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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">problendo</journal-id><journal-title-group><journal-title xml:lang="ru">Проблемы Эндокринологии</journal-title><trans-title-group xml:lang="en"><trans-title>Problems of Endocrinology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0375-9660</issn><issn pub-type="epub">2308-1430</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/probl12266</article-id><article-id custom-type="elpub" pub-id-type="custom">problendo-12266</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>Обзоры</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Reviews</subject></subj-group></article-categories><title-group><article-title>Гипогликемический синдром у пациентов с моноклональными гаммапатиями</article-title><trans-title-group xml:lang="en"><trans-title>Hypoglycemic syndrome in patients with monoclonal gammopathy</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7944-6202</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Соловьев</surname><given-names>Максим Валерьевич</given-names></name><name name-style="western" xml:lang="en"><surname>Solovyev</surname><given-names>Maxim V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н.</p></bio><bio xml:lang="en"><p>MD, PhD</p></bio><email xlink:type="simple">maxsolovej@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/0000-0002-8771-8300</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Юкина</surname><given-names>Марина Юрьевна</given-names></name><name name-style="western" xml:lang="en"><surname>Yukina</surname><given-names>Marina Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н.</p></bio><bio xml:lang="en"><p>MD, PhD</p></bio><email xlink:type="simple">kuronova@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/0000-0002-8520-8702</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Трошина</surname><given-names>Екатерина Анатольевна</given-names></name><name name-style="western" xml:lang="en"><surname>Troshina</surname><given-names>Ekaterina A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, член-корр. РАН</p></bio><bio xml:lang="en"><p>MD, professor. corresponding member of the RAS</p></bio><email xlink:type="simple">troshina@inbox.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 эндокринологии</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Endocrinology Research Centre</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>10</day><month>06</month><year>2020</year></pub-date><volume>65</volume><issue>6</issue><fpage>474</fpage><lpage>480</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Соловьев М.В., Юкина М.Ю., Трошина Е.А., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Соловьев М.В., Юкина М.Ю., Трошина Е.А.</copyright-holder><copyright-holder xml:lang="en">Solovyev M.V., Yukina M.Y., Troshina E.A.</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.probl-endojournals.ru/jour/article/view/12266">https://www.probl-endojournals.ru/jour/article/view/12266</self-uri><abstract><p>Одной из причин развития гипогликемии является синтез аутоиммунных антител к инсулину или его рецептору – инсулиновый аутоиммунный синдром (ИАС). Наибольшее число случаев данного синдрома описано в японской популяции. Синтезируемые АТ к инсулину наиболее часто являются поликлональными иммуноглобулинами. При моноклональной гаммапатии неопределенного значения и множественной миеломе секретируемый патологический моноклональный иммуноглобулин может обладать сродством к человеческому инсулину, что индуцирует развитие ИАС. Длительная персистенция эпизодов гипогликемии неясного генеза требует исключения моноклональной природы секретируемых АТ к инсулину. Нередко наличие патологической секреции длительное время не распознается ввиду отсутствия иных проявлений заболевания. Манифестация гаммапатий представлена широким спектром симптомов и синдромов, требующих совместной работы врачей различных специальностей. В настоящем обзоре суммированы литературные данные об ИАС у пациентов с моноклональными гаммапатиями, заболевание у которых дебютировало с эпизодов спонтанной гипогликемии. Закономерно, что при достижении ремиссии гемобластоза (когда секреция патологического белка минимальна или не определяется) показатели глюкозы, инсулина, АТ к инсулину нормализуются, а при развитии рецидива множественной миеломы возобновляются и эпизоды гипогликемии. Дебют заболевания с клиники ИАС может рассматриваться в качестве нового критерия симптоматической множественной миеломы, диктующего необходимость начала специфической терапии.</p></abstract><trans-abstract xml:lang="en"><p>One of the reasons for the development of hypoglycemia is the synthesis of autoimmune antibodies to insulin or its receptor – insulin autoimmune syndrome (IAS). The largest number of cases of this syndrome is described in the Japanese population. The antibodies to insulin are most often polyclonal immunoglobulins. In monoclonal gammopathy of undetermined significance and multiple myeloma secreted pathological monoclonal immunoglobulin may have an affinity for human insulin, which induces the development of IAS. The prolonged persistence of episodes of hypoglycemia of unknown origin requires the exclusion of the monoclonal nature of secreted antibodies to insulin. Often the presence of pathological secretion for a long time is not recognized due to the absence of other manifestations of the disease. The manifestation of gammopathy is represented by a wide range of symptoms and syndromes requiring the collaboration of doctors of various specialties. This review summarizes the literature on IAS in patients with monoclonal gammopathy, whose disease debuted from episodes of spontaneous hypoglycemia. When hemoblastosis remission is achieved (when the secretion of the pathological protein is minimal or not determined), the glucose, insulin, and antibodies levels of insulin normalize, and when multiple myeloma recurs, episodes of hypoglycemia resume. The onset of the disease from the IAS can be considered as a new criterion for symptomatic multiple myeloma, dictating the need for the initiation of specific therapy.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>инсулиновый аутоиммунный синдром</kwd><kwd>множественная миелома</kwd><kwd>моноклональная гаммапатия неопределенного значения</kwd><kwd>моноклональные антитела к инсулину</kwd><kwd>гипогликемия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>insulin autoimmune syndrome</kwd><kwd>multiple myeloma</kwd><kwd>monoclonal gammopathy of undetermined significance</kwd><kwd>insulin antibodies</kwd><kwd>hypoglycemia</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">Mahapatra M, Mishra P, Makharia G, et al. Acquired von Willebrand’s disease associated with gastrointestinal angiodysplasia and monoclonal gammopathy. 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