Effects of methimazole treatment on growth hormone (GH) response to GH-releasing hormone in patients with hyperthyroidism

1990 ◽  
Vol 123 (6) ◽  
pp. 613-618 ◽  
Author(s):  
Andrea Giustina ◽  
Carlo Ferrari ◽  
Corrado Bodini ◽  
Maria Grazia Buffoli ◽  
Fabio Legati ◽  
...  

Abstract. In vitro studies have demonstrated that thyroid hormones can enhance basal and stimulated growth hormone secretion by cultured pituitary cells. However, both in man and in the rat the effects of high thyroid hormone levels on GH secretion are unclear. The aim of our study was to test the GH response to human GHRH in hyperthyroid patients and to evaluate the effects on GH secretion of short- and long-term pharmacological decrease of circulating thyroid hormones. We examined 10 hyperthyroid patients with recent diagnosis of Graves' disease. Twelve healthy volunteers served as controls. All subjects received a bolus iv injection of GHRH(1-29)NH2, 100 μg. Hyperthyroid patients underwent a GHRH test one and three months after starting antithyroid therapy with methimazole, 10 mg/day po. GH levels at 15, 30, 45, 60 min and GH peak after stimulus were significantly lower in hyperthyroid patients than in normal subjects. The GH peak was also delayed in hyperthyroid patients. After one month of methimazole therapy, most of the hyperthyroid patients had thyroid hormone levels in the normal range, but they did not show significant changes in GH levels after GHRH, and the GH peak was again delayed. After three months of therapy with methimazole, the hyperthyroid patients did not show a further significant decrease in serum thyroid hormone levels. However, mean GH levels from 15 to 60 min were significantly increased compared with the control study. The GH peak after GHRH was also earlier than in the pretreatment study. In conclusion, the GH response to GHRH is inhibited and delayed by hyperthyroidism and returns to the normal pattern after long-term euthyroidism has been achieved with methimazole.

Endocrinology ◽  
1998 ◽  
Vol 139 (2) ◽  
pp. 474-478 ◽  
Author(s):  
Charles C. Gregory ◽  
Carlton E. Dean ◽  
Tom E. Porter

Abstract The importance of thyroid hormone from embryonic through neonatal life has been documented in both avian and mammalian species. However, the regulation of thyroid hormone production during this period is not completely understood. The objective of this study was to characterize expression of chicken TSHβ messenger RNA (mRNA) compared with that of thyroid hormones and GH in embryonic and neonatal chickens. Total pituitary RNA was extracted on embryonic days (e-) 11, 13, 15, 17, and 19 and neonatal days (d-) 1, 3, 6, 9, and 12 and subjected to ribonuclease protection assays (RPA) for chicken TSHβ mRNA. TSHβ mRNA levels increased through e-19, with e-19 levels being greater than those at all other embryonic ages (P < 0.05). Levels decreased markedly on d-1, then slowly increased to d-6 and stayed elevated through d-12. RIAs were performed for T4, T3, and GH at the same ages. Serum T4 levels increased slowly from less than 1.0 ng/ml on e-11 to a peak of 6.6 ng/ml on d-1 (P < 0.05). After the peak on d-1, posthatch T4 levels stabilized between 3.5–4.5 ng/ml through d-12 (P < 0.05). T3 concentrations were less than 0.25 ng/ml on e-11, increased dramatically between e-19 and d-1 (P < 0.05), and remained high throughout the rest of the experiment, with a concentration of 3.25 ng/ml on d-6 (P < 0.05). GH levels for e-11 through e-17 were below the sensitivity of the GH RIA. On e-19, the GH level was 3 ng/ml and continued to increase through d-12 to a level of 130 ng/ml. As thyroid hormone levels were preceded by maximal TSHβ mRNA levels on e-19, we next determined whether TSHβ gene expression on e-19 was under TRH and T3 regulation. E-19 anterior pituitary cells were cultured in serum-free medium with either TRH (10−8) or T3 (10−8) for 20–24 h. Treatment with T3 significantly decreased levels of TSHβ mRNA (P < 0.05). However, TRH did not produce a significant increase in TSHβ mRNA, although TRH did increase TSHβ mRNA by 60%, on the average, in this study. Therefore, these results indicate that an increase in pituitary TSH production probably regulates thyroid hormone levels during late embryonic development and that negative feedback inhibition of TSH production by thyroid hormones also exists at this critical developmental stage.


Author(s):  
J H Parr

Serum concentration of free T3 and, in female patients, FT4, were found to be lower in 20 asymptomatic, moderately-poor or well controlled, diabetics treated with insulin than in a group of non-diabetic subjects. Over a mean 3-month period of the study a significant fall occurred in HbA1 concentration in both groups of diabetics without change in free thyroid hormone levels. The mean capillary blood glucose, fasting free insulin and fasting lipid concentrations, other than high density lipoprotein (HDL) cholesterol, did not change. No correlations were found between the changes in HbA1 and free thyroid hormone concentrations. Improvement in long term metabolic control did not influence free thyroid hormone levels in well controlled and moderately-poor controlled diabetics, taking insulin.


2003 ◽  
Vol 81 (9) ◽  
pp. 890-893 ◽  
Author(s):  
Jörg W Wegener ◽  
Matthias Lee ◽  
Franz Hofmann

Thyroid hormones are known to influence various processes of cell differentiation. Recently, it was reported that hypothyroidism reduces the sensitivity to Ca2+-channel antagonists in the rat uterus. We examined the sensitivity to dihydropyridines of the uterus from mice that had reduced thyroid hormone levels. Isradipine relaxed with the same potency precontracted uterine muscle strips from control and hypothyroid mice, independently from a pseudo-pregnant state. These results demonstrate that hypothyroidism does not change dihydropyridine sensitivity (i.e., the pattern of Ca2+-channel expression) in the murine uterus.Key words: uterus, smooth muscle, Ca2+ channel, isradipine.


2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Carmen Freire ◽  
Rosalina Koifman ◽  
Paula Sarcinelli ◽  
Ana Cristina Rosa ◽  
Ruth Clapauch ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Shariq Rashid Masoodi ◽  
Rameesa Batul ◽  
Khurram Maqbool ◽  
Amir Zahoor ◽  
Mona Sood ◽  
...  

Abstract BACKGROUND: The association between thyroid dysfunction and postoperative mortality is contentious. Thyroid function is frequently depressed during and after cardiopulmonary bypass surgical procedures, and this may adversely affect myocardial performance and postop outcome.OBJECTIVES: To study i) the changes and clinical significance of serum thyroid hormones during cardiopulmonary bypass (CPB), and ii) the association between biochemically assessed peri-op thyroid function and 30-day mortality after CBPSTUDY DESIGN: Prospective Cohort StudySUBJECTS: 279 patients undergoing various cardiac surgeries under cardiopulmonary bypass.METHODS: All consenting patients undergoing open heart surgery in last five years at a tertiary care centre in North-India were studied. The thyroid hormone levels (Total T3, T4 and TSH) were measured before admission, and postoperatively on Day 1 & 7, and 3 months following surgery. The patients’ gender, age, weight, body mass index, heart disease details, previous cardiac surgeries, and cardiac surgery-related data such as pump time, aortic clamping time, hypothermia duration, postoperative hemodynamic status and postoperative use of inotropic drugs were recorded and analysed. Patients were classified as having biochemically overt or subclinical hyperthyroidism or hypothyroidism, normal thyroid function, or non-classifiable state based on preoperative thyroid-stimulating hormone and total T4 values. Outcome data were collected from hospital records. Biochemical thyroid dysfunction was not systematically treated. Outcomes measured were length of ICU stay, postoperative complications and 30-day mortality.RESULTS: There was significant changes in thyroid function in patients undergoing cardiopulmonary bypass surgery (Fig 1). All patients showed a decrease in T3, T4 and TSH after surgery. Post-op complications were observed in 137 patients (49%) most common being atrial fibrillation (34%) followed by acute kidney injury (23%), infections (18%), dyselectrolytemia (7%), bleeding (1.4%) and ARDS (1.4%). Of 263 patients followed, eventually 26 patients expired with a mortality rate of 8.89% (95% CI, 0.4 - 19.4). Perioperatively, there was a significant correlation between 30-day with type of surgery (r, 0.26), aortic clamp time (r, 0.45), CBP time (r, 0.48), number of inotropes used (r, 0.57), hours of mechanical ventilation (r, 0.4), ICU stay (r, 0.13) and post-op complications (r, 0.24), as well as with the reduction in the thyroid hormone levels; 17 (7%), 3 (20%) and 6 (46%) patients of those with pre-op TSH level of <6.5, >6.5 and >10.5 mIU/L expired (p <0.001).CONCLUSION: Pre-op thyroid dysfunction is associated with increased mortality in patients undergoing cardiac surgery with CBP. Excess mortality with elevated serum TSH levels suggests the importance of timely detection and intervention in individuals with thyroid dysfunction undergoing cardiac surgery.Table of Contents oTable 1. Characteristics of patients who expired versus those who survived cardiac surgery with cardiopulmonary bypass (CPB) oFig 1. Changes in serum thyroid hormones during CPB surgery oTable 1. Characteristics of patients who expired versus those who survived cardiac surgery with cardiopulmonary bypass (CPB) oFigures in parenthesis indicate ±Standard Deviation, unless indicated otherwise oFig 1. Changes in serum thyroid hormones during CPB surgery


2005 ◽  
Vol 288 (5) ◽  
pp. R1264-R1272 ◽  
Author(s):  
Samantha J. Richardson ◽  
Julie A. Monk ◽  
Caroline A. Shepherdley ◽  
Lars O. E. Ebbesson ◽  
Frank Sin ◽  
...  

Thyroid hormones are essential for vertebrate development. There is a characteristic rise in thyroid hormone levels in blood during critical periods of thyroid hormone-regulated development. Thyroid hormones are lipophilic compounds, which readily partition from an aqueous environment into a lipid environment. Thyroid hormone distributor proteins are required to ensure adequate distribution of thyroid hormones, throughout the aqueous environment of the blood, and to counteract the avid partitioning of thyroid hormones into the lipid environment of cell membranes. In human blood, these proteins are albumin, transthyretin and thyroxine-binding globulin. We analyzed the developmental profile of thyroid hormone distributor proteins in serum from a representative of each order of marsupials ( M. eugenii; S.crassicaudata), a reptile ( C. porosus), in two species of salmonoid fishes ( S. salar; O. tshawytsch), and throughout a calendar year for sea bream ( S. aurata). We demonstrated that during development, these animals have a thyroid hormone distributor protein present in their blood which is not present in the adult blood. At least in mammals, this additional protein has higher affinity for thyroid hormones than the thyroid hormone distributor proteins in the blood of the adult. In fish, reptile and polyprotodont marsupial, this protein was transthyretin. In a diprotodont marsupial, it was thyroxine-binding globulin. We propose an hypothesis that an augmented thyroid hormone distributor protein network contributes to the rise in total thyroid hormone levels in the blood during development.


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