Introduction: The coronavirus disease 2019 (COVID-19) infection, caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), involves several organs through participation of angiotensin-conversion enzyme 2 (ACE2) receptors. The presence of ACE2 receptors in the liver renders this organ a potential target for the novel coronavirus. Methods: We performed 14 complete autopsies of patients infected with SARS-CoV-2. In each case we stained liver tissue sections with haematoxylin/eosin, Masson blue trichrome stain, periodic acid-Schiff (PAS), Perls, and performed cytokeratin-7 (CK7) immunochemistry. Results: Macroscopically, livers were pale and yellowish in 8 of 14 (57%) patients, and had a nutmeg appearance in the other 6 cases (42%). Histologically, centrolobular necrosis was observed in 12 cases (86%), and was associated with discreet to moderate lobular or portal inflammation. Steatosis was seen in 8 cases (57%), but fibrosis was rare. Cholestasis and discrete bile duct proliferation was observed in 5 cases (36%). Discussion/Conclusion: The main histological changes can be explained by the hypoxic status as a result of severe hypoxemic pneumonia leading to death. Drug toxicity may also play a role in certain cases. Other histological changes may be explained by previous hepatic conditions or underlying hepatic diseases. We concluded that COVID-19 infection was not associated with a specific histopathological pattern of the liver.

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COVID-19 相关死亡中的肝脏：主角还是无辜的旁观者？

简介：由严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 引起的 2019 年冠状病毒病 (COVID-19) 感染通过血管紧张素转换酶 2 (ACE2) 受体的参与涉及多个器官。肝脏中 ACE2 受体的存在使该器官成为新型冠状病毒的潜在目标。方法：我们对感染 SARS-CoV-2 的患者进行了 14 次完整的尸检。在每种情况下，我们都用苏木精/伊红、马森蓝三色染色、高碘酸-希夫 (PAS)、Perls 对肝组织切片进行染色，并进行细胞角蛋白-7 (CK7) 免疫化学。结果：肉眼观察，14 例患者中有 8 例（57%）肝脏呈苍白和黄色，另外 6 例（42%）呈肉豆蔻外观。组织学上，12 例 (86%) 观察到小叶中心坏死，并且与谨慎至中度的小叶或门静脉炎症有关。8 例（57%）出现脂肪变性，但纤维化罕见。在 5 例（36%）中观察到胆汁淤积和离散胆管增生。讨论/结论：主要的组织学变化可以用导致死亡的严重缺氧性肺炎导致的缺氧状态来解释。在某些情况下，药物毒性也可能起作用。其他组织学变化可以用先前的肝脏疾病或潜在的肝脏疾病来解释。我们得出结论，COVID-19 感染与肝脏的特定组织病理学模式无关。主要的组织学变化可以用严重缺氧性肺炎导致死亡导致的缺氧状态来解释。在某些情况下，药物毒性也可能起作用。其他组织学变化可以用先前的肝脏疾病或潜在的肝脏疾病来解释。我们得出结论，COVID-19 感染与肝脏的特定组织病理学模式无关。主要的组织学变化可以用严重缺氧性肺炎导致死亡导致的缺氧状态来解释。在某些情况下，药物毒性也可能起作用。其他组织学变化可以用先前的肝脏疾病或潜在的肝脏疾病来解释。我们得出结论，COVID-19 感染与肝脏的特定组织病理学模式无关。