Pre-existing liver disease is associated with poor outcome in patients with SARS CoV2 infection; The APCOLIS Study (APASL COVID-19 Liver Injury Spectrum Study)
Pre-existing liver disease is associated with poor outcome in patients with SARS CoV2 infection; The APCOLIS Study (APASL COVID-19 Liver Injury Spectrum Study)
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DOI：
10.1007/s12072-020-10072-8
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发表时间：
2020-07-04
影响因子：
6.6
通讯作者：
Omata, Masao
中科院分区：
文献类型：
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作者：
Sarin, Shiv Kumar;Choudhury, Ashok;Omata, Masao
背景和目的COVID-19是一种主要的肺部疾病，根据合并症的不同，可累及多系统。它在已有慢性肝病（CLD）患者中的情况在很大程度上是未知的。我们研究了伴有或不伴有肝硬化的CLD患者的SARS-Cov-2肝损伤模式。方法收集来自13个亚洲国家的已知或新诊断的CLD确诊COVID-19患者的数据。结果共纳入228例患者（185例无肝硬化CLD， 43例有肝硬化CLD），合并症近80%。代谢相关的脂肪肝（113.61%）和病毒病因（26.60%）是常见的。在没有肝硬化的CLD中，糖尿病[57.7% vs 39.7%, OR = 2.1 (1.1-3.7), p = 0.01]和肝硬化中，肥胖[64.3% vs 17.2%, OR = 8.1 (1.9-38.8), p = 0.002]比没有肝硬化的CLD更易发生肝损伤。无肝硬化的CLD患者中有43%表现为急性肝损伤，20%的肝硬化患者表现为急性伴慢性肝功能衰竭[5(11.6%)]或急性代偿失代偿[4(9%)]。肝相关并发症随肝病分期增加（p < 0.05）；Child-Turcotte Pugh评分≥9预示高死亡率[AUROC 0.94, HR = 19.2 (95 CI 2.3-163.3), p < 0.001，敏感性85.7%，特异性94.4%]。失代偿性肝硬化中，57%的患者肝损伤是进行性的，死亡率为43%。胆红素升高和AST/ALT比值预测肝硬化患者的死亡率。结论SARS-Cov-2感染导致CLD患者肝损伤明显，使肝硬化失代偿率达到1 / 5，并使已失代偿者的临床状况进一步恶化。合并糖尿病和肥胖的CLD患者易感，应密切监测。
Background and aims COVID-19 is a dominant pulmonary disease, with multisystem involvement, depending upon comorbidities. Its profile in patients with pre-existing chronic liver disease (CLD) is largely unknown. We studied the liver injury patterns of SARS-Cov-2 in CLD patients, with or without cirrhosis. Methods Data was collected from 13 Asian countries on patients with CLD, known or newly diagnosed, with confirmed COVID-19. Results Altogether,228 patients [185 CLD without cirrhosis and 43 with cirrhosis] were enrolled, with comorbidities in nearly 80%. Metabolism associated fatty liver disease (113, 61%) and viral etiology (26, 60%) were common. In CLD without cirrhosis, diabetes [57.7% vs 39.7%, OR = 2.1 (1.1-3.7), p = 0.01] and in cirrhotics, obesity, [64.3% vs. 17.2%, OR = 8.1 (1.9-38.8), p = 0.002] predisposed more to liver injury than those without these.Forty three percent of CLD without cirrhosis presented as acute liver injury and 20% cirrhotics presented with either acute-on-chronic liver failure [5 (11.6%)] or acute decompensation [4 (9%)]. Liver related complications increased (p < 0.05) with stage of liver disease; a Child-Turcotte Pugh score of 9 or more at presentation predicted high mortality [AUROC 0.94, HR = 19.2 (95 CI 2.3-163.3), p < 0.001, sensitivity 85.7% and specificity 94.4%). In decompensated cirrhotics, the liver injury was progressive in 57% patients, with 43% mortality. Rising bilirubin and AST/ALT ratio predicted mortality among cirrhosis patients. Conclusions SARS-Cov-2 infection causes significant liver injury in CLD patients, decompensating one fifth of cirrhosis, and worsening the clinical status of the already decompensated. The CLD patients with diabetes and obesity are more vulnerable and should be closely monitored.