Decreased prolactin responsiveness to thyrotrophin-releasing hormone and metoclopramide in hyperthyroidism

1985 ◽  
Vol 110 (2) ◽  
pp. 221-226 ◽  
Author(s):  
Sven Röjdmark ◽  
Anders Carlsson

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.

1972 ◽  
Vol 71 (2) ◽  
pp. 209-225 ◽  
Author(s):  
G. Faglia ◽  
P. Beck-Peccoz ◽  
B. Ambrosi ◽  
C. Ferrari ◽  
P. Travaglini

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.


1975 ◽  
Vol 80 (1) ◽  
pp. 42-48 ◽  
Author(s):  
K. W. Wenzel ◽  
H. Meinhold ◽  
H. Schleusener

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.


1924 ◽  
Vol 39 (6) ◽  
pp. 931-955 ◽  
Author(s):  
A. Hiller ◽  
G. C. Linder ◽  
C. Lundsgaard ◽  
D. D. Van Slyke

Determinations of the plasma lipoids and of the respiratory quotient and total metabolism (Tissot method) have been performed with nephritics and normal subjects before and after they ingested fat in the proportion of 1 gm. per kilo body weight. After fat ingestion a greater increase of fatty acids and lecithin was noted in the plasma of nephritics with initially high blood lipoids than in the plasma of normal subjects or of nephritics without constant lipemia. In cholesterol no differences were found. The nephritic patients with constant lipemia were able to burn fat as efficiently as normal individuals. The accumulation of fat in their blood may be due to a disturbance in the mechanism for transferring lipoids from the blood to the tissue depots.


1950 ◽  
Vol 28e (3) ◽  
pp. 97-105
Author(s):  
M. C. Blanchaer ◽  
D. E. Bergsagel ◽  
Pamela Weiss ◽  
Dorothy E. Jefferson

The pyridine nucleotide content of the blood cells (PN/BG) of four normal individuals and five anemic patients was measured repeatedly before and after supplementing the diet with niacin. Daily doses of 50 mgm. nicotinic acid or nicotinamide failed to affect the values in the normal subjects and two well-nourished anemic patients. The same dose of nicotinic acid rapidly raised the PN/BC of three poorly nourished anemic patients to values approximating those of well-nourished subjects with similar degrees of anemia. The results obtained after saturation with niacin confirmed the previous report that the PN/BC is higher in anemic patients than in normal controls and that a negative correlation exists between the pyridine nucleotide values and the severity of the anemia. In spite of continued niacin therapy, correction of the anemia was accompanied by a gradual decrease in the values until they approached those of the normal subjects. The present findings also confirm the earlier report that changes in the PN/BC are apparently independent of moderate variations in the number of circulating leucocytes and reticulocytes and bear no relationship to the size or hemoglobin content of the red cells. The significance of these findings in relation to human niacin nutrition is discussed.


1987 ◽  
Vol 114 (2) ◽  
pp. 275-282 ◽  
Author(s):  
G. R. Rutteman ◽  
R. Stolp ◽  
A. Rijnberk ◽  
S. Loeffler ◽  
J. A. Bakker ◽  
...  

Abstract. Growth hormone (GH), prolactin (Prl) and cortisol secretion was studied in 5 ovariohysterectomized dogs before and after oestradiol implantation and medroxy-progesterone acetate (MPA) administration. MPA was given at regular intervals during a period of 10 months in a total of 12 injections. Short-term effects of oestradiol were restricted to significantly enhanced Prl responses to thyrotropin-releasing hormone (TRH). MPA treatment after oestradiol implantation resulted in significanly elevated basal GH levels in all dogs, with a continuing increase in one dog. Only in the latter dog was a significant decrease in basal Prl levels seen. MPA administration did not significantly change Prl responses to TRH. The GH responses to clonidine were significantly reduced at 9 and 16 weeks of oestradiol and MPA treatment. In the one dog which exhibited the greatest rise in basal GH levels, GH responses were completely abolished at 9, 16 and 43 weeks of oestradiol and MPA treatment. TRH never evoked significant GH responses. Both basal and lysine-vasopressin (LVP)-stimulated cortisol levels were significantly suppressed during combined oestradiol-MPA treatment. These findings denote that in the dog. 1) Oestradiol rapidly induces an enhanced Prl response to TRH. 2) The oestradiol-MPA induced GH overproduction is associated with a reduced responsiveness of GH to clonidine and is not accompanied by GH responsiveness to TRH. 3) Oestradiol-MPA treatment suppresses both basal and LVP-stimulated cortisol secretion.


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.


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.


1980 ◽  
Vol 94 (4) ◽  
pp. 450-458 ◽  
Author(s):  
Naguib A. Samaan ◽  
George E. Elhaj ◽  
Milam E. Leavens ◽  
Robert R. Franklin

Abstract. Twenty-six women, 16 to 40 years of age, with amenorrhoea with or without galactorrhoea and abnormal pituitary fossa tomogram were studied before and after transsphenoidal resection of their pituitary adenomas. The immunoreactive serum prolactin (Prl) was abnormally high both before and after intravenous (iv) administration of thyrotrophin-releasing hormone (TRH) but the rise was blunted. The serum Prl level returned to normal post-operatively in 20 patients, but the subnormal rise after TRH persisted in 23 patients. The basal serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were normal before and after surgery. The peak serum level of LH after administration of the luteinizing hormone-releasing hormone (LRH) was normal but the peak FSH was significantly high before surgery (P < 0.001) and returned to normal post-operatively. Plasma oestradiol (Oe2) was significantly low compared to that after surgery (P < 0.001). Plasma testosterone (T) was significantly higher before surgery than that found in normal women (P < 0.001) and the level fell post-operatively. Plasma androstenedione (A) was higher before surgery than found in normals, but the difference was not significant (P < 0.2). Post-operatively, 23 patients regained their normal menses. Three of these 23 patients continued to have high serum Prl but the serum Oe2 returned to normal. Sixteen of 20 patients who desired pregnancy became pregnant post-operatively. None of the patients required hormonal replacement after surgery. These data indicate that the measurement of LH or FSH at basal and after LRH stimulation, may not be of significant prognostic importance compared with serum Prl and plasma Oe2. Regular menses and pregnancy can occur in some patients in spite of moderately high serum Prl but normal plasma Oe2 levels. Surgical resection of prolactinoma has low morbidity with a high incidence of success resulting in return of normal menses and fertility. The persistent subnormal rise of Prl after TRH post-operatively in the majority of the patients suggests that long-term follow-up for evidence of recurrence is indicated.


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