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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Terapevticheskii arkhiv</journal-id><journal-title-group><journal-title xml:lang="en">Terapevticheskii arkhiv</journal-title><trans-title-group xml:lang="ru"><trans-title>Терапевтический архив</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0040-3660</issn><issn publication-format="electronic">2309-5342</issn><publisher><publisher-name xml:lang="en">LLC Obyedinennaya Redaktsiya</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">31730</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Editorial article</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Передовая статья</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Familial partial lipodystrophy (Dunnigan syndrome) due to LMNA gene mutation: The first description of its clinical case in Russia</article-title><trans-title-group xml:lang="ru"><trans-title>Семейная парциальная липодистрофия (синдром Dunnigan) вследствие мутации в гене LMNA: первое описание клинического случая в России</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Sorkina</surname><given-names>E L</given-names></name><name xml:lang="ru"><surname>Соркина</surname><given-names>Е Л</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Kalashnikova</surname><given-names>M F</given-names></name><name xml:lang="ru"><surname>Калашникова</surname><given-names>М Ф</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Melnichenko</surname><given-names>G A</given-names></name><name xml:lang="ru"><surname>Мельниченко</surname><given-names>Г А</given-names></name></name-alternatives><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Tyulpakov</surname><given-names>A N</given-names></name><name xml:lang="ru"><surname>Тюльпаков</surname><given-names>А Н</given-names></name></name-alternatives><xref ref-type="aff" rid="aff4"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en"></institution></aff><aff><institution xml:lang="ru">«Первый МГМУ им. И.М. Сеченова» Минздрава России</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en"></institution></aff><aff><institution xml:lang="ru">«Первый МГМУ им. И.М. Сеченова» Минздрава России, Москва, Россия</institution></aff></aff-alternatives><aff-alternatives id="aff3"><aff><institution xml:lang="ru">«Эндокринологический научный центр» Минздрава России, Москва, Россия</institution></aff><aff><institution xml:lang="en"></institution></aff></aff-alternatives><aff id="aff4"><institution>«Эндокринологический научный центр» Минздрава России</institution></aff><pub-date date-type="pub" iso-8601-date="2015-03-15" publication-format="electronic"><day>15</day><month>03</month><year>2015</year></pub-date><volume>87</volume><issue>3</issue><issue-title xml:lang="en">VOL 87, NO3 ()</issue-title><issue-title xml:lang="ru">ТОМ 87, №3 (2015)</issue-title><fpage>83</fpage><lpage>87</lpage><history><date date-type="received" iso-8601-date="2020-04-10"><day>10</day><month>04</month><year>2020</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2015, Consilium Medicum</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2015, ООО "Консилиум Медикум"</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="en">Consilium Medicum</copyright-holder><copyright-holder xml:lang="ru">ООО "Консилиум Медикум"</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by-nc-sa/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://ter-arkhiv.ru/0040-3660/article/view/31730">https://ter-arkhiv.ru/0040-3660/article/view/31730</self-uri><abstract xml:lang="en"><p>Hereditary lipodystrophies (HLD) are a heterogeneous group of rare diseases characterized by a complete or partial loss of subcutaneous fat and by the development of metabolic disturbances: diabetes mellitus with obvious insulin resistance and acanthosis nigricans, dyslipidemia, hepatic steatosis, hypertension, and polycystic ovary syndrome. The laminopathy variant familial partial lipodystrophy type 2 or Dunnigan syndrome (FPLD2) is the most common cause of partial LD. The paper describes a family (3 clinical cases) with FPLD2 caused by heterozygous R482W missense mutations in the gene encoding the protein lamin A/C (LMNA; 150330). This observation demonstrates that specialists should be more aware of this disease and make a timely diagnose in cases of concurrent severe metabolic disturbances at a young age, which contributes to more effective treatment of patients and to medical genetic counseling of their families.</p></abstract><trans-abstract xml:lang="ru"><p>Наследственные липодистрофии (НЛД) представляют собой гетерогенную группу редких заболеваний, характеризующихся полной или частичной потерей подкожной жировой клетчатки, а также развитием метаболических нарушений: сахарного диабета с выраженной инсулинорезистентностью и acanthosis nigricans, дислипидемии, стеатоза печени, артериальной гипертонии, синдрома поликистозных яичников. Наиболее частой причиной парциальной липодистрофии (ЛД) является вариант ламинопатий, семейная парциальная ЛД 2-го типа (FPLD2), или синдром Dunnigan. Описана семья (3 клинических случая) с FPLD2, обусловленной гетерозиготной миссенс-мутацией R482W в гене, кодирующем белок ламин A/C (LMNA; 150330). Это наблюдение демонстрирует необходимость увеличения осведомленности специалистов о данном заболевании и своевременно установленного диагноза в случаях сочетания выраженных метаболических нарушений в молодом возрасте, что способствует более эффективному лечению пациентов и проведению медико-генетического консультирования их семей.</p></trans-abstract><kwd-group xml:lang="en"><kwd>lipodystrophy</kwd><kwd>LMNA</kwd><kwd>insulin resistance</kwd><kwd>diabetes mellitus</kwd><kwd>acanthosis nigricans</kwd><kwd>LMNA</kwd><kwd>acanthosis nigricans</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>липодистрофия</kwd><kwd>инсулинорезистентность</kwd><kwd>сахарный диабет</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Den Dunnen J.T., Antonarakis S.E. 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