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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">ometendo</journal-id><journal-title-group><journal-title xml:lang="ru">Ожирение и метаболизм</journal-title><trans-title-group xml:lang="en"><trans-title>Obesity and metabolism</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2071-8713</issn><issn pub-type="epub">2306-5524</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/omet2017311-18</article-id><article-id custom-type="elpub" pub-id-type="custom">ometendo-8794</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>Обзор литературы</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Низкотравматичные переломы и костное ремоделирование при сахарном диабете 2 типа</article-title><trans-title-group xml:lang="en"><trans-title>Fragility fractures and bone remodeling in type 2 diabetes mellitus</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1097-4557</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ялочкина</surname><given-names>Татьяна Олеговна</given-names></name><name name-style="western" xml:lang="en"><surname>Yalochkina</surname><given-names>Tatiana O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Врач-эндокринолог</p><p> </p></bio><bio xml:lang="en"><p>MD, endocrinologist</p></bio><email xlink:type="simple">tatiana540@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/0000-0002-7199-5469</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Белая</surname><given-names>Жанна Евгеньевна</given-names></name><name name-style="western" xml:lang="en"><surname>Belaya</surname><given-names>Zhanna E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>гл. н.с., д.м.н, зав. отделением нейроэндокринологии и остеопатий</p></bio><bio xml:lang="en"><p>Sc.D., Head of Department of neuroendocrinology and bone diseases</p></bio><email xlink:type="simple">jannabelaya@gmail.com</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>&lt;p&gt;ГБУЗ Городская поликлиника №219 ДЗМ;&lt;/p&gt;&#13;
&lt;p&gt;&amp;nbsp;&lt;/p&gt;</institution><country>Россия</country></aff><aff xml:lang="en"><institution>&lt;p&gt;Moscow outpatient clinic N 219&lt;/p&gt;</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>&lt;p&gt;ФГБУ &amp;laquo;Национальный медицинский исследовательский центр эндокринологии&amp;raquo; Минздрава России&lt;/p&gt;</institution><country>Россия</country></aff><aff xml:lang="en"><institution>&lt;p&gt;Endocrinology Research Centre&lt;/p&gt;</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2017</year></pub-date><pub-date pub-type="epub"><day>13</day><month>11</month><year>2017</year></pub-date><volume>14</volume><issue>3</issue><fpage>11</fpage><lpage>18</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Ялочкина Т.О., Белая Ж.Е., 2017</copyright-statement><copyright-year>2017</copyright-year><copyright-holder xml:lang="ru">Ялочкина Т.О., Белая Ж.Е.</copyright-holder><copyright-holder xml:lang="en">Yalochkina T.O., Belaya Z.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://www.omet-endojournals.ru/jour/article/view/8794">https://www.omet-endojournals.ru/jour/article/view/8794</self-uri><abstract><p>Риск низкотравматичных переломов значительно повышен у пациентов с сахарным диабетом 1 и 2 типа (СД1 и СД2), и пациенты с диабетом имеют значительно худшие последствия переломов, в том числе повышения сроков их заживления. Для пациентов с СД1 характерно снижение минеральной плотности кости (МПК), в то время как пациенты с СД2 зачастую имеют более высокую МПК по сравнению с лицами без сахарного диабета. Повышение риска переломов при СД2 частично можно объяснить осложнениями заболевания, увеличивающими риск падений и связанных с ними травм. Однако наиболее значимой причиной выраженной хрупкости костной ткани при СД2 служат различные нарушения ее микроархитектоники, механизмы которых до настоящего времени окончательно не известны. Увеличение МПК у таких пациентов не позволяет использовать для диагностики остеопороза «золотой стандарт» инструментальных методов – рентгеновскую денситометрию. Это определяет поиск новых инструментов оценки групп риска низкотравматичных переломов среди пациентов с СД2. Кроме того, сама по себе группа пациентов с СД2 достаточно гетерогенна, и некоторые исследователи допускают, что практический врач может столкнуться с тремя принципиально разными группами пациентов: больные с остеопорозом и соответствующей потерей МПК с легким течением сахарного диабета; пациенты с остеопорозом, который усугубляется нарушениями состояния костной ткани вследствие сахарного диабета – диабетоостеопороз, и поражением скелета вследствие тяжелого неконтролируемого сахарного диабета без развития остеопороза – диабетической болезнью костей. Для лучшего понимания проблемы повышенной хрупкости скелета у пациентов с СД2 необходимы разработка новых диагностических алгоритмов, а также дальнейшие исследования патогенетических аспектов нарушения костной микроархитектоники у этих пациентов. Настоящий обзор литературы суммирует современные представления о частоте переломов, факторах риска и причинах повреждения костной ткани у пациентов с СД2.</p></abstract><trans-abstract xml:lang="en"><p>Fracture risk is significantly increased in both type 1 and type 2 diabetes and individuals with diabetes experience worse fracture outcomes compared to normoglycemic individuals. Patients with T1DM have decreased bone mineral density (BMD), whereas patients with T2DM demonstrate increased BMD compared to healthy control. The latest studies show increased incidence of low-traumatic fractures in patients with T2DM instead of high bone mineral density (BMD). The risk of osteoporotic fractures in patients with T2DM can be explained by disease complications and increased risk of falls and consequent trauma. However, the most important cause of bone fragility in T2DM is the deterioration in bone microarchitecture, the mechanism of which is not completely understood. High BMD in patients with T2DM does not allow us to use dual-energy X-ray-absorptiometry as a “gold standard” test for diagnosticsof osteoporosis. Consequently,new risk factors and diagnostic algorithm as well as treatment strategy should be developed for patients with T2DM. In addition to this, some researchers considered that the group of T2DM is geterogenous and physicians might face patients with osteoporosis and mild diabetes that add very little to bone fragility; patients with osteoporosis and moderate or severe diabetes which also affects bone tissue –diabetoosteoporosis; and patients without osteoporosis but severe diabetes which cause bone tissue deterioration with the development of diabetic bone disease. New diagnostic tools and algorithm and new experimental research are needed for better understanding bone deterioration in patients with T2DM. This review summarizes our current knowledge on fracture rate, risk factors for fractures and causes of bone deterioration in subjects with T2DM.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>Сахарный диабет 2 типа</kwd><kwd>остеопороз</kwd><kwd>низкотравматические переломы</kwd><kwd>факторы риска</kwd><kwd>табекулярный костный индекс</kwd></kwd-group><kwd-group xml:lang="en"><kwd>type 2 diabetes mellitus</kwd><kwd>osteoporosis</kwd><kwd>risk factors</kwd><kwd>trabecular bone score</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа проведена в рамках государственного задания «Первичный остеопороз и вторичный остеопороз на фоне эндокринопатий, в том числе нарушения костной ткани при сахарном диабете; роль сочетанной эндокринной патологии, дефицита витамина D; генетические и метаболические характеристики орфанных заболеваний костной ткани».</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">Atlas D. 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