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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">diaendo</journal-id><journal-title-group><journal-title xml:lang="ru">Сахарный диабет</journal-title><trans-title-group xml:lang="en"><trans-title>Diabetes mellitus</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2072-0351</issn><issn pub-type="epub">2072-0378</issn><publisher><publisher-name>Endocrinology research centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/DM10316</article-id><article-id custom-type="elpub" pub-id-type="custom">diaendo-10316</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 Studies</subject></subj-group></article-categories><title-group><article-title>Эффект терапии витамином D на маркеры воспаления у больных сахарным диабетом 2 типа и диабетической периферической нейропатией</article-title><trans-title-group xml:lang="en"><trans-title>The effect of vitamin D therapy on inflammatory markers in patients with type 2 diabetes mellitus and diabetic peripheral polyneuropathy</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8611-7095</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Степанова</surname><given-names>Анна Павловна</given-names></name><name name-style="western" xml:lang="en"><surname>Stepanova</surname><given-names>Anna P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант</p></bio><bio xml:lang="en"><p>MD, PhD student</p></bio><email xlink:type="simple">annstepanova12@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1547-0123</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Каронова</surname><given-names>Татьяна Леонидовна</given-names></name><name name-style="western" xml:lang="en"><surname>Karonova</surname><given-names>Tatiana L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор</p></bio><bio xml:lang="en"><p>MD, PhD, Professor</p></bio><email xlink:type="simple">karonova@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр имени В.А. Алмазова; Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Almazov National Medical Research Centre; Pavlov First Saint Petersburg State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>17</day><month>01</month><year>2020</year></pub-date><volume>22</volume><issue>5</issue><fpage>417</fpage><lpage>427</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Степанова А.П., Каронова Т.Л., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Степанова А.П., Каронова Т.Л.</copyright-holder><copyright-holder xml:lang="en">Stepanova A.P., Karonova T.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://www.dia-endojournals.ru/jour/article/view/10316">https://www.dia-endojournals.ru/jour/article/view/10316</self-uri><abstract><sec><title>ОБОСНОВАНИЕ</title><p>ОБОСНОВАНИЕ. Патогенез диабетической периферической нейропатии (ДПН) у больных сахарным диабетом 2 типа (СД2) является многофакторным, и воспаление может занимать одно из важных мест. В последние годы активно изучается влияние терапии препаратами витамина D на улучшение профиля воспалительных показателей.</p></sec><sec><title>ЦЕЛЬ</title><p>ЦЕЛЬ. Изучить изменение маркеров воспаления на фоне терапии различными дозами колекальциферола у больных СД2 и ДПН.</p></sec><sec><title>МЕТОДЫ</title><p>МЕТОДЫ. В одноцентровое открытое рандомизированное исследование включены больные СД2 с ДПН. Шестьдесят семь больных рандомизированы на 2 две группы, где в течение 24 нед Группа I принимала препараты колекальциферола в дозе 5000 МЕ/нед, а Группа II – в дозе 40 000 МЕ/нед. Исходно и в конце исследования определяли индекс массы тела (ИМТ), уровень гликированного гемоглобина (НbA1c), 25(ОН)D, паратиреоидного гормона (ПТГ), интерлейкинов-1β, -6, -10 (ИЛ), С-реактивного белка (СРБ), фактора некроза опухоли альфа (ФНО-α).</p></sec><sec><title>РЕЗУЛЬТАТЫ</title><p>РЕЗУЛЬТАТЫ. Завершили исследование 62 пациента. Группа I (n=31, Ж16), Группа II (n=31, Ж15) исходно были сопоставимы по возрасту, полу, ИМТ и НbA1c. Дефицит/недостаток витамина D был выявлен у 78% больных СД2. Через 24 нед приема колекальциферола в Группе II имелось значимое снижение ИМТ, НbA1c, ИЛ-6 и повышение концентрации ИЛ-10, в то время как в Группе I данных изменений выявлено не было. Установлена корреляционная связь между конечной концентрацией 25(ОН)D и ИЛ-6 (r=-0,378, p=0,036), ИЛ-10 (r=0,483, p=0,006), ИМТ (r=-0,388, p=0,031) и НbA1c (r=-0,388, p=0,031).</p></sec><sec><title>ЗАКЛЮЧЕНИЕ</title><p>ЗАКЛЮЧЕНИЕ. Прием колекальциферола в дозе 40 000 МЕ/нед. в течение 24 нед ассоциирован со снижением ИМТ, улучшением гликемического контроля и профиля провоспалительных маркеров у больных СД2 и ДПН. Результаты исследования демонстрируют, что нормализация уровня 25(ОН)D может быть одним из модифицируемых факторов, влияющих на развитие и прогрессирование ДПН у больных СД2.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>BACKGROUND</title><p>BACKGROUND: The pathogenesis of diabetic peripheral neuropathy (DPN) in patients with type 2 diabetes mellitus (T2DM) is multifactorial, and includes increased inflammation. In recent years, the effect of vitamin D therapy on improving the profile of inflammatory parameters has been actively studied.</p></sec><sec><title>AIMS</title><p>AIMS: The aim of this study was to assess inflammation markers before and after various doses of cholecalciferol therapy in T2DM with DPN.</p></sec><sec><title>MATERIALS AND METHODS</title><p>MATERIALS AND METHODS: Single-center open randomized study included T2DM patients with PDN. Sixty-seven patients were randomized into 2 groups. For 24 weeks Group I have been taking a dosage of cholecalciferol 5,000 IU/week, and Group II a dosage of 40,000 IU/week. At the baseline and in the end of the research there have been studied body mass index (BMI), glycated hemoglobin (HbA1c), 25-hydroxyvitamin D (25(OH)D), PTH, interleukin-1β, -6, -10 (IL), C-reactive protein (CRP), tumor necrosis factor -α (TNFα).</p></sec><sec><title>RESULTS</title><p>RESULTS: Sixty-two patients completed the study. Group I (n=31, F16), Group II (n=31, F15) were initially compared by age, sex, BMI and НbA1clevel. Vitamin D deficiency/insufficiency was detected in 78% of patients with T2DM. After 24 weeks of therapy with cholecalciferol in Group II there was a significant decrease in BMI, HbA1c, IL-6 levels and an increase in IL-10 levels while no changes were found in Group I. There has been established a correlation between the final level of 25(OH)D and IL-6 (r=-0.378, p=0.036), IL-10 (r=0.483, p=0.006), BMI (r=-0.388, p=0.031) and НbA1c(r=-0.388, p=0.031).</p></sec><sec><title>CONCLUSION</title><p>CONCLUSION: The intake of cholecalciferol at a dosage of 40,000 IU/week for 24 weeks is associated with a decrease in BMI, improvement of glycemic control and pro-inflammatory markers profile in patients with T2DM with DPN. Study results showed that the normalization of serum 25(OH)D level can be one of the modifying factors for the development and progression of DPN in patients with T2DM.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>диабетическая периферическая нейропатия</kwd><kwd>интерлейкины-1β</kwd><kwd>-6</kwd><kwd>-10</kwd><kwd>25(OH)D</kwd><kwd>недостаток/дефицит витамина D</kwd><kwd>терапия колекальциферолом</kwd></kwd-group><kwd-group xml:lang="en"><kwd>diabetic peripheral neuropathy (DPN)</kwd><kwd>interleukins-1β</kwd><kwd>-6</kwd><kwd>-10</kwd><kwd>25(OH)D</kwd><kwd>vitamin D deficiency</kwd><kwd>сholecalciferol 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">Pop-Busui R, Boulton AJ, Feldman EL, et al. Diabetic neuropathy: a position statement by the american diabetes association. 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