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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="en"><front><journal-meta><journal-id journal-id-type="publisher-id">rpcardio</journal-id><journal-title-group><journal-title xml:lang="en">Rational Pharmacotherapy in Cardiology</journal-title><trans-title-group xml:lang="ru"><trans-title>Рациональная Фармакотерапия в Кардиологии</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1819-6446</issn><issn pub-type="epub">2225-3653</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.20996/1819-6446-2009-5-2-49-54</article-id><article-id custom-type="elpub" pub-id-type="custom">rpcardio-619</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="en"><subject>ORIGINAL STUDIES</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group></article-categories><title-group><article-title>NEW PATHOGENIC MECHANISMS OF THE CHRONIC PERICARDITIS</article-title><trans-title-group xml:lang="ru"><trans-title>О НОВЫХ ЗВЕНЬЯХ ПАТОГЕНЕЗА ХРОНИЧЕСКОГО ПЕРИКАРДИТА</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кочмашева</surname><given-names>В. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kochmasheva</surname><given-names>V. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>620102 Екатеринбург, ул. Волгоградская, 185</p></bio><email xlink:type="simple">kochmasheva@okb1.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Рождественская</surname><given-names>Е. Д.</given-names></name><name name-style="western" xml:lang="en"><surname>Rozhdestvenskaya</surname><given-names>E. D.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кафедра терапии</p><p>620028 Екатеринбург, ул. Репина, 3</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Беликов</surname><given-names>Е. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Belikov</surname><given-names>E. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>620149 Екатеринбург, ул.Волгоградская, 185а</p></bio><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Дергунова</surname><given-names>М. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Dergunova</surname><given-names>M. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>620149 Екатеринбург, ул.Волгоградская, 185а</p></bio><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Архипов</surname><given-names>М. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Arhipov</surname><given-names>M. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кафедра терапии</p><p>620028 Екатеринбург, ул. Репина, 3</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>Свердловская областная клиническая больница №1</institution><country>Russian Federation</country></aff><aff xml:lang="ru" id="aff-2"><institution>Уральская государственная медицинская академия</institution><country>Russian Federation</country></aff><aff xml:lang="ru" id="aff-3"><institution>Свердловское областное патологоанатомическое бюро</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2009</year></pub-date><pub-date pub-type="epub"><day>08</day><month>01</month><year>2016</year></pub-date><volume>5</volume><issue>2</issue><fpage>49</fpage><lpage>54</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Kochmasheva V.V., Rozhdestvenskaya E.D., Belikov E.S., Dergunova M.A., Arhipov M.V., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Кочмашева В.В., Рождественская Е.Д., Беликов Е.С., Дергунова М.А., Архипов М.В.</copyright-holder><copyright-holder xml:lang="en">Kochmasheva V.V., Rozhdestvenskaya E.D., Belikov E.S., Dergunova M.A., Arhipov M.V.</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.rpcardio.online/jour/article/view/619">https://www.rpcardio.online/jour/article/view/619</self-uri><abstract><sec><title>Aim</title><p>Aim. To determine the main mechanisms of chronic pericarditis (CP) on the basis of chronic pericardium inflammation study with morphological, laboratory and instrumental methods.</p></sec><sec><title>Material and methods</title><p>Material and methods. 139 patients with CP were involved in the study. The analysis of clinical data, results of laboratory and instrumental examination as well as morphological data of 27 pericardectomies was performed.</p></sec><sec><title>Results</title><p>Results. The morphological features in 92,5% of cases did not depend on disease aetiology. Inflammation signs are founded in 74,1% of pericardium samples. Inflammatory reaction of adjacent fatty tissue and changes of the pericardium nervous system also was revealed. The levels of immune status markers in patients with CP significantly depended on inflammation activity and they did not depend on disease causes. Anti-inflammatory cytokine levels (receptor antagonist of IL-1 alpha (RAIL-1 alpha) above 700 pg/ml is founded in patients with subclinical disease feature. RAIL level below 300 pg/ml took place in serious and recurring CP.</p></sec><sec><title>Conclusion</title><p>Conclusion. CP is a result of pericardium inflammation with involving adjacent fatty tissue and with changes of the pericardium nervous system. Relationship between disease clinical course and RAIL-1 level was found. CP progression and new pathogenesis mechanisms is discussed. </p></sec></abstract><trans-abstract xml:lang="ru"><sec><title>Цель</title><p>Цель. Выделить ведущие механизмы формирования хронического перикардита (ХП) на основании изучения морфологической картины хронического воспаления серозной оболочки сердца, его лабораторных и инструментальных маркеров.</p></sec><sec><title>Материал и методы</title><p>Материал и методы. Проведен анализ клинических данных, результатов лабораторных и инструментальных методов исследования 139 больных c перикардитом и данных морфологического изучения материала, полученного в ходе 27 перикардэктомий.</p></sec><sec><title>Результаты</title><p>Результаты. Морфологическая картина ХП, по данным гистоморфологического изучения операционного материала, в 92,5% наблюдений не зависела от этиологии заболевания; признаки воспаления выявлены в 74,1% препаратов, причем обнаружена воспалительная реакция жировой клетчатки, прилежащей к перикарду, и изменения его нервного аппарата. Показатели иммунного статуса у больных перикардитом достоверно зависели от активности воспалительного процесса, но не от причины заболевания. Титры противовоспалительного цитокина – рецепторного антагониста интерлейкина-1 альфа (РАИЛ-1), превышающие 700 пг/мл, отмечены у больных с субклиническим течением заболевания, уровни РАИЛ-1 менее 300 пг/мл – при тяжелом, рецидивирующем течении ХП.</p></sec><sec><title>Заключение</title><p>Заключение. ХП является результатом воспаления серозной оболочки сердца, протекающего с вовлечением прилежащей жировой ткани и изменениями нервного аппарата перикарда. Выявлена взаимосвязь течения ХП с уровнями РАИЛ-1. Результаты исследования позволили детализировать процесс формирования ХП и охарактеризовать новые звенья патогенеза хронического воспаления серозной оболочки сердца.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>хронический перикардит</kwd><kwd>этиология</kwd><kwd>морфологические изменения</kwd><kwd>воспаление</kwd><kwd>интерлейкины</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic pericarditis</kwd><kwd>etiology</kwd><kwd>morphological changes</kwd><kwd>inflammation</kwd><kwd>interleukins</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Европейские рекомендации по диагностике и лечению заболеваний перикарда: методические рекомендации. Часть 1. Доказательная кардиология 2004;(3):19-32.</mixed-citation><mixed-citation xml:lang="en">Европейские рекомендации по диагностике и лечению заболеваний перикарда: методические рекомендации. Часть 1. 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