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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">mrj</journal-id><journal-title-group><journal-title xml:lang="ru">Современная ревматология</journal-title><trans-title-group xml:lang="en"><trans-title>Modern Rheumatology Journal</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1996-7012</issn><issn pub-type="epub">2310-158X</issn><publisher><publisher-name>IMA-PRESS, LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/1996-7012-2014-3-23-27</article-id><article-id custom-type="elpub" pub-id-type="custom">mrj-556</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 INVESTIGATIONS</subject></subj-group></article-categories><title-group><article-title>Сахарный диабет и гипергликемия у больных ревматоидным артритом</article-title><trans-title-group xml:lang="en"><trans-title>Diabetes mellitus and hyperglycemia in patients with rheumatoid arthritis</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>Кондратьева</surname><given-names>Л. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kondratyeva</surname><given-names>L. V.</given-names></name></name-alternatives><email xlink:type="simple">kondratyeva.liubov@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>Панафидина</surname><given-names>Т. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Panafidina</surname><given-names>T. A.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Герасимова</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Gerasimova</surname><given-names>E. V.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Горбунова</surname><given-names>Ю. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Gorbunova</surname><given-names>Yu. N.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Попкова</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Popkova</surname><given-names>T. V.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Насонов</surname><given-names>Е. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Nasonov</surname><given-names>E. L.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой», Москва, Россия&#13;
115552, Москва, Каширское ш., 34А</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology, Moscow, Russia 34A, Kashirskoe Shosse, Moscow 115522</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2014</year></pub-date><pub-date pub-type="epub"><day>22</day><month>09</month><year>2014</year></pub-date><volume>8</volume><issue>3</issue><fpage>23</fpage><lpage>27</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Кондратьева Л.В., Панафидина Т.А., Герасимова Е.В., Горбунова Ю.Н., Попкова Т.В., Насонов Е.Л., 2014</copyright-statement><copyright-year>2014</copyright-year><copyright-holder xml:lang="ru">Кондратьева Л.В., Панафидина Т.А., Герасимова Е.В., Горбунова Ю.Н., Попкова Т.В., Насонов Е.Л.</copyright-holder><copyright-holder xml:lang="en">Kondratyeva L.V., Panafidina T.A., Gerasimova E.V., Gorbunova Y.N., Popkova T.V., Nasonov E.L.</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://mrj.ima-press.net/mrj/article/view/556">https://mrj.ima-press.net/mrj/article/view/556</self-uri><abstract><p>Провоспалительные цитокины, участвующие в патогенезе ревматоидного артрита (РА), способны тормозить продукцию инсулина и вызывать инсулинорезистентность периферических тканей. Возможно, при РА увеличивается риск развития нарушений углеводного обмена (НУО): сахарного диабета (СД), гипергликемии натощак (ГН), нарушения толерантности к глюкозе. Больные с сочетанием РА и СД относятся к категории наиболее тяжелых пациентов с неблагоприятным прогнозом макро- и микрососудистых осложнений.</p><p>Цель исследования – оценить частоту НУО (СД и ГН) в когорте пациентов с РА и их возможное влияние на течение артрита.</p><sec><title>Материал и методы</title><p>Материал и методы. В исследование было включено 165 пациентов (28 мужчин, 137 женщин), средний возраст – 55 [47; 61] лет, наблюдающихся в ФГБНУ НИИР им. В.А.Насоновой с диагнозом РА. Серопозитивными по ревматоидному фактору были 86,3% больных, по антителам к циклическому цитруллинированному пептиду – 78,8%. Активность РА была низкой у 29,1% пациентов, умеренной – у 48,5%, высокой – у 22,4%. Глюкокортикоиды (ГК) получали 40,6% больных (в средней дозе 5 [5; 7,5] мг/сут), метотрексат – 72,7%, лефлуномид 8,5%, генно-инженерные биологические препараты – 23,7%. Проводили опрос пациентов для выявления осведомленности о наличии НУО и исследование уровня глюкозы натощак в венозной плазме для скрининга гипергликемии. Измеряли рост и массу тела пациентов, рассчитывали индекс массы тела (ИМТ).</p></sec><sec><title>Результаты исследования</title><p>Результаты исследования. НУО имелись у 21 (12,7%) из 165 пациентов с РА. Только 11 (6,7%) из 165 пациентов с РА знали о наличии у них СД (2 случая СД 1-го типа, 9 случаев СД 2-го типа), у оставшихся 10 больных НУО (у 8 больных – ГН, у 2 – СД 2-го типа) обнаружены при лабораторном обследовании. Пациенты с СД и ГН имели большое число болезненных суставов (ЧБС), более высокие оценку общего состояния здоровья пациента (ООЗП) и DAS28, чем больные с нормогликемией, но не отличались по длительности РА, уровню острофазовых показателей (СОЭ, СРБ), числу припухших суставов. Избыточная масса тела отмечена у 57 (34,5%), ожирение – у 39 (23,6%) пациентов. На фоне приема ГК уровень глюкозы был ниже (5,1 [4,7; 5,5]), чем у больных без ГК-терапии (5,4 [5,0; 5,9] ммоль/л, p=0,001), и коррелировал с ИМТ (r=0,3, p=0,01).</p></sec><sec><title>Заключение</title><p>Заключение. Продемонстрированы большая частота СД и ГН при РА, низкая осведомленность о них больных, а также взаимосвязь НУО с активностью артрита, преимущественно за счет изменения субъективных показателей (ООЗП, ЧБС). На уровень глюкозы в крови при РА могут оказывать влияние прием ГК и ИМТ.</p></sec></abstract><trans-abstract xml:lang="en"><p>Proinflammatory cytokines involved in the pathogenesis of rheumatoid arthritis (RA) are able to inhibit the production of insulin and to cause insulin resistance in peripheral tissues. Conceivably RA increases the risk of developing carbohydrate metabolic disturbances (CMDs), such as diabetes mellitus (DM), fasting hyperglycemia (FH), and impaired glucose tolerance. Patients with a concurrence of RA and DM belong to a category of the most critically ill patients with a poor prognosis of macro- and microvascular complications.</p><sec><title>Objective</title><p>Objective: to estimate the rate of CMDs (DM and FH) in a cohort of patients with RA and their possible impact on the course of arthritis.</p></sec><sec><title>Subjects and methods</title><p>Subjects and methods. The investigation enrolled 165 patients (28 men and 137 women) aged 55 [47; 61] years who were diagnosed with RA and followed up at the V.A. Nasonova Research Institute of Rheumatology. The patients who were seropositive for rheumatoid factor and anti-cyclic citrullinated peptide antibodies were 86.3 and 78.8%, respectively. RA activity was low in 29.1% of the patients, moderate in 48.5%, and high in 22.4%. Glucocorticoids (GC) were taken at a mean dose of 5 [5; 7.5] mg/day by 40.6% of the patients; methotrexate, leflunomide, and genetically engineered biological agents were used by 72.7, 8.5, and 23.7%, respectively. A survey was conducted among the patients to find out their awareness of the presence of CMDs and fasting venous plasma glucose levels were determined to screen for hyperglycemia. Height and weight were measured and body mass index (BMI) was calculated.</p></sec><sec><title>Results</title><p>Results. CMDs were present in 21 (12.7%) of the 165 patients with RA. Only 11 (6.7%) of the 165 patients were aware of having DM (2 cases with type 1 DM and 9 with type 2 DM); laboratory tests revealed CMDs in the remaining 10 patients (8 cases with FH and 2 with type 2 DM). The patients with DM and FH had a large number of tender joints (TJN) and high scores of general health survey (GHS) and DAS28 than those with normal blood glycose levels, but did not differ in RA duration, acute-phase indicators (erythrocyte sedimentation rate, C-reactive protein), and the number of swollen joints. Fifty-seven (34.5%) patients were overweight and 39 (23.6%) were obese. In the patients who took GC, glucose levels were lower (5.1 [4.7; 5.5]) than in those who did not (5.4 [5.0; 5.9] mmol/l; p = 0.001) and correlated with BMI ((r = 0.3; p = 0.01).</p></sec><sec><title>Conclusion</title><p>Conclusion. The investigation demonstrated the high rate of DM and FH in RA, but low patient awareness of these conditions, as well as the relationship of CMDs to arthritis activity mainly due to the changes of subjective indices (GHS and TJN). The intake of GC and BMI may affect blood glucose levels in RA.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>ревматоидный артрит</kwd><kwd>нарушения углеводного обмена</kwd><kwd>сахарный диабет</kwd><kwd>гипергликемия натощак</kwd><kwd>индекс массы тела.</kwd></kwd-group><kwd-group xml:lang="en"><kwd>rheumatoid arthritis</kwd><kwd>carbohydrate metabolic disturbances</kwd><kwd>diabetes mellitus</kwd><kwd>fasting hyperglycemia</kwd><kwd>body mass index.</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">Насонов ЕЛ, Каратеев ДЕ. 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