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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">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/2079-701X-2015-13-80-85</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-340</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>БОЛЕЗНИ ГЕПАТОБИЛИАРНОЙ СИСТЕМЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>DISEASES OF THE HEPATOBILIARY SYSTEM</subject></subj-group></article-categories><title-group><article-title>Аммиак как нейро- и гепатотоксин: клинические аспекты</article-title><trans-title-group xml:lang="en"><trans-title>Ammonia as a neuro- and hepatotoxin: clinical aspects</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>Буеверов</surname><given-names>А. О.</given-names></name><name name-style="western" xml:lang="en"><surname>Bueverov</surname><given-names>A. O.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Первый Московский государственный медицинский университет им. И.М. Сеченова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>First Moscow State Medical University named after I.M. Sechenov</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>30</day><month>12</month><year>2015</year></pub-date><volume>0</volume><issue>13</issue><fpage>80</fpage><lpage>85</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Буеверов А.О., 2015</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="ru">Буеверов А.О.</copyright-holder><copyright-holder xml:lang="en">Bueverov A.O.</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.med-sovet.pro/jour/article/view/340">https://www.med-sovet.pro/jour/article/view/340</self-uri><abstract><p>Аммиак - наиболее хорошо изученный и, по-видимому, важнейший патогенетический фактор печеночной энцефалопатии (ПЭ). Патогенез ПЭ имеет некоторые различия в зависимости от варианта повреждения печени. Помимо нейротоксических, аммиак обладает универсальными цитотоксическими, в том числе гепатотоксическими свойствами. Недавно проведенное исследование позволило констатировать наличие гипераммониемии у пациентов с начальными изменениями печени, что ведет к латентной когнитивной дисфункции, проявляющейся нарушением реакции в стрессовых ситуациях. Медикаментозная терапия ПЭ направлена в первую очередь на предотвращение образования и ускорение метаболизма аммиака. Назначение метаболитов орнитина уменьшает гипераммониемию, способствует улучшению когнитивных функций и снижению активности трансаминаз, в том числе у пациентов с патологией печени на доцирротической стадии.</p></abstract><trans-abstract xml:lang="en"><p>Ammonia is the most studied and, apparently, the most critical pathogenetic factor for hepatic encephalopathy (HE). The pathogenesis of PE is varied depending on the type of liver damage. Apart from neurotoxic properties, ammonia has general cytotoxic as well as hepatotoxic effects. A recent study allowed to register presence of hyperammonemia in patients with initial liver changes leading to latent cognitive dysfunction, which manifests itself in impaired reaction in stressful situations. Drug therapy of PE is primarily aimed at prevention and acceleration of metabolism of ammonia. Administration of ornithine metabolites reduces hyperammonemia, improves cognitive function and reduces enzyme activity, including in patients at pre-cirrhotic stage.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>аммиак</kwd><kwd>печеночная энцефалопатия</kwd><kwd>лечение</kwd><kwd>орнитин</kwd><kwd>ammonia</kwd><kwd>hepatic encephalopathy</kwd><kwd>treatment</kwd><kwd>ornithine</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">Bernal W, Hall C, Karvellas CJ et al. 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