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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">10.14412/1996-7012-2023-6-59-64</article-id><article-id custom-type="elpub" pub-id-type="custom">mrj-1504</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>Применение гепсидина в качестве маркера для диагностики характера анемии у больных с высокой активностью ревматоидного артрита</article-title><trans-title-group xml:lang="en"><trans-title>The use of hepcidin as a marker for diagnosing the type of anemia in patients with high activity of rheumatoid arthritis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Семашко</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Semashko</surname><given-names>A. S.</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"><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;</p><p>кафедра ревматологии, 125993, Москва, ул. Баррикадная, 2/1, стр. 1</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522;</p><p>Department of Rheumatology, 2/1, Barrikadnaya Street, Build. 1, Moscow 125993</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Галушко</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Galushko</surname><given-names>E. A.</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><email xlink:type="simple">egalushko@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гордеев</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Gordeev</surname><given-names>A. V.</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"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Зоткин</surname><given-names>Е. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Zotkin</surname><given-names>E. G.</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-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»;&#13;
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;&#13;
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>2023</year></pub-date><pub-date pub-type="epub"><day>19</day><month>12</month><year>2023</year></pub-date><volume>17</volume><issue>6</issue><fpage>59</fpage><lpage>64</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Семашко А.С., Лила А.М., Галушко Е.А., Гордеев А.В., Зоткин Е.Г., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Семашко А.С., Лила А.М., Галушко Е.А., Гордеев А.В., Зоткин Е.Г.</copyright-holder><copyright-holder xml:lang="en">Semashko A.S., Lila A.M., Galushko E.A., Gordeev A.V., Zotkin E.G.</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/1504">https://mrj.ima-press.net/mrj/article/view/1504</self-uri><abstract><p>Анемия остается одним из наиболее распространенных видов сопутствующей патологии, которая влияет на прогноз основного заболевания и качество жизни пациентов.</p><p>Цель исследования – оценка информативности определения уровня сывороточного гепсидина для дифференциальной диагностики анемии хронического воспаления (АХВ) у пациентов с активным ревматоидным артритом (РА).</p><sec><title>Материал и методы</title><p>Материал и методы. В исследование включено 47 больных РА с анемией, последовательно поступивших на стационарное лечение в ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой». Критерием анемии, согласно рекомендациям ВОЗ, считали снижение уровня гемоглобина ˂ 120 г/л для женщин и ˂ 130 г/л для мужчин. Контрольная группа состояла из 29 больных без анемии. У всех пациентов определяли индекс DAS28, исследовали клинические и биохимические показатели крови: сывороточное железо, общую железосвязывающую способность сыворотки, гепсидин, цитокины, включая интерлейкин (ИЛ) 6 и фактор некроза опухоли α (ФНОα).</p></sec><sec><title>Результаты и обсуждение</title><p>Результаты и обсуждение. Из 47 пациентов с активным РА и анемией только у 13 (28%) была диагностирована изолированная АХВ. Железодефицитная анемия (ЖДА) была выявлена в 17 (36%) случаях, у остальных 17 больных отмечался смешанный генез анемии (АХВ + ЖДА). Больные с изолированной АХВ имели статистически значимо более высокий уровень гепсидина (120,3±56,1 пг/мл) по сравнению с лицами контрольной группы (90,3±37,9 пг/мл) и пациентами с РА + ЖДА. При изолированной АХВ уровни ИЛ6, ФНОα, ревматоидного фактора и антител к циклическому цитруллинированному пептиду были в 2 раза выше (р&lt;0,05), чем при РА с дефицитом железа (как при ЖДА, так и при смешанном генезе анемии). Только в случаях изолированной АХВ уровень гепсидина коррелировал с концентрацией ИЛ6 (r=0,8), у пациентов с ЖДА и анемией смешанного генеза, а также у больных без анемии такой взаимосвязи не выявлено. Корреляции с уровнем ФНОα ни в одной подгруппе не обнаружено. Заключение. Уровень гепсидина является информативным показателем для дифференциальной диагностики характера анемии при активном воспалении. У больных РА с АХВ определялась максимальная концентрация гепсидина в сыворотке крови, а при ЖДА она оказалась ниже референсных значений. Продемонстрированы важность оси гепсидин – ИЛ6, а также отсутствие влияния провоспалительного цитокина ФНОα на метаболизм железа. Ключевые слова: гепсидин; анемия; труднолечимый пациент; ревматоидный артрит. &gt; ˂ 0,05), чем при РА с дефицитом железа (как при ЖДА, так и при смешанном генезе анемии). Только в случаях изолированной АХВ уровень гепсидина коррелировал с концентрацией ИЛ6 (r=0,8), у пациентов с ЖДА и анемией смешанного генеза, а также у больных без анемии такой взаимосвязи не выявлено. Корреляции с уровнем ФНОα ни в одной подгруппе не обнаружено.</p></sec><sec><title>Заключение</title><p>Заключение. Уровень гепсидина является информативным показателем для дифференциальной диагностики характера анемии при активном воспалении. У больных РА с АХВ определялась максимальная концентрация гепсидина в сыворотке крови, а при ЖДА она оказалась ниже референсных значений. Продемонстрированы важность оси гепсидин – ИЛ6, а также отсутствие влияния провоспалительного цитокина ФНОα на метаболизм железа.</p></sec></abstract><trans-abstract xml:lang="en"><p>Anemia is still one of the most common comorbidities that affects the prognosis of the underlying disease and the quality of life of patients.</p><sec><title>Objective</title><p>Objective: to evaluate the value of serum hepcidin level determination for the differential diagnosis of anemia of chronic disease/inflammation (ACD) in patients with active rheumatoid arthritis (RA).</p></sec><sec><title>Material and methods</title><p>Material and methods. The study included 47 patients with RA with anemia consecutively admitted to V.A. Nasonova Research Institute of Rheumatology for inpatient treatment. According to WHO recommendations, the criterion for anemia was a decrease in hemoglobin level ˂ 120 g/l in women and ˂ 130 g/l in men. The control group consisted of 29 patients without anemia. In all patients, the DAS28 index was determined, and clinical and biochemical blood parameters were examined: serum iron, total iron-binding capacity of serum, hepcidin, cytokines, including interleukin (IL) 6 and tumor necrosis factor α (TNFα).</p></sec><sec><title>Results and discussion</title><p>Results and discussion. Of 47 patients with active RA and anemia, only 13 (28%) were diagnosed with isolated ACD. Iron deficiency anemia (IDA) was found in 17 (36%), the remaining 17 patients had a mixed genesis of anemia (ACD + IDA). Patients with isolated ACD had a statistically significant higher level of hepcidin(120.3±56.1 pg/ml) compared to the control group (90.3±37.9 pg/ml) and to patients with RA + IDA. In isolated ACD, the levels of IL6, TNFα, rheumatoid factor and antibodies to cyclic citrullinated peptide were 2 times higher (p&lt;0.05) than in RA with iron deficiency (both in IDA and in mixed genesis of anemia). Only in isolated ACD did the hepcidin level correlate with the IL6 concentrations (r=0.8); no such correlation was found in patients with IDA and anemia of mixed origin or in patients without anemia. No correlation with TNFα levels was found in any subgroup. Conclusion. Hepcidin levels are an informative indicator for the differential diagnosis of the type of anemia during active inflammation. In RA patients with ACD, the maximum hepcidin concentration in blood serum was determined, and in IDA it was found to be lower than the reference values. The importance of the hepcidin – IL6 axis and the lack of influence of the proinflammatory cytokine TNFα on iron metabolism were demonstrated. Keywords: hepcidin; anemia; difficult-to-treat patient; rheumatoid arthritis&gt; ˂ 0.05) than in RA with iron deficiency (both in IDA and in mixed genesis of anemia). Only in isolated ACD did the hepcidin level correlate with the IL6 concentrations (r=0.8); no such correlation was found in patients with IDA and anemia of mixed origin or in patients without anemia. No correlation with TNFα levels was found in any subgroup.</p></sec><sec><title>Conclusion</title><p>Conclusion. Hepcidin levels are an informative indicator for the differential diagnosis of the type of anemia during active inflammation. In RA patients with ACD, the maximum hepcidin concentration in blood serum was determined, and in IDA it was found to be lower than the reference values. The importance of the hepcidin – IL6 axis and the lack of influence of the proinflammatory cytokine TNFα on iron metabolism were demonstrated.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>гепсидин</kwd><kwd>анемия</kwd><kwd>труднолечимый пациент</kwd><kwd>ревматоидный артрит</kwd></kwd-group><kwd-group xml:lang="en"><kwd>hepcidin</kwd><kwd>anemia</kwd><kwd>difficult-to-treat patient</kwd><kwd>rheumatoid arthritis</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование выполнено в рамках государственного задания по теме №1021051503137-7.</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">Busby AD, Wason J, Pratt AG, et al. The role of comorbidities alongside patient and disease characteristics on long-term disease activity in RA using UK inception cohort data. 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