scholarly journals Novel uses of thyroid hormones in cardiovascular conditions

Endocrine ◽  
2019 ◽  
Vol 66 (1) ◽  
pp. 115-123 ◽  
Author(s):  
Salman Razvi

Abstract Thyroid hormone levels are reduced in cardiovascular diseases and this phenomenon is associated with worse outcomes. It is unclear whether the changes in thyroid hormone bioavailability to the affected myocardium are beneficial or if this is a maladaptive response. Experimental studies from animal models of acute myocardial infarction (AMI) suggest that thyroid hormone treatment may be beneficial. There is limited data available on the use of thyroid hormones in patients with AMI and heart failure and this suggests that treatment to normalise thyroid hormone levels may be safe and potentially efficacious. Similarly, evidence of thyroid hormone therapy in patients undergoing cardiac surgery or during cardiac transplantation is limited. It is therefore difficult to draw any firm conclusions about benefits or risks of thyroid hormone treatment in these conditions. Large scale clinical trials of thyroid hormones in patients with cardiac conditions are required to confirm safety and evaluate efficacy. Furthermore, it needs to be elucidated which hormone to administer (thyroxine or triiodothyronine), when in the disease pathway to treat, dose of thyroid hormone to administer, and which parameters to utilise to assess safety and efficacy. Until these important questions are answered thyroid hormone therapy in cardiovascular diseases must remain within the research domain.

2020 ◽  
Vol 66 (3) ◽  
pp. 6-14
Author(s):  
Daniil V. Borisov ◽  
Diliara N. Gubaeva ◽  
Evgeniy A. Praskurnichiy

Cardiovascular diseases remain the leading cause of death all over the world. Thyroid hormones play a significant role in the regulation of cardiac function. According to a number of researches, patients with cardiovascular diseases usually have a decrease in the concentration of thyroid hormones in the blood serum, which may be associated with a poor prognosis. Today it still remains unclear whether the change in the bioavailability of thyroid hormones in the myocardium is a favorable physiological mechanism or a replication of an adaptation disorder. Experimental researches suggest that thyroid hormone therapy may be applied in clinical cardiology. This review describes the results of researches examining the use of thyroid hormones in patients with cardiovascular diseases, as well as experiment data on animal models. The available data on the use of thyroid hormones in patients with acute myocardial infarction and heart failure allow us to suggest that normalization of thyroid hormone levels is a safe and potentially effective treatment method in the group of patients with cardiovascular disease. At the same time, the data on the use of thyroid hormones in patients who have undergone an open-heart surgery or heart transplantation are limited. However, at present, it is difficult to draw unambiguous conclusions about the benefits, as well as about the possible risk of using thyroid hormones in the described conditions. Large-scale clinical researches are required to confirm the safety and evaluate the effectiveness of such therapy. Moreover, it is necessary to set parameters for evaluating the safety and effectiveness and understand which hormone (thyroxine or triiodothyronine), what dosage and at what stage of the disease should be applied. Until we do not have answers for these questions, thyroid hormone therapy in patients with cardiovascular diseases should remain within the research field.


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.


2005 ◽  
Vol 90 (12) ◽  
pp. 6498-6507 ◽  
Author(s):  
Robin P. Peeters ◽  
Serge van der Geyten ◽  
Pieter J. Wouters ◽  
Veerle M. Darras ◽  
Hans van Toor ◽  
...  

Context: Pronounced alterations in serum thyroid hormone levels occur during critical illness. T3 decreases and rT3 increases, the magnitudes of which are related to the severity of disease. It is unclear whether these changes are associated with decreased tissue T3 concentrations and, thus, reduced thyroid hormone bioactivity. Patients and Study Questions: We therefore investigated, in 79 patients who died after intensive care and who did or did not receive thyroid hormone treatment, whether total serum thyroid hormone levels correspond to tissue levels in liver and muscle. Furthermore, we investigated the relationship between tissue thyroid hormone levels, deiodinase activities, and monocarboxylate transporter 8 expression. Results: Tissue iodothyronine levels were positively correlated with serum levels, indicating that the decrease in serum T3 during illness is associated with decreased levels of tissue T3. Higher serum T3 levels in patients who received thyroid hormone treatment were accompanied by higher levels of liver and muscle T3, with evidence for tissue-specific regulation. Tissue rT3 and the T3/rT3 ratio were correlated with tissue deiodinase activities. Monocarboxylate transporter 8 expression was not related to the ratio of the serum over tissue concentration of the different iodothyronines. Conclusion: Our results suggest that, in addition to changes in the hypothalamus-pituitary-thyroid axis, tissue-specific mechanisms are involved in the reduced supply of bioactive thyroid hormone in critical illness.


Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 4218-4228 ◽  
Author(s):  
Yves Debaveye ◽  
Björn Ellger ◽  
Liese Mebis ◽  
Theo J. Visser ◽  
Veerle M. Darras ◽  
...  

To delineate the metabolic fate of thyroid hormone in prolonged critically ill rabbits, we investigated the impact of two dose regimes of thyroid hormone on plasma 3,3′-diiodothyronine (T2) and T4S, deiodinase type 1 (D1) and D3 activity, and tissue iodothyronine levels in liver and kidney, as compared with saline and TRH. D2-expressing tissues were ignored. The regimens comprised either substitution dose or a 3- to 5- fold higher dose of T4 and T3, either alone or combined, targeted to achieve plasma thyroid hormone levels obtained by TRH. Compared with healthy animals, saline-treated ill rabbits revealed lower plasma T3 (P = 0.006), hepatic T3 (P = 0.02), and hepatic D1 activity (P = 0.01). Substitution-dosed thyroid hormone therapy did not affect these changes except a further decline in plasma (P = 0.0006) and tissue T4 (P = 0.04). High-dosed thyroid hormone therapy elevated plasma and tissue iodothyronine levels and hepatic D1 activity, as did TRH. Changes in iodothyronine tissue levels mimicked changes in plasma. Tissue T3 and tissue T3/reverse T3 ratio correlated with deiodinase activities. Neither substitution- nor high-dose treatment altered plasma T2. Plasma T4S was increased only by T4 in high dose. We conclude that in prolonged critically ill rabbits, low plasma T3 levels were associated with low liver and kidney T3 levels. Restoration of plasma and liver and kidney tissue iodothyronine levels was not achieved by thyroid hormone in substitution dose but instead required severalfold this dose. This indicates thyroid hormone hypermetabolism, which in this model of critical illness is not entirely explained by deiodination or by sulfoconjugation.


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.


2020 ◽  
Vol 36 (5) ◽  
Author(s):  
Sabeen Nasir ◽  
Sara Ziaullah ◽  
Sadaf Alam ◽  
Muhammad Mumtaz Khan

Objectives: To study the morphological spectrum of endometrial changes with the thyroid hormone levels in infertile women. Methods: This cross sectional study was conducted at Department of Pathology, Peshawar Medical College, Health Care Centre and Madina Medical Laboratory, Peshawar from April 2013 to August 2013. Total 160 cases of infertile women were included in the study. Biopsies were taken on 22-23rd day of menstrual cycle. Statistical Analysis was performed using SPSS version 19 statistical program. Difference between endometrial findings of patients with normal thyroid profile and abnormal one were analyzed for statistical significance using Chi square test. Probability values p ≤ 0.05 were considered statistically significant. Results: In our study, majority infertile women were euthyroid (80%), followed by hyperthyroid (18%) and only two% to be hypothyroid. The correlation of endometrial morphology with thyroid hormones levels turned out to be insignificant. While correlating histological details of endometrial biopsy with thyroid hormone status, we found significant association of leukocytic infiltrate with thyroid hormone levels. Conclusion: This study shows that thyroid hormones may have role in early leukocytic infiltration into stroma, and a possibility of immune modulation by altered thyroid hormones in causing infertility. doi: https://doi.org/10.12669/pjms.36.5.1791 How to cite this:Nasir S, Ziaullah S, Alam S, Khan MM. Morphological spectrum of endometrium with thyroid hormone profile in infertile female population of Khyber Pakhtunkhwa province of Pakistan. Pak J Med Sci. 2020;36(5):---------. doi: https://doi.org/10.12669/pjms.36.5.1791 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


1974 ◽  
Vol 12 (8) ◽  
pp. 31-32

Thyrotrophin-releasing hormone (TRH - Roche) is a synthetic tripeptide, L-pyroglutamyl-L-histidyl-L-proline-amide, which is identical with the porcine, ovine and human hypothalamic hormone that promotes the secretion of thyrotrophin. Secreted in the hypothalamus, it passes down the capillaries of the pituitary stalk to the anterior pituitary and there causes release of thyrotrophin. Thyroid hormones (triiodo-thyronine (T3) and thyroxine (T4)) interfere with the thyrotrophin (TSH)-releasing action of TRH, so that excess thyroid hormones block TSH release in response to TRH; conversely when thyroid hormone levels are low, increased secretion of TSH occurs. The hypothalamic secretion of TRH is probably directly influenced by the concentration of thyroid hormones in the blood reaching it. In addition TRH promotes the secretion of prolactin from the pituitary. TRH-Roche is marketed in Britain for use in hospitals in diagnostic tests of thyroid and of pituitary-hypothalamic function.


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