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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">32259</article-id><article-id pub-id-type="doi">10.17116/terarkh20178985-12</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">Molecular genetic predictors of resistance to anti-Helicobacter pylori therapy</article-title><trans-title-group xml:lang="ru"><trans-title>Молекулярно-генетические предикторы резистентности к антихеликобактерной терапии</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Maev</surname><given-names>I V</given-names></name><name xml:lang="ru"><surname>Маев</surname><given-names>И В</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Andreev</surname><given-names>D N</given-names></name><name xml:lang="ru"><surname>Андреев</surname><given-names>Д Н</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en"></institution></aff><aff><institution xml:lang="ru">ФГБОУ ВО «Московский государственный медико-стоматологический университет им. А.И. Евдокимова» Минздрава России</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2017-08-15" publication-format="electronic"><day>15</day><month>08</month><year>2017</year></pub-date><volume>89</volume><issue>8</issue><issue-title xml:lang="en">VOL 89, NO8 ()</issue-title><issue-title xml:lang="ru">ТОМ 89, №8 (2017)</issue-title><fpage>5</fpage><lpage>12</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 ©; 2017, Consilium Medicum</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2017, ООО "Консилиум Медикум"</copyright-statement><copyright-year>2017</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/32259">https://ter-arkhiv.ru/0040-3660/article/view/32259</self-uri><abstract xml:lang="en"><p>In current clinical practice, there is no optimal empirical therapy for Helicobacter pylori (H. pylori) infection and there is a progressive decrease in the efficiency of classical eradication therapy (ET) regimens. The variability in the efficiency of ET in a specific patient is largely due to the heterogeneous molecular genetic mechanisms underlying the resistance of the microorganism to the components of the treatment regimens. The basis of the mechanisms for antibiotic resistance in H. pylori is mainly the point mutations in some genes, which determine alterations in the mechanisms of action of drugs, such as clarithromycin (domain V of 23S rRNA), metronidazole (rdxA, frxA), amoxicillin (pbp1A), tetracycline (16S rRNA), and levofloxacin (gyrA). The predictors of resistance to ET are also the CagA-negative status of the microorganism and the presence of the vacA s2 allele. There are a number of host genetic determinants (the CYP2C19 genotype (*1/*1, *1/*17, *17/*17) and the MDR1 3435 T/T genotype (in an Asian population)) that reduce the efficiency of ET, by altering the pharmacokinetics of proton pump inhibitors. In addition, the IL-1β-511 C/C polymorphism that affects gastric acid secretion is a predictor of the inefficiency of ET.</p></abstract><trans-abstract xml:lang="ru"><p>Аннотация В настоящее время в клинической практике отсутствует оптимальная эмпирическая терапия инфекции Helicobacter pylori (H. pylori) и отмечается прогрессивное снижение эффективности классических схем эрадикационной терапии (ЭТ). Во многом вариативность эффективности ЭТ у конкретного пациента объясняется гетерогенными молекулярно-генетическими механизмами, лежащими в основе резистентности микроорганизма к компонентам схем лечения. В основе механизмов формирования резистентности H. pylori к антибактериальным препаратам преимущественно лежат точечные мутации в определенных генах, обусловливающие альтерацию механизмов действия препаратов: кларитромицин (V домен 23S рРНК), метронидазол (rdxA, frxA), амоксицилин (pbp1A), тетрациклин (16S рРНК), левофлоксацин (gyrA). Предикторами резистентности к ЭТ также являются отрицательный статус микроорганизма по CagA и наличие аллеля VacA s2. Существует ряд генетических детерминант макроорганизма, снижающих эффективность ЭТ, изменяя фармакокинетику ингибиторов протонного насоса: генотип CYP2C19 (*1/*1, *1/*17, *17/*17) и MDR1 3435 T/T (для азиатской популяции). Кроме того, полиморфизм IL-1β-511 С/C, влияющий на кислотопродукцию в желудке, является предиктором неэффективности ЭТ.</p></trans-abstract><kwd-group xml:lang="en"><kwd>Helicobacter pylori</kwd><kwd>eradication therapy</kwd><kwd>resistance</kwd><kwd>antibiotics</kwd><kwd>proton pump inhibitors</kwd><kwd>CagA</kwd><kwd>VacA</kwd><kwd>CYP2C19</kwd><kwd>MDR1</kwd><kwd>and IL1β</kwd><kwd>Helicobacter pylori</kwd><kwd>CagA</kwd><kwd>vacA</kwd><kwd>CYP2C19</kwd><kwd>MDR1</kwd><kwd>IL-1β</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>эрадикационная терапия</kwd><kwd>резистентность</kwd><kwd>антибактериальные препараты</kwd><kwd>ингибиторы протонного насоса</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Маев И.В., Самсонов А.А., Андреев Д.Н., Гречушников В.Б., Коровина Т.И. Клиническое значение инфекции Helicobacter pylori. 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