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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">pulmo</journal-id><journal-title-group><journal-title xml:lang="ru">Пульмонология</journal-title><trans-title-group xml:lang="en"><trans-title>PULMONOLOGIYA</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0869-0189</issn><issn pub-type="epub">2541-9617</issn><publisher><publisher-name>Scientific and Practical Journal “PULMONOLOGIYA” LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18093/0869-0189-2015-25-4-425-432</article-id><article-id custom-type="elpub" pub-id-type="custom">pulmo-599</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>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL STUDIES</subject></subj-group></article-categories><title-group><article-title>Генетические особенности у больных гриппом А / H1N1 / 09, осложненным пневмонией</article-title><trans-title-group xml:lang="en"><trans-title>Genetic features of patients with influenza A / H1N1 / 09 complicated by pneumonia</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>Романова</surname><given-names>Е. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Romanova</surname><given-names>E. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д. м. н., профессор кафедры госпитальной терапии и эндокринологии ГБОУ ВПО "Читинская государственная медицинская академия" Минздрава России; тел.: (924) 5760299</p></bio><bio xml:lang="en"><p>MD, Professor at Department of Hospital Internal Medicine and Endocrinology, Chita State Medical Academy, Healthcare Ministry of Russia; tel.: (924) 5760299</p></bio><email xlink:type="simple">elenarchita@yandex.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>Говорин</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Govorin</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д. м. н., профессор, зав. кафедрой факультетской терапии ГБОУ ВПО "Читинская государственная медицинская академия" Минздрава России, тел.: (3022) 354324, факс: (3022) 323058</p></bio><bio xml:lang="en"><p>MD, Professor, Head of Department of General Internal Medicine; Chita State Medical Academy, Healthcare Ministry of Russia; tel.: (3022) 354324, fax: (3022) 323058</p></bio><email xlink:type="simple">pochta@medacadem.chita.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ГБОУ ВПО "Читинская государственная медицинская академия" Минздрава России: 672020, Чита, ул. Горького 39А</institution><country>Россия</country></aff><aff xml:lang="en"><institution>State Institution "Chita State Medical Academy", Healthcare Ministry of Russia: 39A, Gor'kogo str., Chita, 672090, Russia</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>21</day><month>10</month><year>2015</year></pub-date><volume>25</volume><issue>4</issue><fpage>425</fpage><lpage>432</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Романова Е.Н., Говорин А.В., 2015</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="ru">Романова Е.Н., Говорин А.В.</copyright-holder><copyright-holder xml:lang="en">Romanova E.N., Govorin A.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://journal.pulmonology.ru/pulm/article/view/599">https://journal.pulmonology.ru/pulm/article/view/599</self-uri><abstract><p>Целью исследования явилось выявление особенностей полиморфизмов генов цитокинов (фактор некроза опухоли – TNF G308A, интерлейкины – IL 10 C592A, IL 10 C819T, IL 10 G1082A), гена регуляторной молекулы воспаления (CD14 C159T) и регуляции сосудистого тонуса (еNOS C786T) у пациентов с гриппом A / H1N1, осложненном пневмонией.</p><sec><title>Материалы и методы</title><p>Материалы и методы. Обследованы пациенты, находившиеся на лечении по поводу пневмонии на фоне гриппа А / H1N1 / 09: 1я группа (n = 37) – с тяжелыми пневмониями; 2я (n = 74) – с нетяжелыми пневмониями; 3я (n = 115) – здоровые лица. Молекулярно-генетическое исследование проводилось методом полимеразной цепной реакции. У больных гриппом А / H1N1, осложненным пневмонией, чаще встречалось гомозиготное носительство аллели G полиморфизма (308 G/A) гена TNF по сравнению с контрольной группой. У заболевших значительно преобладала G аллель гена IL10 (1082 G/A), преимущественно в виде гомозиготного носительства. У пациентов с гриппозными пневмониями превалировала С аллель гена IL 10 (592 C/A), в большей степени в виде гомозиготного варианта. Гомозиготное носительство гена IL 10 (819 C/Т) Т/Т и гена CD14 (159 C/Т) Т/Т оказалось значительно ниже по сравнению с группой здоровых лиц. Установлено преобладание гомозиготы Т/Т полиморфизма (786 C/Т) гена еNOS среди заболевших гриппозной пневмонией.</p></sec><sec><title>Результаты</title><p>Результаты. Прогностическими факторами риска развития пневмонии у больных гриппом А / H1N1 явились полиморфизмы гена IL 10 592 CС, 819 CС, 1082 GG. Наибольшее значение в прогнозировании тяжелого течения пневмонии при гриппе А / H1N1 имеют гаплотипы TNF (308 GG); IL 10 (819 CC); (1082 GG). В качестве предикторов развития острого повреждения легких / острого респираторного дистресс синдрома и летального исхода у больных гриппом А / H1N1 / 09 выявлены гаплотипы TNF (308 GG); IL 10 (819 CC); (1082 GG) и TNF (308 GG); IL 10 (819 CC); (1082 GG); CD14 (159 CС) соответственно.</p></sec><sec><title>Заключение</title><p>Заключение. Изучение генетического статуса пациента при гриппе А / H1N1 позволит оценивать тяжесть заболевания и прогнозировать возможные осложнения.</p></sec></abstract><trans-abstract xml:lang="en"><p>The aim of this study was to investigate polymorphisms of cytokine genes (TNF G308A, IL 10 C592A, IL 10 C819T, IL 10 G1082A), and molecular regulation of inflammation (CD14 C159T) and vascular tone (еNOS C786T) in patients with A / H1N1 flu complicated by pneumonia.</p><sec><title>Methods</title><p>Methods. Patients hospitalized for pneumonia complicating influenza A / H1N1 / 09 were involved in the study: 37 patients with severe pneumonia, 74 patients with non severe pneumonia and 115 healthy subjects as controls. Polymerase chain reaction (PCR) was used for molecular investigations.</p></sec><sec><title>Results</title><p>Results. Patients with influenza A / H1N1 complicated by pneumonia carried the homozygous G allele of TNF gene polymorphism (308 G/A) and the homozygous G allele of IL 10 gene polymorphism (1082 G/A) more often compared with controls. Patients with pneumonia more often carried IL 10 gene 592 C/A allele and largely as homozygous variant. Frequencies of homozygous IL 10 gene polymorphism (819 C/T) T/T and CD14 gene polymorphism (159 C/T) T/T were significantly lower compared with healthy subjects. On contrary, the homozygous T/T polymorphism (786 C/T) of еNOS gene was more common in patients with pneumonia. Prognostic risk factors for occurrence of pneumonia in patients with influenza А / H1N1 were IL 10 gene polymorphisms 592 CC, 819 CC, and 1082 GG. TNF (308 GG); IL 10 (819 CC) and (1082 GG) haplotypes had the highest prognostic value for severe pneumonia in patients with influenza A / H1N1. TNF (308 GG); IL 10 (819 CC); (1082 GG) and TNF (308 GG); IL 10 (819 CC); (1082 GG) and CD14 (159 CC) haplotypes predicted ARDS and death in patients with influenza A / H1N1 / 09, respectively.</p></sec><sec><title>Conclusion</title><p>Conclusion. Identifying genetic status in a patient with influenza A / H1N1 could predict severity and complications of the disease.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>грипп А / H1N1</kwd><kwd>пневмония</kwd><kwd>полиморфизм генов</kwd><kwd>цитокины</kwd><kwd>эндотелиальная NO синтаза.</kwd></kwd-group><kwd-group xml:lang="en"><kwd>influenza A / H1N1</kwd><kwd>pneumonia</kwd><kwd>polymorphism</kwd><kwd>cytokines</kwd><kwd>endothelial NO synthase</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">Kolobukhina L.V., Merkulova L.N., Shchelkanov M.Yu. et al. 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