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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">10.14412/1996-7012-2025-6-48-55</article-id><article-id custom-type="elpub" pub-id-type="custom">mrj-1878</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>Периферическая артериальная болезнь в ревматологии</article-title><trans-title-group xml:lang="en"><trans-title>Peripheral arterial disease in rheumatology</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-5781-2964</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Середавкина</surname><given-names>Н. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Seredavkina</surname><given-names>N. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Наталия Валерьевна Середавкина</p><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>Nataliya Valerievna Seredavkina</p><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><email xlink:type="simple">n_seredavkina@mail.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/0000-0003-3552-2522</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Решетняк</surname><given-names>Т. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Rheshetnyak</surname><given-names>T. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А; 125993, Москва, ул. Баррикадная, 2/1, стр. 1</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522; 2/1, Barrikadnaya Street, Build. 1, Moscow 125993</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4285-0869</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Глухова</surname><given-names>С. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Glukhova</surname><given-names>S. I.</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"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6068-3080</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Лила</surname><given-names>А. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Lila</surname><given-names>A. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А; 125993, Москва, ул. Баррикадная, 2/1, стр. 1</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522; 2/1, Barrikadnaya Street, Build. 1, Moscow 125993</p></bio><xref ref-type="aff" rid="aff-2"/></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><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»; ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology; Russian Medical Academy of Continuing Professional Education, Ministry of Health of Russia</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>22</day><month>12</month><year>2025</year></pub-date><volume>19</volume><issue>6</issue><fpage>48</fpage><lpage>55</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Середавкина Н.В., Решетняк Т.М., Глухова С.И., Лила А.М., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Середавкина Н.В., Решетняк Т.М., Глухова С.И., Лила А.М.</copyright-holder><copyright-holder xml:lang="en">Seredavkina N.V., Rheshetnyak T.M., Glukhova S.I., Lila A.M.</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/1878">https://mrj.ima-press.net/mrj/article/view/1878</self-uri><abstract><p>Цель исследования – оценить частоту поражения сосудов по типу облитерирующего тромбангиита (ОТ) и его взаимосвязь с клинико-лабораторными проявлениями у больных системной красной волчанкой (СКВ) и антифосфолипидным синдромом (АФС).</p><sec><title>Материал и методы</title><p>Материал и методы. В исследование включено 172 пациента (30 мужчин и 142 женщины): 22 (13%) с изолированным «первичным» АФС (ПАФС), 66 (38%) с СКВ и 84 (49%) с СКВ + АФС. Медиана возраста составила 36 [30; 46] лет. Длительность болезни в группе СКВ + АФС была больше, чем в группах ПАФС и СКВ (медиана – соответственно 17 [9; 21]; 5 [2; 13] и 7 [3; 12] лет; р&lt;0,05). Все пациенты находились на стационарном лечении в ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой» в связи с обострением основного заболевания и прошли комплексное обследование.</p></sec><sec><title>Результаты и обсуждение</title><p>Результаты и обсуждение. Поражение сосудов по типу ОТ было зарегистрировано у 17 (10%) из 172 пациентов: 1 с ПАФС, 13 с СКВ + АФС и 3 с СКВ. На развитие ОТ у больных СКВ + АФС влияли следующие факторы: дислипидемия (отношение шансов, ОШ 10,74; 95% доверительный интервал, ДИ 3,29–34,99; р&lt;0,01), артериальная гипертензия (ОШ 7,19; 95% ДИ 1,98–26,07; р&lt;0,01) и синдром Рейно (ОШ 7,72; 95% ДИ 2,61–22,82, р&lt;0,01). В результате многофакторного анализа получена прогностическая модель, согласно которой число асептических некрозов костей, число язв голеней за весь срок заболевания, тип тромбоза, длительность АФС, дебют заболевания с признаков АФС, сетчатое ливедо, повышенные уровни IgG-антител к кардиолипину, к β2-гликопротеину 1, общего холестерина, СРБ и увеличение числа лейкоцитов ассоциируются с большей вероятностью развития ОТ у больных СКВ и/или АФС.</p></sec><sec><title>Заключение</title><p>Заключение. Факторами риска развития ОТ у больных СКВ и АФС являются асептические некрозы костей, трофические язвы голеней, длительность АФС, сетчатое ливедо, повышенные уровни IgG-антител к кардиолипину, к β2-гликопротеину 1, общего холестерина, СРБ и увеличение числа лейкоцитов.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Objective</title><p>Objective: to assess the frequency of thromboangiitis obliterans (TAO) vascular lesions and its association with clinical and laboratory manifestations in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS).</p></sec><sec><title>Material and methods</title><p>Material and methods. The study included 172 patients (30 men and 142 women): 22 (13%) with isolated “primary” APS (pAPS), 66 (38%) with SLE, and 84 (49%) with SLE + APS. The median age was 36 [30; 46] years. Disease duration in the SLE + APS group was longer than in the pAPS and SLE groups (median 17 [9; 21], 5 [2; 13], and 7 [3; 12] years, respectively; p&lt;0.05). All patients were hospitalized at the V.A. Nasonova Research Institute of Rheumatology due to exacerbation of the underlying disease and underwent a comprehensive examination.</p></sec><sec><title>Results and discussion</title><p>Results and discussion. Vascular lesions of the TAO type were recorded in 17 (10%) of 172 patients: 1 with pAPS, 13 with SLE + APS, and 3 with SLE. The development of TAO in patients with SLE + APS was influenced by the following factors: dyslipidemia (odds ratio, OR 10.74; 95% confidence interval, CI 3.29–34.99; p&lt;0.01), arterial hypertension (OR 7.19; 95% CI 1.98–26.07; p&lt;0.01), and Raynaud’s syndrome (OR 7.72; 95% CI 2.61–22.82; p&lt;0.01). As a result of multivariate analysis, a prognostic model was obtained, according to which the number of aseptic bone necroses, the number of lower leg ulcers over the entire disease course, the type of thrombosis, APS duration, disease onset with APS manifestations, livedo reticularis, elevated levels of IgG antibodies to cardiolipin, to β2-glycoprotein 1, total cholesterol, C-reactive protein (CRP), and an increase in leukocyte count are associated with a higher probability of TAO development in patients with SLE and/or APS.</p></sec><sec><title>Conclusion</title><p>Conclusion. Risk factors for the development of TAO in patients with SLE and APS are aseptic bone necroses, trophic ulcers of the lower legs, APS duration, livedo reticularis, elevated levels of IgG antibodies to cardiolipin, to β2-glycoprotein 1, total cholesterol, CRP, and an increased leukocyte count.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>облитерирующий тромбангиит</kwd><kwd>антифосфолипидные антитела</kwd><kwd>системная красная волчанка</kwd><kwd>антифосфолипидный синдром</kwd></kwd-group><kwd-group xml:lang="en"><kwd>thromboangiitis obliterans</kwd><kwd>antiphospholipid antibodies</kwd><kwd>systemic lupus erythematosus</kwd><kwd>antiphospholipid syndrome</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование не имело спонсорской поддержки</funding-statement><funding-statement xml:lang="en">The investigation has not been sponsored</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">Lambert M, Hatron PY. 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