THE EFFECTS OF A SYNTHETIC THYROTROPHIN RELEASING HORMONE (TRH) IN NORMAL AND ENDOCRINOPATHIC SUBJECTS

1972 ◽  
Vol 71 (2) ◽  
pp. 209-225 ◽  
Author(s):  
G. Faglia ◽  
P. Beck-Peccoz ◽  
B. Ambrosi ◽  
C. Ferrari ◽  
P. Travaglini
Keyword(s):  
Oral Administration ◽  
Standard Dose ◽  
Poor Response ◽  
Normal Subjects ◽  
Graves Disease ◽  
Pituitary Tumours ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Secondary Hypothyroidism ◽  
Normal Increase

ABSTRACT The effects of thyrotrophin releasing hormone (TRH) on plasma thyrotrophin (HTSH), thyroxine iodine (T4-I), growth hormone (HGH) and cortisol were studied in healthy and endocrinopathic subjects. In normal subjects rapid iv injection of 100, 200, 400, 600, 800 μg of TRH caused definite increases in plasma HTSH with a dose-response correlation between 100 and 200 μg; the peak occurred at 20–30 min at any dose level; iv infusion of 1000 μg over 30 min was followed by highly variable rises in plasma HTSH; the oral administration of 20 mg caused a definite and prolonged increase. In endocrinopathic subjects a standard dose of 600 μg of TRH was rapidly iv injected: 5 euthyroid patients with high 131I thyroidal uptake showed a normal increase in HTSH; 10 cases of Graves' disease, 5 of hyperactive adenomas as well as 4 normal subjects pre-treated with triiodothyronine showed no response; out of 5 cases of Graves' disease re-investigated after remission 3 showed no response, while 2 had an exaggerated response; 5 cases of primary myxoedema showed a very marked and prolonged response; out of 2 patients with idiopathic secondary hypothyroidism 1 did not respond at all and 1 showed a large and prolonged increase with a late peak; out of 4 cases of secondary hypothyroidism due to pituitary tumours, 2 gave normal responses, 1 showed a very marked and prolonged rise and 1 had a poor response; the same subject, after selective adenomectomy, however, had an exaggerated response; 12 euthyroid patients with pituitary tumours were examined: 3 did not respond at all, 4 had a normal increase in plasma HTSH and 5 gave a prolonged and exaggerated response. The serum T4-I showed an upward trend after TRH iv; however, the increase was not present in all instances. After oral administration of TRH a more definite increase was reached. It was demonstrated that TRH does not promote the release of HGH and ACTH.

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.

SOME ASPECTS OF HYPOTHALAMIC-PITUITARY FUNCTION IN PATIENTS WITH ANOREXIA NERVOSA

1976 ◽  
Vol 81 (2) ◽  
pp. 252-262 ◽  
Author(s):  
P. Travaglini ◽  
P. Beck-Peccoz ◽  
C. Ferrari ◽  
B. Ambrosi ◽  
A. Paracchi ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Serum Testosterone ◽  
Normal Subjects ◽  
Control Group ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Mean ◽  
Normal Increase ◽  
Lh Rh ◽  
Serum Tsh

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.

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.

FAILURE OF PITUITARY RESPONSE TO THYROTROPHIN-RELEASING HORMONE IN EUTHYROID GRAVES' DISEASE

The Lancet ◽  
1971 ◽  
Vol 298 (7714) ◽  
pp. 14-16 ◽  
Author(s):  
N.F. Lawton ◽  
R.P. Ekins ◽  
J.D.N. Nabarro
Keyword(s):  
Graves Disease ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

EFFECT OF SYNTHETIC THYROTROPHIN-RELEASING FACTOR ON PITUITARY TSH SECRETION IN NORMAL SUBJECTS AND PATIENTS WITH HYPOTHALAMIC-PITUITARY DISORDERS

1973 ◽  
Vol 73 (2) ◽  
pp. 233-249 ◽  
Author(s):  
Makoto Otsuki ◽  
Hidetaro Mori ◽  
Shigeaki Baba ◽  
Naohisa Hiroshige
Keyword(s):  
Normal Subjects ◽  
Pituitary Insufficiency ◽  
Tumour Invasion ◽  
Secondary Hypothyroidism ◽  
Chromophobe Adenoma ◽  
Tsh Secretion ◽  
Normal Increase ◽  
The Stability ◽  
Slow Intravenous Infusion ◽  
Different Doses

ABSTRACT Different doses of thyrotrophin-releasing factor (TRF) were administered by three different routes (intravenous, subcutaneous and oral) to 87 normal subjects in order to standardize the "TRF test" for the pituitary TSH reserve. The results were: 1) Intravenous single injection may be suitable as a routine TRF test because of the stability of TSH response to TRF and the reliability of TRF administration. 2) The maximum TSH increases were dose-related between 50 and 400 μg, so that we can recommend the use of 50 μg of TRF as a screening test for TSH secretion. 3) Oral administration and slow intravenous infusion of TRF with estimation of thyroxine levels can be useful as an indirect test of pituitary TSH reserve when TSH assays are not available. According to these results, the TRF test was performed in patients with hypothalamic-pituitary disorders. A normal increase in plasma TSH occurred in 10 out of 20 patients with operated pituitary chromophobe adenoma following the administration of 50 or 100 μg of TRF. Two patients showed no rise in plasma TSH after receiving 50 or 100 μg of TRF but a normal rise after receiving 400 or 600 μg of TRF. Little or no rise in the plasma TSH levels occurred following the administration of 100 μg TRF in pituitary chromophobe adenoma and Sheehan's syndrome who had a long standing pituitary insufficiency and secondary hypothyroidism. However, some cases with craniopharyngioma and pinealoma, accompanied with a low level of thyroid function, showed a normal TSH responses to 50 μg of TRF. Since the pituitary of these cases remained intact from tumour invasion, they should be assumed to have tertiary (hypothalamic) hypothyroidism. Of particular interest is the fact that the patients with suprahypophyseal tumour surprisingly showed a supernormal TSH response to 50 μg of TRF.

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.

Thyrotrophin-releasing hormone responsiveness and degradation in children with chronic renal failure: effect of time of evolution

1982 ◽  
Vol 99 (4) ◽  
pp. 508-516 ◽  
Author(s):  
C. Marti Henneberg ◽  
J. M. Domenech ◽  
E. Montoya
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Normal Subjects ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Degradation Rates

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.

INFLUENCE OF ANAESTHETICS ON BASAL, PERPHENAZINE-INDUCED AND THYROTROPHIN RELEASING HORMONE-INDUCED PROLACTIN SECRETION IN OVARIECTOMIZED, OESTROGEN-TREATED RATS

1975 ◽  
Vol 66 (2) ◽  
pp. 151-157 ◽  
Author(s):  
D. M. LAWSON ◽  
R. R. GALA
Keyword(s):  
Central Nervous System ◽  
Anterior Pituitary ◽  
Chloral Hydrate ◽  
Direct Action ◽  
Prolactin Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Site Of Action ◽  
The Central Nervous System ◽  
Normal Increase

SUMMARY Plasma levels of prolactin were determined, by radioimmunoassay, in ovariectomized, oestrogen-treated rats after administration of ether, sodium pentobarbitone, urethane, chloral hydrate or ketamine. These anaesthetics, when administered alone, induced sustained increases in the plasma level of prolactin (continuous ether inhalation), no change in prolactin secretion (urethane), or depressions in the level of prolactin (sodium pentobarbitone, chloral hydrate and ketamine). These same anaesthetics when given before perphenazine failed to alter the stimulatory effect of this phenothiazine on prolactin secretion. Sodium pentobarbitone did not alter the normal increase in prolactin concentration after intra-arterial administration of synthetic thyrotrophin releasing hormone (TRH). These results indicated that anaesthetics do not affect the response of either the central nervous system or the anterior pituitary to perphenazine or TRH although they affect prolactin secretion when administered alone. The site of action of anaesthetics must, therefore, be different from that of perphenazine or perphenazine must be capable of overcoming their influence by direct action on the pituitary.

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