PARTIAL FAILURE OF ANTERIOR PITUITARY AND THYROID PRESENTING AS MYXOEDEMA

1975 ◽  
Vol 79 (4) ◽  
pp. 688-690
Author(s):  
A. D. Toft ◽  
W. J. Irvine

ABSTRACT The development of a sensitive radioimmunoassay of plasma thyrotrophin (TSH) and the isolation and synthesis of thyrotrophin-releasing hormone (TRH) allows a precise evaluation of the disordered brain-thyroid axis. The present report describes a patient who presented with myxoedema due to partial failure of both the anterior pituitary and the thyroid gland. The degree of impaired function of either gland alone would not have caused her clinical presentation.

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.


1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).


1985 ◽  
Vol 109 (4) ◽  
pp. 499-504 ◽  
Author(s):  
E. Iversen ◽  
P. Laurberg

Abstract. Recently we found small amounts of TRH immunoreactivity in the thyroid gland of dogs and pigs. In the present study we investigated if exogenous TRH influences the release of T4, T3 and cAMP from the follicular cells, and calcitonin and somatostatin from the C-cells of perfused dog thyroid lobes. 10−5 mol/l TRH inhibited the TSH induced iodothyronine and cAMP release from the thyroid while 10−8 mol/l TRH had no effect. The relative proportions of T4 and T3 in thyroid secretion were not altered by TRH infusion. TRH did not influence the basal or the Ca++ induced release of somatostatin and calcitonin. Hence TRH has a direct inhibitory effect on the hormone secretion from thyroidal follicular cells. This opens the possibility that TRH in the thyroid participate in the regulation of thyroid hormone secretion. Even though the concentration of TRH found to be effective is high our results may indicate that TRH in the thyroid participates in the regulation of thyroid hormone secretion as an antagonist to TSH.


1985 ◽  
Vol 107 (1) ◽  
pp. 83-87 ◽  
Author(s):  
L. Persson ◽  
M. Nilsson ◽  
E. Rosengren

ABSTRACT The biosynthesis of polyamines, an ubiquitous group of amines shown to be essential for normal cellular growth and differentiation, was studied in the rat anterior pituitary gland during the different stages of the oestrous cycle. The activity of ornithine decarboxylase (ODC), which catalyses the rate-limiting step in the biosynthesis of polyamines, was low during oestrus, metoestrus and dioestrus. However, a marked transitory rise in ODC activity was found in the pituitary gland on the evening of pro-oestrus. The rise in ODC activity was accompanied by an increase in the pituitary content of the polyamines putrescine and spermidine. Ovariectomy did not significantly change the basal ODC activity in the pituitary gland. Oestrogen treatment of ovariectomized rats resulted in a marked stimulation of pituitary polyamine biosynthesis. The largest effects were observed when oestrogen was given as two injections 72 h apart, which gave rise to levels of ODC activity comparable to those observed on the evening of pro-oestrus. The increase in polyamine synthesis in the anterior pituitary gland during pro-oestrus appeared not to be related to the preovulatory secretion of LH or prolactin, since neither LH-releasing hormone nor thyrotrophin-releasing hormone (which induces a secretion of prolactin) affected pituitary ODC activity. The observed biosynthesis of polyamines may be associated with the cellular proliferation which occurs in the anterior pituitary gland at oestrus. J. Endocr. (1985) 107, 83–87


1983 ◽  
Vol 102 (4) ◽  
pp. 481-485 ◽  
Author(s):  
Sven Röjdmark

Abstract. The responsiveness of anterior pituitary lactotrophs and thyrotrophs to cimetidine (Cim) was investigated in healthy volunteers. Four-hundred mg Cim, injected iv, raised the serum prolactin level (Prl) from 14 ± 2 to 58 ± 9 ng/ml (P < 0.001), but left the serum thyrotrophin level (TSH) unaffected. Acute hypercalcaemia, induced by iv infusion of calcium, blunted this Cim-elicited Prl response by 35 ± 4% (P < 0.01). Iv injection of 25 μg thyrotrophin-releasing hormone (TRH) had similar Prl-releasing potency as 400 mg Cim, and raised the Prl level from 14 ± 1 to 51 ± 6 ng/ml (P < 0.001). In contrast to Cim, TRH also increased the TSH level significantly. Although oral pre-treatment with Cim for 3 days (1000 mg/day) failed to affect the Prl response to TRH in this study, iv injection of the drug more than doubled the above mentioned Prl response to TRH. The TSH response to TRH remained unaffected both by oral and by iv administration of Cim. These results imply that acute changes in serum calcium affect the release pattern of Prl, and that iv administration of Cim may add Prl-releasing power to TRH in healthy individuals.


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.


1978 ◽  
Vol 12 (2) ◽  
pp. 114-119 ◽  
Author(s):  
K. M. TAYLOR ◽  
G. S. WRIGHT ◽  
W. F. BREMNER ◽  
W. H. BAIN ◽  
P. K. CAVES ◽  
...  

1984 ◽  
Vol 103 (2) ◽  
pp. 165-171 ◽  
Author(s):  
M. Mori ◽  
M. Murakami ◽  
T. Iriuchijima ◽  
H. Ishihara ◽  
I. Kobayashi ◽  
...  

ABSTRACT An influence of thyrotrophin-releasing hormone (TRH) on TSH heterogeneity in close association with de-novo biosynthesis was studied in rat anterior pituitary glands. Hemipituitary glands from adult male rats were incubated in Krebs–Henseleit–glucose media containing [3H]glucosamine and [14C]alanine for 3 and 6 h in the presence or absence of 10 ng TRH per ml. Fractions of TSH in the pituitary extracts were obtained using affinity chromatography coupled with an anti-rat TSH globulin. These TSH fractions were analysed by isoelectric focusing. The control pituitary glands were composed of four component peaks (isoelectric point (pI) 8·7, 7·8, 5·3 and 2·5) of [3H]glucosamine and [14C]alanine incorporated into TSH, and the amounts of radioactivity of these components were increased with the incubation time. Of these peaks, radioactive components of pI 8·7 and 7·8 coincided with the non-radioactive TSH components measured by radioimmunoassay. Addition of TRH increased incorporation of [14C]alanine into TSH in each of the components to a greater extent than that of [3H]glucosamine. In addition, new components with pI 7·2, 6·5 and 6·2, each component corresponding to each unlabelled TSH component, were demonstrated in the presence of TRH. Because addition of TRH did not change the amounts of [14C]alanine-labelled TSH in the media, the newly formed components were assumed to be connected with protein synthesis occurring in the anterior pituitary gland, which may be specific substances in response to TRH administration. These results indicate that TRH principally elicits an increase in protein synthesis in TSH at the anterior pituitary level, resulting in an alteration of TSH heterogeneity. J. Endocr. (1984) 103, 165–171


1992 ◽  
Vol 132 (1) ◽  
pp. 93-100 ◽  
Author(s):  
R. Peeters ◽  
N. Buys ◽  
D. Vanmontfort ◽  
J. Van Isterdael ◽  
E. Decuypere ◽  
...  

ABSTRACT The influence of TRH and TSH injections on plasma concentrations of tri-iodothyronine (T3) and thyroxine (T4) was investigated in neonatal (injection within 0·5 h after delivery) and growing lambs and in normal, pregnant and lactating adult ewes (all 2 years old and originating from Suffolk, Milksheep and Texal cross-breeds). Neonatal lambs had higher levels of T3, T4 and GH compared with all other groups, whereas prolactin and TSH were higher in lactating ewes. In all animals, injections of TRH increased plasma concentrations of prolactin and TSH after 15 min but not of GH at any time. Small increases in T3 and T4 were observed in neonatal lambs, without any effect on the T3 and T4 ratio, after prolactin administration, whereas prolactin did not influence plasma concentrations of T3 or T4 in all other experimental groups. Similar results for thyroid hormones were obtained after TRH or TSH injections. It was therefore concluded that the effects observed after TRH challenge were mediated by the release of TSH. With the possible exception of neonatal lambs, plasma concentrations of T3 after administration of TRH or TSH were always increased before those of T4; the increase in T3 occurred within 0·5–1 h compared with 2–4 h for T4 in all experimental groups. This resulted in an increased ratio of plasma T3 to T4 up to 4 h after injection. It is concluded that, in sheep, TRH and TSH preferentially release T3 from the thyroid gland probably by a stimulatory effect of TSH on the intrathyroidal conversion of T3 to T4. Journal of Endocrinology (1992) 132, 93–100


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