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

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.

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.


1971 ◽  
Vol 51 (3) ◽  
pp. 483-488 ◽  
Author(s):  
G. MILHAUD ◽  
P. RIVAILLE ◽  
M. S. MOUKHTAR ◽  
E. BINET ◽  
J. C. JOB

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.


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.


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.


1976 ◽  
Vol 81 (2) ◽  
pp. 252-262 ◽  
Author(s):  
P. Travaglini ◽  
P. Beck-Peccoz ◽  
C. Ferrari ◽  
B. Ambrosi ◽  
A. Paracchi ◽  
...  

ABSTRACT The secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyrotrophin (TSH) and prolactin (PRL, was studied in 17 women suffering from anorexia nervosa. The mean basal serum LH was reduced (8.4 ± 0.8 se mIU/ml; P < 0.001 vs normal controls), while LH increase after gonadotrophin-releasing hormone (LH-RH) appeared to be normal in 9 cases and impaired in 6 cases. The mean basal FSH did not significantly differ from normal subjects (3.9 ± 0.5 mIU/ml), while LH-RH administration elicited an exaggerated increase in 7 cases and a normal increase in 8 cases: the mean FSH response was significantly higher than in controls (P < 0.02). Plasma oestradiol-17β was reduced (20.4 ± 0.4 pg/ml; P < 0.001) while the serum testosterone levels were normal (0.73 ± 0.09 ng/ml). Clomiphene administration induced an increase in gonadotrophins in only 1 out of 7 patients. The mean serum TSH concentration was normal (2.3 ± 0.4 μU/ml), while serum thyroxine and triiodothyronine and free thyroxine index, though generally in the normal range, were significantly lower than values obtained in a control group (6.1 ± 0.4 μg/100 ml, P< 0.005; 102.3±7.7 ng/100 ml, P <0.005; 3.8±0.3, P < 0.05). Though the mean serum TSH increase after thyrotrophin-releasing hormone (TRH) was normal (12.0 ± 2.3 μU/ml), there were 4 impaired and 1 exaggerated increases, and 8 patients showed a delayed and frequently prolonged response. The increase in serum T3 after TRH appeared lower than in normal subjects (36.3 ± 1.8 ng/100 ml, P < 0.001). Serum PRL levels in basal conditions were higher than in the controls (19.4 ± 4.1 ng/ml, P < 0.001) while the increase in PRL after TRH was exaggerated in only 2 patients. The present data suggest that the primary failure in gonadotrophin secretion in anorexia nervosa occurs at hypothalamic level; moreover the data on TSH and PRL secretion also point to the existence of a hypothalamic disorder in this disease.


1982 ◽  
Vol 99 (4) ◽  
pp. 508-516 ◽  
Author(s):  
C. Marti Henneberg ◽  
J. M. Domenech ◽  
E. Montoya

Abstract. In order to study the hypothalamic-pituitarythyroid function in children with chronic renal failure (CRF), the serum levels of l-thyroxine (l-T4), l-triiodothyronine (l-T3), reverse T3 (rT3), thyrotrophin (TSH) and prolactin (Prl) were measured by radioimmunoassay (RIA). Values were compared with those of normal subjects. Low levels of l-T4 were present in CRF patients as compared to controls. l-T3 was also found to be low but less than l-T4, and rT3 was lower in patients with long evolution. No alterations were observed in TSH basal levels, whereas Prl values in patients were high. After thyrotrophin-releasing hormone (TRH) administration, TSH and Prl rose to similar levels in both groups, but high values were maintained throughout (120 min) in CRF. A significant negative correlation was found between the peak rise of the TSH response and the CRF evolution time. The l-T3 response to TRH administration (120 min) was similar in both CRF and controls. The rate of in vivo and in vitro exogenous TRH degradation was decreased in patients with CRF or by their sera, respectively. Our data seem to confirm that the hypothyroid syndrome described in CRF patients is of hypothalamic origin, and the low in vivo and in vitro TRH degradation rates are a consequence of this state.


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.


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


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