Liptak Peter, Nosakova Lenka, Rosolanka Robert, Skladany Lubomir, Banovcin Peter
Clinic of Internal Medicine-Gastroenterology, University Hospital in Martin, Jessenius Faculty of Medicine in Martin, Comenius University, Martin 03601, Slovakia.
Clinic of Infectology and Travel Medicine, University Hospital in Martin, Jessenius Faculty of Medicine in Martin, Comenius University, Martin 03601, Slovakia.
World J Hepatol. 2023 Jan 27;15(1):41-51. doi: 10.4254/wjh.v15.i1.41.
The coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has had a significant impact on the lives of millions of people, especially those with other concomitant diseases, such as chronic liver diseases. To date, seven coronaviruses have been identified to infect humans. The main site of pathological action of these viruses is lung tissue. However, a substantial number of studies have proven that SARS-CoV-2 shows affinity towards several organs, including the gastrointestinal tract and the liver. The current state of evidence points to several proposed mechanisms of liver injury in patients with COVID-19 and their combination. Liver impairment is considered to be the result of the direct effect of the virus on the hepatic tissue cells, a systemic reaction consisting of inflammation, hypoxia and cytokine storm, drug-induced liver injury, with the possible contribution of a perturbed gut-liver axis. Reactivation of chronic hepatic disease could be another factor for liver impairment in patients with SARS-CoV-2 infection. Acute-on-chronic liver failure (ACLF) is a relatively new syndrome that occurs in 10%-30% of all hospitalized patients with chronic liver disease. It is crucial to recognize high-risk patients due to the increased morbidity and mortality in these cases. Several published studies have reported virus infection as a trigger factor for ACLF. However, to date, there are few relevant studies describing the presence of ACLF in patients with acute SARS-CoV-2 infection. In this minireview we summarize the current state of knowledge regarding the relation between ACLF and acute SARS-CoV-2 infection.
由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的2019冠状病毒病(COVID-19)大流行对数以百万计的人的生活产生了重大影响,尤其是那些患有其他伴随疾病的人,如慢性肝病患者。迄今为止,已确定有七种冠状病毒可感染人类。这些病毒的主要病理作用部位是肺组织。然而,大量研究证明,SARS-CoV-2对包括胃肠道和肝脏在内的多个器官具有亲和力。目前的证据状况指向了COVID-19患者肝损伤的几种可能机制及其组合。肝损伤被认为是病毒对肝组织细胞直接作用的结果,是一种由炎症、缺氧和细胞因子风暴组成的全身反应,药物性肝损伤,以及肠道-肝脏轴紊乱可能起到的作用。慢性肝病的再激活可能是SARS-CoV-2感染患者肝损伤的另一个因素。慢加急性肝衰竭(ACLF)是一种相对较新的综合征,在所有住院的慢性肝病患者中发生率为10%-30%。由于这些病例的发病率和死亡率增加,识别高危患者至关重要。几项已发表的研究报告称病毒感染是ACLF的触发因素。然而,迄今为止,很少有相关研究描述急性SARS-CoV-2感染患者中ACLF的存在情况。在本综述中,我们总结了关于ACLF与急性SARS-CoV-2感染之间关系的当前知识状况。