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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">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/2079-701X-2020-8-120-127</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-5689</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>РЕВМАТОЛОГИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>RHEUMATOLOGY</subject></subj-group></article-categories><title-group><article-title>Минеральная плотность костной ткани и риск переломов у больных ревматическими заболеваниями</article-title><trans-title-group xml:lang="en"><trans-title>Bone mineral density and fracture risk in patients with rheumatic diseases</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2809-0197</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Добровольская</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Dobrovolskaya</surname><given-names>O. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Добровольская Ольга Валерьевна, к.м.н., научный сотрудник лаборатории остеопороза</p><p>115522, Россия, Москва, Каширское шоссе, д. 34А</p></bio><bio xml:lang="en"><p>Olga V. Dobrovolskaya, Cand. of Sci. (Med.), researcher of the Laboratory for Osteoporosis</p><p>34А, Kashirskoe shosse, Moscow, 115522, Russia</p></bio><email xlink:type="simple">olgavdobr@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/0000-0002-8155-6101</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ефремова</surname><given-names>А. О.</given-names></name><name name-style="western" xml:lang="en"><surname>Efremova</surname><given-names>A. O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ефремова Арина Олеговна, младший научный сотрудник лаборатории остеопороза</p><p>115522, Россия, Москва, Каширское шоссе, д. 34А</p></bio><bio xml:lang="en"><p>Arina O. Efremova, junior researcher of the Laboratory for Osteoporosis</p><p>34А, Kashirskoe shosse, Moscow, 115522, Russia</p></bio><email xlink:type="simple">epid@irramn.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/0000-0003-0961-9785</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Демин</surname><given-names>Н. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Demin</surname><given-names>N. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Демин Николай Викторович, младший научный сотрудник лаборатории остеопороза,</p><p>115522, Россия, Москва, Каширское шоссе, д. 34А</p></bio><bio xml:lang="en"><p>Nikolay V. Demin, junior researcher of the Laboratory for Osteoporosis</p><p>34А, Kashirskoe shosse, Moscow, 115522, Russia</p></bio><email xlink:type="simple">epid@irramn.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/0000-0003-4739-4302</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Торопцова</surname><given-names>Н. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Toroptsova</surname><given-names>N. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Торопцова Наталья Владимировна, д.м.н., заведующая лабораторией остеопороза</p><p>115522, Россия, Москва, Каширское шоссе, д. 34А</p></bio><bio xml:lang="en"><p>Natalia V. Toroptsova, Dr. of Sci. (Med.), Head of the Laboratory for Osteoporosis</p><p>34А, Kashirskoe shosse, Moscow, 115522, Russia</p></bio><email xlink:type="simple">torop@irramn.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>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>2020</year></pub-date><pub-date pub-type="epub"><day>14</day><month>07</month><year>2020</year></pub-date><volume>0</volume><issue>8</issue><fpage>120</fpage><lpage>127</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Добровольская О.В., Ефремова А.О., Демин Н.В., Торопцова Н.В., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Добровольская О.В., Ефремова А.О., Демин Н.В., Торопцова Н.В.</copyright-holder><copyright-holder xml:lang="en">Dobrovolskaya O.V., Efremova A.O., Demin N.V., Toroptsova N.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.med-sovet.pro/jour/article/view/5689">https://www.med-sovet.pro/jour/article/view/5689</self-uri><abstract><sec><title>Введение</title><p>Введение: снижение минеральной плотности кости (МПК) и риск переломов при ревматических заболеваниях (РЗ) обусловлены патогенетическими механизмами, лежащими в основе РЗ, и воздействием лекарственных препаратов, применяемых для их лечения, на кость.</p></sec><sec><title>Цель исследования</title><p>Цель исследования: оценить состояние МПК, частоту и риск переломов у женщин постменопаузального возраста с различными РЗ.</p></sec><sec><title>Материал и методы</title><p>Материал и методы: в исследование включены 260 женщин в постменопаузе – медиана возраста 61 год (54; 68 лет) с системной склеродермией (ССД), ревматоидным артритом (РА) и остеоартритом (ОА). Пациентки проанкетированы и обследованы с помощью двухэнергетической рентгеновской абсорбциометрии; всем рассчитан 10-летний риск переломов с использованием алгоритма FRAX®.</p></sec><sec><title>Результаты</title><p>Результаты: сниженная МПК обнаружена у 210 (81%) женщин с РЗ, при этом остеопороз (ОП) выявлен у 43% женщин с ССД, 31% – с РА и 17% – с ОА. При всех РЗ ОП чаще встречался в поясничном отделе позвоночника, чем в проксимальном отделе бедра. Частота низкоэнергетических переломов в анамнезе была 35, 29 и 20% у лиц с ССД, РА и ОА соответственно. Самыми частыми переломами среди женщин с ССД и РА были переломы позвонков, а у пациенток с ОА – предплечья. 10-летний риск новых переломов по FRAX® и потребность в противоостеопоротическом лечении у женщин с ОА были меньше, чем у пациенток с ССД и РА (р &lt; 0,0001). Среди всех обследованных лиц 44% пациенток нуждались в патогенетической противоостеопоротической терапии, а в реальной практике ее получали 25% женщин. Чаще всего пациентки с РЗ лечились золедроновой кислотой, алендронатом и парентеральной формой ибандроната.</p></sec><sec><title>Заключение</title><p>Заключение: частота ОП и 10-летний риск переломов при аутоиммунных РЗ были значимо больше, чем при ОА. Структура низкоэнергетических переломов при РЗ различна: при аутоиммунных процессах и приеме глюкокортикоидов (ГК) значимо чаще происходили компрессионные переломы позвонков. Патогенетическая терапия ОП женщинам в постменопаузе с РЗ проводится недостаточно часто, что может быть причиной повторных низкоэнергетических переломов.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction: Decrease in bone mineral density (BMD) and risk of fractures in rheumatic diseases (RD) is caused by the pathogenetic mechanisms underlying RD and the effects of drugs used to treat them on bone.</p></sec><sec><title>Aim of the study</title><p>Aim of the study: to assess the condition of BMD, frequency and risk of fractures in postmenopausal women with different RD.</p></sec><sec><title>Material and methods</title><p>Material and methods: The study enrolled 260 women in postmenopause (median age 61 years) (54; 68 year) with systemic scleroderma (SS), rheumatoid arthritis (RA) and osteoarthritis (OA). Patients were sanitized and examined using dual energy X-ray absorptiometry; a 10-year risk of fractures was calculated using the FRAX® algorithm.</p></sec><sec><title>Results</title><p>Results: A reduced BMD was observed in 210 (81%) women with RD, while osteoporosis (OP) was found in 43% of women with SS, 31% of women with RA and 17% of women with OA. In all RD, osteoporosis was more common in the lumbar spine than in the proximal femur. The frequency of low-energy fractures in the anamnesis was 35, 29 and 20 percent for those with SS, RA and OA, respectively. The most frequent fractures among women with SS and RA were vertebral fractures, and in patients with OA - forearm fractures. The 10-year risk of new fractures according to FRAX® and the need for antiosteoporotic treatment in women with OA was less than in patients with SS and RA (p &lt; 0.0001). Of all patients examined, 44% needed pathogenetic antiosteoporotic therapy, and in actual practice 25% of women received it. Patients with RA were most often treated with zoledronic acid, alendronate and parenteral form of ibandronate.</p></sec><sec><title>Conclusions</title><p>Conclusions: The frequency of OPs and the 10-year risk of fractures in autoimmune RD was significantly higher than in OA. The structure of low-energy fractures in RD is different: in autoimmune processes and glucocorticoids (GC) intake, spinal compression fractures were significantly more common. Pathogenetic treatment for OP in women in post-menopause with RD is not performed frequently enough, which may cause repeated low-energy fractures.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>минеральная плотность кости</kwd><kwd>ревматоидный артрит</kwd><kwd>системная склеродермия</kwd><kwd>остеоартрит</kwd><kwd>FRAX®</kwd><kwd>риск переломов</kwd><kwd>потребность в противоостеопоротической терапии</kwd></kwd-group><kwd-group xml:lang="en"><kwd>bone mineral density</kwd><kwd>rheumatoid arthritis</kwd><kwd>systemic scleroderma</kwd><kwd>osteoarthritis</kwd><kwd>FRAX®</kwd><kwd>fracture risk</kwd><kwd>need for antiosteoporotic therapy</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">Braun T., Schett G. Pathways for Bone Loss in Inflammatory Disease. 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