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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/2079-701X-2022-16-23-216-223</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-7329</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ЭНДОКРИНОЛОГИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ENDOCRINOLOGY</subject></subj-group></article-categories><title-group><article-title>Физиологические эффекты тиреоидных гормонов в аспекте коморбидности и здорового долголетия</article-title><trans-title-group xml:lang="en"><trans-title>Physiological effects of thyroid hormones in the aspect of comorbidity and healthy longevity</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8520-8702</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Трошина</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Troshina</surname><given-names>E. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Трошина Екатерина Анатольевна - член-корреспондент РАН, доктор медицинских наук, профессор, заместитель директора – директор Института клинической эндокринологии.</p><p>117036, Москва, ул. Дмитрия Ульянова, д. 11</p></bio><bio xml:lang="en"><p>Ekaterina A. Troshina - Corr. Member RAS, Dr. Sci. (Med.), Professor, Deputy Director - Director of the Institute of Clinical Endocrinology, National Medical Research Center for Endocrinology.</p><p>11, Dmitry Ulyanov St., Moscow, 117036</p></bio><email xlink:type="simple">troshina@inbox.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6420-8674</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Терехова</surname><given-names>М. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Terekhova</surname><given-names>M. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Терехова Мария Александровна – студент.</p><p>119991, Москва, ул. Трубецкая, д. 8, стр. 2</p></bio><bio xml:lang="en"><p>Maria A. Terekhova - Student, Sechenov First Moscow State Medical University (Sechenov University).</p><p>8, Bldg. 2, Trubetskaya St., Moscow, 119991</p></bio><email xlink:type="simple">terexova@list.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр эндокринологии</institution><country>Россия</country></aff><aff xml:lang="en"><institution>National Medical Research Center for Endocrinology</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Первый Московский государственный медицинский университет имени И.М. Сеченова (Сеченовский Университет)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Sechenov First Moscow State Medical University (Sechenov University)</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>20</day><month>01</month><year>2023</year></pub-date><volume>0</volume><issue>23</issue><fpage>216</fpage><lpage>223</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Трошина Е.А., Терехова М.А., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Трошина Е.А., Терехова М.А.</copyright-holder><copyright-holder xml:lang="en">Troshina E.A., Terekhova M.A.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.med-sovet.pro/jour/article/view/7329">https://www.med-sovet.pro/jour/article/view/7329</self-uri><abstract><p>На сегодняшний день одни из первых позиций в структуре заболеваемости и смертности занимают неинфекционные заболевания, среди которых различные нарушения эндокринной системы играют решающую роль. Патология эндокринной системы ухудшает течение прочих заболеваний и является значимым неблагоприятным фактором в повышении смертности, в том числе от сердечно-сосудистых катастроф. В структуре эндокринных заболеваний патология щитовидной железы занимает 2-е место, причем за последние десятилетия отмечено увеличение заболеваемости и распространенности патологий щитовидной железы в старших возрастных группах. Тиреоидные гормоны снижают концентрацию холестерина, фосфолипидов и триглицеридов в плазме, при том что количество свободных жирных кислот может увеличиваться. И напротив, снижение секреции тиреоидных гормонов резко увеличивает концентрацию в плазме холестерина и фосфолипидов, а также почти всегда является причиной резкого увеличения отложения жира в печени. При наличии дислипидемии и артериальной гипертензии первичный гипотиреоз можно рассматривать как фактор риска развития атеросклероза и, соответственно, ишемической болезни сердца, особенно у лиц пожилого возраста. В условиях хронического дефицита йода ряд аутоиммунных факторов может играть существенную роль в развитии зоба. У больных с эндемическим зобом выявляют ферментные дефекты синтеза тиреоидных гормонов, что еще больше стимулирует аутоиммунную агрессию и дегенеративные изменения в щитовидной железе, приводя к постепенному снижению функциональной активности железы – гипотиреозу. Йододефицитные и аутоиммунные заболевания щитовидной железы нередко являются составляющими континуума коморбидности, что требует персонализации их лечения с учетом рисков взаимовлияний различных патологий.</p></abstract><trans-abstract xml:lang="en"><p>Currently, non-infectious diseases, among which various disorders of the endocrine system play a decisive role, occupy one of the first positions in the structure of morbidity and mortality. Endocrine pathology worsens the course of other diseases and is a significant adverse factor in increasing mortality, including cardiovascular accidents. Thyroid pathology ranks second in the structure of endocrine diseases, and an increase in the incidence and prevalence of thyroid pathology in older age groups has been noted in recent decades. Thyroid hormones reduce the concentration of cholesterol, phospholipids and triglycerides in the plasma, while the amount of free fatty acids may increase. Conversely, decreased secretion of thyroid hormones dramatically increases the plasma concentration of cholesterol and phospholipids, and is almost always the cause of a sharp increase in fat deposition in the liver. In the presence of dyslipidemia and arterial hypertension, primary hypothyroidism can be considered as a risk factor for atherosclerosis and, accordingly, ischemic heart disease, especially in the elderly. In conditions of chronic iodine deficiency, a number of autoimmune factors may play a significant role in goiter development. Patients with endemic goiter reveal enzymatic defects in the synthesis of thyroid hormones, which further stimulates autoimmune aggression and degenerative changes in the thyroid gland, leading to a gradual decrease in the functional activity of the gland – hypothyroidism. Iodine deficiency and autoimmune diseases of the thyroid gland are often components of a continuum of comorbidity, which requires personalization of their treatment, taking into account the risks of mutual influences of various pathologies.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>щитовидная железа</kwd><kwd>гипотиреоз</kwd><kwd>тиреотоксикоз</kwd><kwd>аутоиммунный тиреоидит</kwd><kwd>дефицит йода</kwd><kwd>метаболизм</kwd><kwd>тиреотропный гормон гипофиза</kwd><kwd>старение</kwd><kwd>левотироксин натрия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>thyroid</kwd><kwd>hypothyroidism</kwd><kwd>thyrotoxicosis</kwd><kwd>autoimmune thyroiditis</kwd><kwd>iodine deficiency</kwd><kwd>metabolism</kwd><kwd>thyroid hormone</kwd><kwd>aging</kwd><kwd>levothyroxine sodium</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование выполнено за счет средств госзадания «Эпидемиологические и молекулярно-клеточные характеристики опухолевых, аутоиммунных и йододефицитных тиреопатий как основа профилактики осложнений и персонализации лечения», Рег. №АААА-А20-120011790180-4.</funding-statement><funding-statement xml:lang="en">The study was funded by the state task “Epidemiological and molecular-cell characteristics of tumor, autoimmune and iodine deficiency thyreopathies as a basis for prevention of complications and personalization of treatment”, Registration: №АААА-А20-120011790180-4.</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Taylor P.N., Albrecht D., Scholz A., Gutierrez-Buey G., Lazarus J.H., Dayan C.M., Okosieme O.E. 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