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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">bloodjour</journal-id><journal-title-group><journal-title xml:lang="ru">Гематология и трансфузиология</journal-title><trans-title-group xml:lang="en"><trans-title>Russian journal of hematology and transfusiology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0234-5730</issn><issn pub-type="epub">2411-3042</issn><publisher><publisher-name>ООО Издательский дом «Практика»</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.35754/0234-5730-2024-69-4-442-450</article-id><article-id custom-type="elpub" pub-id-type="custom">bloodjour-593</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 СТАТЬИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL ARTICLES</subject></subj-group></article-categories><title-group><article-title>Роль окислительного стресса в костной ткани в патогенезе остеопении у больных хроническим лимфолейкозом</article-title><trans-title-group xml:lang="en"><trans-title>The role of oxidative stress in bone tissue in the pathogenesis of osteopenia in patients with chronic lymphocytic leukemia</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6487-9083</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Осиков</surname><given-names>М. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Osikov</surname><given-names>M. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Осиков Михаил Владимирович, доктор медицинских наук, профессор, заведующий кафедрой патофизиологии; руководитель научного отдела</p><p>454092, г. Челябинск; 454048, г. Челябинск</p></bio><bio xml:lang="en"><p>Mikhail V Osikov, Dr. Sci. (Med.), Professor, Head of Pathophysiology Department</p><p>454092, Chelyabinsk; 454048, Chelyabinsk</p></bio><email xlink:type="simple">prof.osikov@yandex.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/0000-0001-7241-1325</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Коробкин</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Korobkin</surname><given-names>E. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Коробкин Егор Александрович, ассистент кафедры  патофизиологии; врач-гематолог</p><p>454092, г. Челябинск; 454048, г. Челябинск</p></bio><bio xml:lang="en"><p>Egor A. Korobkin, Assistant Professor of Pathophysiology Department </p><p>454092, Chelyabinsk; 454048, Chelyabinsk</p></bio><email xlink:type="simple">doktore77@yandex.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/0000-0003-4922-3742</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Коробкин</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Korobkin</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Коробкин Александр Владимирович, кандидат медицинских наук, главный внештатный гематолог</p><p>454048, г. Челябинск</p></bio><bio xml:lang="en"><p>Alexander V. Korobkin, Cand. Sci. (Med.), Chief freelance hematologist</p><p>454048, Chelyabinsk</p></bio><email xlink:type="simple">akoro@rambler.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Южно-Уральский государственный медицинский университет» Министерства здравоохранения Российской Федерации; ГБУЗ «Челябинская областная клиническая больница»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>South State Medical University; Chelyabinsk Regional Clinical Hospital</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ГБУЗ «Челябинская областная клиническая больница»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Chelyabinsk Regional Clinical Hospital</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>28</day><month>12</month><year>2024</year></pub-date><volume>69</volume><issue>4</issue><fpage>442</fpage><lpage>450</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Осиков М.В., Коробкин Е.А., Коробкин А.В., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Осиков М.В., Коробкин Е.А., Коробкин А.В.</copyright-holder><copyright-holder xml:lang="en">Osikov M.V., Korobkin E.A., Korobkin A.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.htjournal.ru/jour/article/view/593">https://www.htjournal.ru/jour/article/view/593</self-uri><abstract><sec><title>Введение</title><p>Введение. Снижение минеральной плотности кости (МПК), развитие остеопении и остеопороза возникают у больных хроническим лимфолейкозом (ХЛЛ). У больных ХЛЛ риск развития переломов костей в результате остеопороза выше по сравнению со здоровыми лицами. Патогенез остеодеструктивного процесса при ХЛЛ мало изучен и может быть обусловлен избыточной генерацией активных форм кислорода и/или угнетением антиокислительной защиты.</p></sec><sec><title>Цель</title><p>Цель: исследовать взаимосвязь между показателями окислительного стресса в костной ткани и показателями остеопении у больных ХЛЛ. Материалы и  методы. В исследование были включены 48  больных ХЛЛ мужского пола в  возрасте 50–70  лет, разделенных, на основании остеоденситометрии (Т-показатель от –1,0 стандартного отклонения (СО) до –2,5 СО), на группу 1 (n = 34) без признаков остеопении и группу 2 (n = 14) — с признаками остеопении. МПК, Т- и Z-критерии оценивали в поясничном отделе позвоночника, шейке проксимального отдела бедренной кости (ШПОБК), проксимальном отделе бедренной кости. В гомогенате костной ткани определяли содержание продуктов окислительной модификации белков (ОМБ) спектрофотометрически в спонтанном и металл-катализируемом режимах, резервноадаптационный потенциал; общий антиоксидантный статус.</p></sec><sec><title>Результаты</title><p>Результаты. У 30 % больных ХЛЛ выявили остеопению по данным остеоденситометрии в ШПОБК. У больных ХЛЛ и остеопенией в костной ткани наблюдали признаки окислительного стресса: накапливались в спонтанном режиме детекции ранние продукты ОМБ нейтрального и основного характера, поздние продукты нейтрального характера, в  индуцированном режиме  — ранние и  поздние продукты ОМБ нейтрального и  основного характера, снижался резервно-адаптационный потенциал, общий антиоксидантный статус. Признаки остеопении в ШПОБК у больных ХЛЛ нарастали по мере увеличения содержания в костной ткани ранних и поздних продуктов ОМБ в спонтанном и в металл-индуцированном режиме детекции, снижения общего антиоксидантного статуса в костной ткани.</p></sec><sec><title>Заключение</title><p>Заключение. На основании полученных данных возможна модернизация диагностических критериев и терапевтических подходов.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. A decrease in bone mineral density (BMD), the development of osteopenia and osteoporosis is observed in patients with chronic lymphocytic leukemia (CLL). Patients with CLL are at a higher risk of developing fractures due to osteoporosis compared to healthy age-matched individuals. The pathogenesis of the osteodestructive process in CLL has been poorly studied and may be associated with excessive generation of reactive oxygen species and/or inhibition of antioxidant defense.</p></sec><sec><title>Aim</title><p>Aim: to investigate the relationship between indicators of oxidative stress in bone tissue and indicators of osteopenia in patients with CLL.</p></sec><sec><title>Materials and methods</title><p>Materials and methods. The study included 48 male patients with CLL aged 50–70 years, divided into group 1 (n = 34) without signs of osteopenia and group 2 (n = 14) with signs of osteopenia based on osteodensitometry (T-score from –1.0 SD to –2.5 SD). BMD, T- and Z-scores were assessed in the lumbar spine, proximal femoral neck (PFC), and proximal femur. In the bone tissue homogenate, the content of products of oxidative modification of proteins (OMP) was determined spectrophotometrically in spontaneous and metal-catalyzed modes, reserve-adaptation potential, and general antioxidant status.</p></sec><sec><title>Results</title><p>Results. Osteopenia was detected in 30 % of patients with CLL according to osteodensitometry in the neck of the proximal femur. In patients with CLL and osteopenia, signs of oxidative stress were observed in the bone tissue: early OMP products of a neutral and basic nature, late products of a neutral nature accumulated in the spontaneous detection mode; early and late OMP products of a neutral and basic nature accumulated in the induced mode; reserve-adaptive potential, the general antioxidant status decreased. Signs of osteopenia in the PFC in patients with CLL in the femoral neck increased as the content of early and late OMP products in the bone tissue increased in spontaneous and metal-induced detection modes, and the general antioxidant status in the bone tissue decreased.</p></sec><sec><title>Conclusion</title><p>Conclusion. Based on the data obtained, it is possible to modernize diagnostic criteria and therapeutic approaches.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>хронический лимфолейкоз</kwd><kwd>минеральная плотность кости</kwd><kwd>остеопения</kwd><kwd>окислительный стресс</kwd><kwd>окислительная модификация белков</kwd><kwd>редокс-статус</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic lymphocytic leukemia</kwd><kwd>bone mineral density</kwd><kwd>osteopenia</kwd><kwd>oxidative stress</kwd><kwd>oxidative modification of proteins</kwd><kwd>redox status</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование не имело спонсорской поддержки.</funding-statement><funding-statement xml:lang="en">The study had no sponsorship.</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">Никитин Е.А., Бялик Т.Е., Зарицкий А.Ю. и др. 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