INFLUENCE OF CHANGES IN THE LEVEL OF HORMONES OF THE THYROID GLAND ON ARTERIAL PRESSURE, REMODELING PROCESS OF MYOCARDIUM AND FUNCTIONING OF THE NERVOUS SYSTEM

Kostrikova Iu. A., Pustovoit A. L., Yarmola T. I., Tkachenko L. A., Talash V. V.

LITERATURE REVIEWS

Scentific article

The necessity for writing this article follows from the author’s own clinical experience. Counseling for therapeutic pathology in patients with a neurological profile, there was a tendency to ignore the study of the level of thyroid hormones in patients with arterial hypertension by family doctors, caused them to require constant correction of antihypertensive drugs, their frequent alteration and lack of effectiveness. Establishing a diagnosis of secondary arterial hypertension is unprecedented because it allows doctors to directly act on the cause of changes in blood pressure by normalizing hormonal status, while false diagnosis of essential hypertension leads to symptomatic use of antihypertensive drugs without affecting the etiological factor. There is also a lack of understanding by the patients of the essence of the thyroid gland pathology established in them, which indicates a low level of educational activities in this direction. Along with the problem of high blood pressure, a change in thyroid function is not new. However, in recent years there have been many reports of a deeper study of the effects of changes in hormone levels in thyroid hyperfunction and hypofunction on blood pressure, myocardial functional ability and the nervous system that are worthy of public attention, given the prevalence of both hypertension and thyroid disease. Differential treatment of secondary arterial hypertension of thyroid genesis is associated primarily with early prevention of lifethreatening complications (myocardial infarction, heart failure, stroke, nephrosclerosis), as well as changes in the central nervous system (dyscirculatory encephalopathy) in order to improve the quality of patient’s life. The determination of the functional ability of the thyroid gland in patients with therapeutic and neurological profiles should be included in the list of general clinical examination methods, since its change determines the course of comorbid pathology and worsens the prognosis. There is a need to study the clinical manifestations of changes in the level of thyroid hormones in patients with a therapeutic and neurological profile in order to gain a deeper understanding of the mechanisms of pathogenesis and to further develop diagnostic patterns and quickly correct existing conditions. A promising direction in medicine is the study of the functional state of the thyroid gland in patients with demyelinating diseases, taking into account their symptoms of pathology of the cardiovascular system, as well as lesions of the musculoskeletal system, renal pathology, pathology of the gastrointestinal tract. It is advisable to carry out active sanitary-educational work among patients with thyroid diseases, as well as work with family medicine doctors, general practitioners and neuropathologists in advanced training departments.

hyperthyroidism, hypothyroidism, arterial hypertension, myocardial remodeling, fibrosis.

1. Pankiv VI. YoddefItsitni zahvoryuvannya. Navchalniy posibnik. Chernivtsi: BDMA; 2001. 100 s. [in Ukrainian].
2. Contreras-Jurado C, García-Serrano L, Gómez-Ferrería M, Costa C, Paramio MY, Aranda A. The thyroid hormone receptors as modulators of skin proliferation and inflammation. J Biol Chem. 2011 Jul 8;286(27):24079-9. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC3129189/ DOI: 10.1074/jbc.M111.218487
3. Yao QY, Xu BL, Wang JY, Liu HC, Zhang SC, Tu CT. Inhibition by curcumin of multiple sites of the transforming growth factorbeta1 signalling pathway ameliorates the progression of liver fibrosis induced by carbon tetrachloride in rats. BMC Complement Altern Med. 2012 Sep;12(1):156. Available from: https://www.ncbi.nlm.nih.gov/pubmed/22978413 DOI: 10.1186/1472-6882-12-156
4. Cheng SY, Leonard JL, Davis PJ. Molecular aspects of thyroid hormone actions. EndocrRev. 2010;31(2):139-41. Available from: https://www. ncbi.nlm.nih.gov/pmc/articles/PMC2852208/ DOI: 10.1210/er.2009-0007
5. Gregory AB. Mechanisms of thyroid hormone actions. J Clin Invest. 2012 Sep 4;122(9):3035-8. Available from: https://www.ncbi.nlm.nih.gov/ pmc/articles/PMC3433956/ DOI: 10.1172/JCI60047
6. Ojamaa K. Signaling mechanisms in thyroid hormone-induced cardiac hypertrophy. Vascul Pharmacol. 2010 Mar–Apr;52(3-4):113-6.
7. Größl T, Hammer E, Bien-Möller S, Geisler A, Pinkert S, Röger C, et al. A novel artificial microrna expressing aav vector for phospholamban silencing in cardiomyocytes improves Ca2+ uptake into the sarcoplasmic reticulum. PLoS One. 2014;9(3):e92188. Available from: //www.ncbi. nlm.nih.gov/pmc/articles/PMC3966758/ DOI: 10.1371/journal.pone.0092188
8. Bianco AC, Anderson G, Forrest D, Galton VA, Gereben B, Kim BW, et al. Report of the American Thyroid Association task force on approaches and strategies to investigate thyroid hormone economy and action. Thyroid. 2014 Jan 1;24(1):88-168.
9. Von Hafe M, Neves JS, Vale C, Borges-Canha M, Leite-Moreira A. The impact of thyroid hormone dysfunction on ischemic heart disease. Endocr Connect. 2019 May;8(5):76-14.
10. Leo DL, Lee SY, Braverman EL. Hyperthyroidism. Lancet. 2016 Aug 27;388(10047):906-18.
11. Rentziou G, Saltiki K, Manios E, Stamatelopoulos K, Koroboki E, Vemmou A, et al. Effects of recombinant human thyrotropin administration on 24-hour arterial pressure in female undergoing evaluation for differentiated thyroid cancer. Int J Endocrinol. 2014 Aug 18:art.270213.
12. Abuzaid AS, Birch N. The controversies of hyponatraemia in hypothyroidism. Sultan Qaboos Univ Med J. 2015 May;15(2):207-15.
13. Katerenchuk VI, Beregova OP. Sertsevo-sudinni maski gipotireozu. Vnutrennyaya meditsina [Internet]. 2007. [tsitovano 2019 Cherv.25];3(3). Dostupno: www.internal.mif-ua.com [in Ukrainian].
14. Mazza A, Beltramello G, Armigliato M, Montemurro D, Zorzan S, Zuin M, et al. Arterial hypertension and thyroid disorders: What is important to know in clinical practice? Annales d’Endocrinologie. 2011 Sep;72(4):296-7.
15.  Spitzweg C, Reincke M. Thyroid diseases and hypertension. Internist (Berl). 2010 May;51(5):603-4.
16. Chopra S, Cherian D, Jacob JJ. The thyroid hormone, parathyroid hormone and vitamin D associated hypertension. Indian J Endocrinol Metab. 2011 Oct 15;l4:354-60. Available from: https://www.ncbi.nlm.nih.gov/pubmed/22145139 DOI: 10.4103/2230-8210.86979
17. Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev. 2014 Apr;94(2):355-82.
18. Gommeren K, van Hoek I, Lefebvre HP, Benchekroun G, Smets P, Daminet S. Effect of thyroxine supplementation on glomerular filtration rate in hypothyroid dogs. J Vet Intern Med. 2009;23:844-5.
19. Sedaghat K, Zahediasl S, Ghasemi A. The influence of thyroid states upon responses of the rat aorta to catecholamines. Gestational hypothyroidism-induced changes in L-type calcium channels of rat aorta smooth muscle and their impact on the responses to vasoconstrictors. IJBMS. 2015 Feb;18(2):172-7.
20. Liamis G, Filippatos TD, Liontos A, Elisaf MS. Hypothyroidism-associated hyponatremia: mechanisms, implications and treatment. EJE. 2017 Jun 27;176(1):15.
21. Razvi S, Jabbar A, Pingitore A, Danzi S, Biondi B, Klein I, et al. Thyroid hormones and cardiovascular function and diseases. JACC. 2018 Apr;71(16):1781-96.
22. Mourtzinis G, Adamsson Eryd S, Rosengren A, Björck L, Adiels M, Johannsson G, et al. Primary aldosteronism and thyroid disorders in atrial fibrillation: A Swedish nationwide case-control study. Eur J Prev Cardiol. 2018 May;25(7):694-7. Available from: https://www.ncbi.nlm.nih. gov/pubmed/29473461 DOI: 10.1177/2047487318759853
23. Pantos C, Mourouzis I, Cokkinos DV. New insights into the role of thyroid hormone in cardiacremodeling: time to reconsider? Heart Fail Rev. 2011 Jan;16(1):79-96. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20668933 DOI: 10.1007/s10741-010-9185-3
24. Makino A, Suarez J, Wang H, Belke DD, Scott BT, Dillmann WH. Thyroid hormone receptor-beta is associated with coronary angiogenesis during pathological cardiac hypertrophy. Endocrinology. 2009 Apr;150(4):2008-15.
25. Louzada RA, Carvalho DP. Similarities and differences in the peripheral actions of thyroid hormones and their metabolites. Front. Endocrinol. 2018 Jul 19;9:394.
26.  Pol CJ, Muller A, Zuidwijk MJ, Van Deel ED, Kaptein E, Saba A, et al. Left-ventricular remodeling after myocardial infarction is associated with a cardiomyocyte-specific hypothyroid condition. Endocrinol. 2011;152:669-79.
27. Cokkinos DV, Chryssanthopoulos S. Thyroid hormones and cardiac remodeling. Heart Fail Rev. 2016;21:365-72.
28. Chen J, Ortmeier SB, Savinova OV, Nareddy VB, Beyer AJ, Wang D, et al. Thyroid hormone induces sprouting angiogenesis in adult heart of hypothyroid mice through the PDGF-Akt pathway. J Cell Mol Med. 2012;16:2726-35.
29. Nehme A, Zouein FA, Zayeri ZD, Zibara K. An Update on the tissue renin angiotensin system and its role in physiology and pathology. J. Cardiovasc. Dev. Dis. 2019 March 29;6(14):1-17.
30. Komatsu Y, Waku T, Iwasaki N, Ono W, Yamaguchi C, Yanagisawa J. Global analysis of DNA methylation in early-stage liver fibrosis. BMC Med Genomics. 2012 Jan 27;5:5.
31. Pavlova TV, redaktor. Vliyanie patologii schitovidnoy zhelezyi na nervnuyu sistemu. Neyrokognitivnyiy status pri endemicheskih formah patologii schitovidnoy zhelezyi. Voprosyi epidemiologii, etiologii, klassifikatsii i morfogeneza zabolevaniy schitovidnoy zhelezyi. Belgorod; 2004. s. 39-58. [in Russian].
32. Usova NN. Yodsoderzhaschie tireoidnyie gormonyi i ih vliyanie na nervnuyu sistemu. Meditsinskie novosti. 2012;4:11-5. [in Russian].
33. Canepa C, Srinivasan R, Muhith A. Reversible and unilateral corticospinal tract disease secondary to autoimmune free-T3-thyrotoxicosis. BMJ Case Rep. 2017 Aug 7:1-6.

«Bulletin of problems biology and medicine» Issue 2 Part 2 (151), 2019 year, 49-53 pages, index UDK 616.12-008.331.1:616.127-005.8

10.29254/2077-4214-2019-2-2-151-49-53