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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">10.14412/1996-7012-2016-1-37-40</article-id><article-id custom-type="elpub" pub-id-type="custom">mrj-669</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>КЛИНИЧЕСКИЕ НАБЛЮДЕНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL OBSERVATIONS</subject></subj-group></article-categories><title-group><article-title>Выраженный и быстрый терапевтический эффект тофацитиниба в комбинации с подкожным метотрексатом у пациентки с ревматоидным артритом, имеющей факторы неблагоприятного прогноза, резистентной к стандартным базисным средствам и генно-инженерным биологическим препаратам (клинический случай)</article-title><trans-title-group xml:lang="en"><trans-title>The marked and rapid therapeutic effect of tofacitinib in combination with subcutaneous methotrexate in a rheumatoid arthritis patient with poor prognostic factors who is resistant to standard disease-modifying antirheumatic drugs and biologicals: A clinical case</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>Демидова</surname><given-names>Н. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Demidova</surname><given-names>N. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><email xlink:type="simple">natasha-demidova@mail.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>Лучихина</surname><given-names>Е. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Luchikhina</surname><given-names>E. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Каратеев</surname><given-names>Д. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Karateev</surname><given-names>D. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><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»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>24</day><month>03</month><year>2016</year></pub-date><volume>10</volume><issue>1</issue><fpage>37</fpage><lpage>40</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Демидова Н.В., Лучихина Е.Л., Каратеев Д.Е., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Демидова Н.В., Лучихина Е.Л., Каратеев Д.Е.</copyright-holder><copyright-holder xml:lang="en">Demidova N.V., Luchikhina E.L., Karateev D.E.</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/669">https://mrj.ima-press.net/mrj/article/view/669</self-uri><abstract><p>В настоящее время общепризнана необходимость достижения при ревматоидном артрите (РА) клинической ремиссии или как минимум низкой активности болезни. Представлено клиническое наблюдение пациентки с диагнозом РА, у которой наблюдались неэффективность стандартной базисной противовоспалительной терапии метотрексатом (МТ) в дозе 25 мг/нед, вторичная неэффективность ингибиторов фактора некроза опухоли α (адалимумаба) и неэффективность/плохая переносимость антагониста рецепторов интерлейкина 6 тоцилизумаба. Это определило необходимость назначения тофацитиниба (ТОФА) – препарата с другим механизмом действия. ТОФА – первое лекарственное средство из новой группы иммуномодулирующих и противовоспалительных препаратов, ингибиторов внутриклеточных киназ. На фоне терапии ТОФА была достигнута ремиссия заболевания, что дает основание рассматривать этот синтетический препарат как метод терапии, потенциально конкурирующий с терапией биологическими агентами.</p></abstract><trans-abstract xml:lang="en"><p>Today, it is generally accepted that it is necessary to achieve clinical remission in rheumatoid arthritis (RA) or as minimum a low disease activity. The paper describes a clinical case of a female patient diagnosed with RA who was observed to have inefficiency of standard disease-modifying antirheumatic therapy with methotrexate 25 mg/week, secondary inefficiency of tumor necrosis factor-α inhibitors (adalimumab), and inefficiency/poor tolerance of the interlukin-6 receptor antagonist tocilizumab. This determined the need to use fofacitinib (TOFA), a drug with another mechanism of action. TOFA is the first agent from a new group of immunomodulatory and anti-inflammatory drugs, intracellular kinase inhibitors. Disease remission could be achieved during therapy with TOFA, which enables one to consider this synthetic drug as a therapy option that potentially competes with therapy with biologicals.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ревматоидный артрит</kwd><kwd>генно-инженерные биологические препараты</kwd><kwd>ингибиторы JAK-киназ</kwd><kwd>тофацитиниб</kwd></kwd-group><kwd-group xml:lang="en"><kwd>rheumatoid arthritis</kwd><kwd>biologicals</kwd><kwd>JAK kinase inhibitors</kwd><kwd>tofacitinib</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">Smolen J, Aletaha D, Bijlsma JW, et al. Treating rheumatoid arthritis to target: recommendations of an international task force. Ann Rheum Dis. 2010 Apr;69(4):631-7. doi: 10.1136/ard.2009.123919. Epub 2010 Mar 9.</mixed-citation><mixed-citation xml:lang="en">Smolen J, Aletaha D, Bijlsma JW, et al. 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