Bender Joshua M, Worman Howard J
Department of Medicine, Vagelos College of Physicians and Surgeons Columbia University New York New York USA.
Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons Columbia University New York New York USA.
JGH Open. 2021 Aug 24;5(10):1166-1171. doi: 10.1002/jgh3.12645. eCollection 2021 Oct.
While many studies have reported on liver injury in patients with coronavirus disease 2019 (COVID-19), none have specifically addressed the significance of hepatic jaundice. We aimed to determine the clinical consequences and etiologies of jaundice in patients with COVID-19.
We retrospectively analyzed clinical features, laboratory abnormalities, and rates of survival and intensive care unit admission in 551 patients with COVID-19, hospitalized between 1 March 2020, and 31 May 2020 at a tertiary care academic medical center. Hepatic jaundice was defined as a serum total bilirubin concentration >2.5 mg/dL and a direct bilirubin concentration >0.3 mg/dL that was >25% of the total. Liver injury was characterized as cholestatic, mixed, or hepatocellular at the time of peak serum total bilirubin concentration by calculating the R factor.
Hepatic jaundice was present in 49 (8.9%) patients and associated with a mortality rate of 40.8% and intensive care unit admission rate of 69.4%, both significantly higher than for patients without jaundice. Jaundiced patients had an increased frequency of fever, leukopenia, leukocytosis, thrombocytopenia, hypotension, hypoxemia, elevated serum creatinine concentration, elevated serum procalcitonin concentration, and sepsis. Nine jaundiced patients had isolated hyperbilirubinemia. Of the 40 patients with abnormally elevated serum alanine aminotransferase or alkaline phosphatase activities, 62.5% had a cholestatic, 20.0% mixed, and 17.5% hepatocellular pattern of liver injury.
Hepatic jaundice in patients with COVID-19 is associated with high mortality. The main etiologies of liver dysfunction leading to jaundice appear to be sepsis, severe systemic inflammation, and hypoxic/ischemic hepatitis.
尽管许多研究报告了2019冠状病毒病(COVID-19)患者的肝损伤情况,但尚无研究专门探讨肝性黄疸的意义。我们旨在确定COVID-19患者黄疸的临床后果及病因。
我们回顾性分析了2020年3月1日至2020年5月31日在一家三级医疗学术医学中心住院的551例COVID-19患者的临床特征、实验室异常情况以及生存率和重症监护病房入住率。肝性黄疸定义为血清总胆红素浓度>2.5mg/dL且直接胆红素浓度>0.3mg/dL,且直接胆红素浓度占总胆红素浓度的比例>25%。通过计算R因子,在血清总胆红素浓度峰值时将肝损伤分为胆汁淤积型、混合型或肝细胞型。
49例(8.9%)患者出现肝性黄疸,其死亡率为40.8%,重症监护病房入住率为69.4%,均显著高于无黄疸患者。黄疸患者发热、白细胞减少、白细胞增多、血小板减少、低血压、低氧血症、血清肌酐浓度升高、血清降钙素原浓度升高及脓毒症的发生率增加。9例黄疸患者仅有单纯高胆红素血症。在血清丙氨酸氨基转移酶或碱性磷酸酶活性异常升高的40例患者中,62.5%为胆汁淤积型肝损伤,20.0%为混合型,17.5%为肝细胞型。
COVID-19患者的肝性黄疸与高死亡率相关。导致黄疸的肝功能障碍的主要病因似乎是脓毒症、严重全身炎症及缺氧/缺血性肝炎。