Результаты исследований: Научные публикации в периодических изданиях › Обзорная статья › Рецензирование
Поражение печени у больных COVID-19. / Вологжанин, Дмитрий Александрович; Голота, Александр Сергеевич; КАМИЛОВА , ТАТЬЯНА АСКАРОВНА; Макаренко, Станислав Вячеславович; Щербак, Сергей Григорьевич.
в: Медицина экстремальных ситуаций, № 1, 01.2022, стр. 12-19.Результаты исследований: Научные публикации в периодических изданиях › Обзорная статья › Рецензирование
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TY - JOUR
T1 - Поражение печени у больных COVID-19
AU - Вологжанин, Дмитрий Александрович
AU - Голота, Александр Сергеевич
AU - КАМИЛОВА , ТАТЬЯНА АСКАРОВНА
AU - Макаренко, Станислав Вячеславович
AU - Щербак, Сергей Григорьевич
PY - 2022/1
Y1 - 2022/1
N2 - The clinical spectrum of SARS-CoV-2 infection continues to expand, raising important fundamental issues regarding the SARS-CoV-2 cellular tropism and pathogenic mechanisms. Liver damage is observed in patients with all forms of COVID-19, especially severe and critical forms, which could be due to the direct viral damage, immune dysregulation (systemic inflammatory response and cytokine storm), hypoxia-ischemia, drug-induced hepatotoxicity, and concomitant chronic disorders. Liver damage, defined primarily by elevated transaminase levels, is often observed in patients with COVID-19 and correlates with clinical outcomes, including mortality. Diagnostic criteria, pathogenesis, clinical characteristics, treatment, and prognosis of liver injury in COVID-19 should be clarified in further clinical trials. Currently, there is a critical shortage of proven treatment options for patients with COVID-19, resulting in an urgent need to study the multiple organ failure and liver damage pathogenesis in patients with this disease. The review provides information about the pathophysiological mechanisms of the SARS-CoV-2-induced liver damage and the development of liver failure in COVID-19. Information sources were searched in the PubMed database using the keywords “liver damage in COVID-19” and “immune liver damage in COVID-19”.
AB - The clinical spectrum of SARS-CoV-2 infection continues to expand, raising important fundamental issues regarding the SARS-CoV-2 cellular tropism and pathogenic mechanisms. Liver damage is observed in patients with all forms of COVID-19, especially severe and critical forms, which could be due to the direct viral damage, immune dysregulation (systemic inflammatory response and cytokine storm), hypoxia-ischemia, drug-induced hepatotoxicity, and concomitant chronic disorders. Liver damage, defined primarily by elevated transaminase levels, is often observed in patients with COVID-19 and correlates with clinical outcomes, including mortality. Diagnostic criteria, pathogenesis, clinical characteristics, treatment, and prognosis of liver injury in COVID-19 should be clarified in further clinical trials. Currently, there is a critical shortage of proven treatment options for patients with COVID-19, resulting in an urgent need to study the multiple organ failure and liver damage pathogenesis in patients with this disease. The review provides information about the pathophysiological mechanisms of the SARS-CoV-2-induced liver damage and the development of liver failure in COVID-19. Information sources were searched in the PubMed database using the keywords “liver damage in COVID-19” and “immune liver damage in COVID-19”.
KW - COVID-19
KW - concomitant chronic liver disease
KW - coronavirus SARS-CoV-2
KW - drug-induced hepatotoxicity
KW - immune liver damage
KW - liver damage
KW - сsystemic hepatotoxicity
KW - COVID-19
KW - concomitant chronic liver disease
KW - coronavirus SARS-CoV-2
KW - drug-induced hepatotoxicity
KW - immune liver damage
KW - liver damage
KW - сsystemic hepatotoxicity
UR - http://www.scopus.com/inward/record.url?scp=85135136800&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/4ca5e6e1-b48e-39e5-ba63-2dc9b44792c5/
U2 - 10.47183/mes.2022.009
DO - 10.47183/mes.2022.009
M3 - Обзорная статья
SP - 12
EP - 19
JO - Медицина экстремальных ситуаций
JF - Медицина экстремальных ситуаций
SN - 2306-6326
IS - 1
ER -
ID: 101141386