Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with streak gonad syndrome

1983 ◽  
Vol 102 (2) ◽  
pp. 179-184 ◽  
Author(s):  
P. Bösze ◽  
Zs. Kóvacs ◽  
J. Egyed ◽  
J. László ◽  
G. Szilágyi

Abstract. Plasma TSH and Prl responses to iv TRH (200 μg) were studied in 21 euthyroid patients with streak gonad syndrome which is characterised by high levels of FSH and LH and low level of oestrogen and in 9 healthy women. The syndrome is associated with a variety of chromosome complements. Basal TSH and Prl responses to TRH were normal in patients with streak gonads irrespective of their chromosomal complements. Peak levels of both the TSH and Prl occurred at 15–30 min following TRH. The data might suggest that in hypergonadotrophic oestrogen deficiency neither the TSH nor the Prl response to TRH are attenuated. It does not seem that the associated chromosome anomalies alter the TSH and Prl responses to TRH in euthyroid affected patients.

1986 ◽  
Vol 111 (1) ◽  
pp. 10-16 ◽  
Author(s):  
Antti Kauppila ◽  
Jorma Heikkinen ◽  
Lasse Viinikka

Abstract. We evaluated the clinical applicability of a 2-h test in which the prolactin (Prl) responses to thyrotrophin releasing hormone (TRH) (200 μg iv) and the dopamine antagonist, metoclopramide (MC; 10 mg iv) were studied successively, 1 h apart. Nine healthy women were studied with TRH-MC test and with another test in which MC alone was used or the drugs were given in opposite order. The preceding TRH injection did not affect the Prl responses to MC, nor did preceding MC affect the Prl response to TRH. With the TRH-MC test, Prl responses to TRH and MC were significantly lowered in amenorrhoea (N = 8) and hyperprolactinaemia (N = 15) regardless of whether or not treated with bromocriptine, and to MC only in oligomenorrhoea (n = 11). In normoprolactinaemic galactorrhoea (N = 7) the responses were similar as in healthy women. The ratio between Prl responses to TRH and MC was significantly higher in women with bromocriptine-treated hyperprolactinaemia (1.06 ± 0.8, so) than in healthy controls (0.34 ± 0.13). The capacity of pituitary lactotrophs to secrete Prl in response TRH and MC can be evaluated with a 2-h test which has potential for investigation of pituitary Prl dynamics in gynaecological endocrine disorders, particularly in amenorrhoea and hyperprolactinaemia.


1981 ◽  
Vol 98 (3) ◽  
pp. 451-455 ◽  
Author(s):  
Olavi Ylikorkala ◽  
Seppo Kivinen ◽  
Lasse Viinikka

Abstract. The regulation of prolactin (Prl) and thyrotrophin (TSH) secretions during early human gestation was studied in 30 healthy women. Twelve women were treated with oral sulpiride, 150 mg daily for two weeks, and the Prl and TSH responses to 220 μg of iv thyrotrophin-releasing hormone (TRH) were measured before and at the end of sulpiride administration. Eight women were given 200 mg of sulpiride im, and 4 of them received 200 μg of TRH 30 min later. In 4 women the order of the TRH and sulpiride injections was reversed. Six women were studied as controls. Oral sulpiride treatment induced a significant Prl elevation from 14.6 ± 1.8 μg/l (mean ± sem) to 83.0 ± 4.0 μg/l, whereas the mean TSH levels did not change. Before sulpiride intake, TRH caused a mean maximal increment of 42.9 ± 4.7 μg/l in the Prl levels and an increment of 5.6 ± 0.9 IU/l in the TSH levels. During sulpiride administration, TRH caused a mean maximal increment of 16.5 ± 4.7 μg/l in the Prl levels and 3.5 ± 0.6 IU/l in the TSH levels. Both responses were significantly smaller (P < 0.001) during the sulpiride treatment than before. Intramuscular injection of sulpiride raised the mean Prl concentration by 282 ± 32 μg/l (P < 0.001) and the mean TSH concentration by 0.5 ± 0.1 IU/l (P < 0.05). The Prl elevation was 502 ± 109 μg/l when sulpiride was injected after TRH. A preceding im sulpiride injection caused no changes in Prl and TSH responses to TRH. These results show that in addition to Prl also TSH secretion is partially controlled by the dopaminergic system during early human pregnancy.


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 68 (2) ◽  
pp. 363-366 ◽  
Author(s):  
W. Wildmeister ◽  
F. A. Horster

ABSTRACT Gold-fishes (carassius auratus) were injected with synthetic thyrotrophin releasing hormone (TRH) in concentrations of 25 μg to 1000 μg/fish. TRH did not provoke endocrine exophthalmos.


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.


2002 ◽  
pp. 323-332 ◽  
Author(s):  
A Sartorio ◽  
G De Nicolao ◽  
D Liberati

OBJECTIVE: The quantitative assessment of gland responsiveness to exogenous stimuli is typically carried out using the peak value of the hormone concentrations in plasma, the area under its curve (AUC), or through deconvolution analysis. However, none of these methods is satisfactory, due to either sensitivity to measurement errors or various sources of bias. The objective was to introduce and validate an easy-to-compute responsiveness index, robust in the face of measurement errors and interindividual variability of kinetics parameters. DESIGN: The new method has been tested on responsiveness tests for the six pituitary hormones (using GH-releasing hormone, thyrotrophin-releasing hormone, gonadotrophin-releasing hormone and corticotrophin-releasing hormone as secretagogues), for a total of 174 tests. Hormone concentrations were assayed in six to eight samples between -30 min and 120 min from the stimulus. METHODS: An easy-to-compute direct formula has been worked out to assess the 'stimulated AUC', that is the part of the AUC of the response curve depending on the stimulus, as opposed to pre- and post-stimulus spontaneous secretion. The weights of the formula have been reported for the six pituitary hormones and some popular sampling protocols. RESULTS AND CONCLUSIONS: The new index is less sensitive to measurement error than the peak value. Moreover, it provides results that cannot be obtained from a simple scaling of either the peak value or the standard AUC. Future studies are needed to show whether the reduced sensitivity to measurement error and the proportionality to the amount of released hormone render the stimulated AUC indeed a valid alternative to the peak value for the diagnosis of the different pathophysiological states, such as, for instance, GH deficits.


The Lancet ◽  
1975 ◽  
Vol 305 (7899) ◽  
pp. 162 ◽  
Author(s):  
R. Hall ◽  
P.R. Hunter ◽  
J.S. Price ◽  
C.Q. Mountjoy

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