATMENT

1977 ◽  
Vol 84 (1) ◽  
pp. 23-35 ◽  
Author(s):  
E. Rutlin ◽  
E. Haug ◽  
P. A. Torjesen
Keyword(s):  
Growth Hormone ◽  
Human Subjects ◽  
Serum Levels ◽  
Normal Male ◽  
Oestrogen Treatment ◽  
Thyrotrophin Releasing Hormone ◽  
Basal Serum ◽  
Menopausal Women ◽  
Menstruating Women ◽  
Post Menopausal

ABSTRACT The serum levels of thyrotrophin (TSH), prolactin (PRL) and growth hormone (GH) and the response of these hormones to 500 μg thyrotrophin-releasing hormone (TRH) iv were studied in menstruating women. in post-menopausal women before and after 2 mg oestradiol valerate for 5 consecutive days, and in men on long term oestrogen treatment. Oestrogen treatment had no effect on basal serum TSH levels, which were within the normal range in all groups. The TSH response to TRH was not different in menstruating and post-menopausal women and was not changed in the latter group after oestrogen treatment. In men treated chronically with oestrogens, the TSH response to TRH was similar to that found in normal male subjects. There was no difference in basal levels of serum PRL between males and menstruating females. In the post-menopausal women, however, basal levels of serum PRL was significantly decreased, but rose during oestrogen treatment to serum levels normally found in menstruating women. In the oestrogen treated males basal serum PRL levels were significantly higher than in untreated men. The PRL response to TRH was significantly greater in females than in males, but in the oestrogen treated males the PRL response to TRH was greatly increased and almost of the same magnitude as the response in females. There was no difference in PRL response between menstruating and post-menopausal women, and oestrogen treatment of the latter group had no significant effect on the PRL response. Basal levels of serum GH did not differ between the groups. In the group of 9 post-menopausal women one subject showed a small GH response to TRH prior to oestrogen treatment, while 7 subjects showed GH responses to TRH after oestrogen treatment. In the group of 5 chronically oestrogen treated men, 2 subjects had increased serum levels of GH after TRH. Thus our data show that oestrogen administration may induce PRL release in human subjects, while oestrogens seem to play a far less important role in the regulation of GH and TSH secretion.

RESPONSE OF NORMAL, HYPOTHYROID AND HYPOTHALAMO-PITUITARY INSUFFICIENT CHILDREN TO SYNTHETIC THYROTROPHIN-RELEASING HORMONE

1971 ◽  
Vol 51 (3) ◽  
pp. 483-488 ◽  
Author(s):  
G. MILHAUD ◽  
P. RIVAILLE ◽  
M. S. MOUKHTAR ◽  
E. BINET ◽  
J. C. JOB
Keyword(s):  
Time Course ◽  
Solid Phase ◽  
Thyroid Stimulating Hormone ◽  
Normal Children ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Secretion ◽  
Course Changes ◽  
Serum Tsh ◽  
Tsh Deficiency

SUMMARY Thyrotrophin-releasing hormone (TRH) was synthesized by the solid phase technique, administered to 13 children, and the time-course changes in the serum level of thyroid-stimulating hormone (TSH) assessed. In eight normal children, peak levels of TSH occurred 20 min after the injection, and circulating TSH remained significantly raised for 60 min. In three hypothyroid children, the increase in serum TSH was much greater than in normal children, suggesting the existence of large pituitary TSH stores. In two hypopituitary children with TSH deficiency, TSH reserves seemed normal. One of these patients had a craniopharyngioma; after operation, the increase in serum TSH was reduced. These results show that assay of serum TSH after administration of synthetic TRH provides a test which distinguishes pituitary from hypothalamic defects affecting TSH secretion.

The Effect of Thyrotrophin-Releasing Hormone on Serum TSH, T4, and T3Levels in Endemic and Sporadic Nontoxic Goitre

1974 ◽  
Vol 6 (06) ◽  
pp. 501-506 ◽  
Author(s):  
G. Rothenbuchner ◽  
D. Koutras ◽  
S. Raptis ◽  
J. Birk ◽  
U. Loos ◽  
...  
Keyword(s):  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Tsh

Basal and TRH stimulated serum levels of TSH in patients with hyperprolactinaemia and in subjects on oestrogen treatment

1983 ◽  
Vol 102 (2) ◽  
pp. 173-178 ◽  
Author(s):  
Eva M. Erfurth ◽  
Pavo Hedner ◽  
Anders Nilsson
Keyword(s):  
Serum Level ◽  
Serum Levels ◽  
Plasma Prolactin ◽  
Thyroid Antibodies ◽  
Elevated Plasma ◽  
Oestrogen Treatment ◽  
Pituitary Dysfunction ◽  
Basal Serum ◽  
The Mean ◽  
Serum Tsh

Abstract. In 21 hyperprolactinaemic patients without other signs of pituitary dysfunction the mean basal serum level of TSH was 4.4 ± 0.47 μU/ml that was significantly (P < 0.001) higher than controls (2.5 ± 0.16 μU/ml and oestrogen treated individuals (2.4 ± 0.29 μU/ml). The TSH increase was more pronounced (P < 0.05) in hyperprolactinaemic patients without sellar enlargement and with moderately elevated plasma prolactin levels (155 ± 42 μg/ml) than in patients with sellar enlargement and higher plasma prolactin levels (857 ± 306 μg/ml). The serum levels of thyroxine and triiodothyronine in the hyperprolactinaemic patients did not differ significantly from controls. Patients with thyroid antibodies were excluded. The increased basal serum level of TSH in hyperprolactinaemia is compatible with the concept of a reduced dopaminergic tonus as the mechanism for both changes. In patients with advanced hyperprolactinaemia and sellar enlargement the high prolactin level may induce some inhibition of TSH release and explain their lower basal serum level of TSH that was probably not due to pituitary compression as they responded normally to TRH. The TSH response to TRH was significantly (P < 0.05) correlated to the basal serum TSH in all groups. The regression lines were very similar for hyperprolactinaemic patients and controls suggesting that in hyperprolactinaemia the thyrotroph has not changed its mode of response to TRH. In contrast, oestrogen treated subjects in addition to dependence on basal serum TSH levels showed a genuinely augmented response to TRH (164.6 ± 20.3%, P < 0.01) compared to controls.

ABNORMAL RESPONSE OF THYROTROPHIN AND GROWTH HORMONE TO THYROTROPHIN RELEASING HORMONE IN CHRONIC RENAL FAILURE

1975 ◽  
Vol 79 (4) ◽  
pp. 635-643 ◽  
Author(s):  
Koichi Hasegawa ◽  
Yoshiki Matsushita ◽  
Seima Otomo ◽  
Noboru Hamada ◽  
Yoshiki Nishizawa ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Healthy Subjects ◽  
Maximum Level ◽  
Serum Levels ◽  
Thyrotrophin Releasing Hormone ◽  
The Mean ◽  
Maximum Increment ◽  
Serum Gh ◽  
Serum Tsh

ABSTRACT Serum levels of TSH and GH were measured by radioimmunoassay after iv injection of 500 μg of TRH in 9 undialysed patients and 12 dialysed patients with chronic renal failure and in 6 healthy subjects. The basal level of the serum TSH was significantly higher in patients with chronic renal failure than that in healthy subjects. In healthy subjects, serum TSH rose to a maximum level 30 min after TRH injection, while in patients with chronic renal failure, serum TSH rose to a maximum level 60 min after TRH injection. The mean maximum increment of serum TSH in healthy subjects was significantly higher than that in patients with chronic renal failure. Although TSH levels rapidly decreased after initial rise at 30 min after TRH administration in healthy subjects, these did not show significant changes at 60 and 120 min compared with values at 30 min after TRH administration in both dialysed and undialysed patients. The basal level of serum GH was significantly higher in dialysed patients with chronic renal failure than in healthy subjects. Serum GH level was much higher in dialysed patients at 30 min after TRH injection compared with that in healthy subjects. These findings may indicate that the response of the pituitary to TRH is abnormal and that the turnover of TSH and GH is decreased in patients with chronic renal failure.

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