Digestive Diseases Section, Yale University School of Medicine, New Haven, Connecticut; VA-Connecticut Healthcare System, West Haven, Connecticut.
Yale University School of Medicine, New Haven, Connecticut.
Clin Gastroenterol Hepatol. 2021 Oct;19(10):2182-2191.e7. doi: 10.1016/j.cgh.2021.05.022. Epub 2021 May 15.
BACKGROUND & AIMS: Coronavirus-19 disease (COVID-19) is associated with hepatocellular liver injury of uncertain significance. We aimed to determine whether development of significant liver injury during hospitalization is related to concomitant medications or processes common in COVID-19 (eg, ischemia, hyperinflammatory, or hypercoagulable states), and whether it can result in liver failure and death.
There were 834 consecutive patients hospitalized with COVID-19 who were included. Clinical, medication, and laboratory data were obtained at admission and throughout hospitalization using an identified database. Significant liver injury was defined as an aspartate aminotransferase (AST) level 5 or more times the upper limit of normal; ischemia was defined as vasopressor use for a minimum of 2 consecutive days; hyperinflammatory state was defined as high-sensitivity C-reactive protein value of 100 mg/L or more, and hypercoagulability was defined as D-dimer 5 mg/L or more at any time during hospitalization.
A total of 105 (12.6%) patients developed significant liver injury. Compared with patients without significant liver injury, ischemia (odds ratio [OR], 4.3; range, 2.5-7.4; P < .0001) and tocilizumab use (OR, 3.6; range, 1.9-7.0; P = .0001) were independent predictors of significant liver injury. Although AST correlated closely with alanine aminotransferase (R = 0.89) throughout hospitalization, AST did not correlate with the international normalized ratio (R = 0.10) or with bilirubin level (R = 0.09). Death during hospitalization occurred in 136 (16.3%) patients. Multivariate logistic regression showed that significant liver injury was not associated with death (OR, 1.4; range, 0.8-2.6; P = .2), while ischemic (OR, 2.4; range, 1.4-4.0; P = .001), hypercoagulable (OR, 1.7; range, 1.1-2.6; P = .02), and hyperinflammatory (OR, 1.9; range, 1.2-3.1; P = .02) disease states were significant predictors of death.
Liver test abnormalities known to be associated with COVID-19 are secondary to other insults, mostly ischemia or drug-induced liver injury, and do not lead to liver insufficiency or death.
冠状病毒病（COVID-19）与意义不明的肝细胞损伤有关。我们旨在确定在住院期间是否出现显著的肝损伤是否与 COVID-19 中常见的合并症或过程有关（例如，缺血、高炎症或高凝状态），以及是否会导致肝功能衰竭和死亡。
连续纳入了 834 例因 COVID-19 住院的患者。通过已确定的数据库在入院时和整个住院期间获取临床、药物和实验室数据。显著肝损伤定义为天门冬氨酸氨基转移酶（AST）水平高于正常上限 5 倍以上；缺血定义为至少连续 2 天使用血管加压药；高炎症状态定义为高敏 C 反应蛋白值≥100mg/L；高凝状态定义为住院期间任何时候 D-二聚体≥5mg/L。
共有 105 例（12.6%）患者发生显著肝损伤。与无显著肝损伤的患者相比，缺血（比值比[OR]，4.3；范围，2.5-7.4；P<0.0001）和托珠单抗使用（OR，3.6；范围，1.9-7.0；P=0.0001）是显著肝损伤的独立预测因子。尽管 AST 在整个住院期间与丙氨酸氨基转移酶（ALT）密切相关（R=0.89），但 AST 与国际标准化比值（INR）（R=0.10）或胆红素水平（R=0.09）不相关。住院期间有 136 例（16.3%）患者死亡。多变量逻辑回归显示，显著肝损伤与死亡无关（OR，1.4；范围，0.8-2.6；P=0.2），而缺血（OR，2.4；范围，1.4-4.0；P=0.001）、高凝状态（OR，1.7；范围，1.1-2.6；P=0.02）和高炎症状态（OR，1.9；范围，1.2-3.1；P=0.02）是死亡的显著预测因子。
与 COVID-19 相关的已知肝功能检查异常继发于其他损伤，主要是缺血或药物性肝损伤，不会导致肝功能不全或死亡。
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