Abenavoli Ludovico, Aquila Isabella, Sacco Matteo A, Procopio Anna C, Cinaglia Pietro, Zanza Christian, Longhitano Yaroslava, Arena Vincenzo, Fagoonee Sharmila, Ricci Pietrantonio, Luzza Francesco
Department of Health Sciences, Magna Grecia University, Catanzaro, Italy -
Department of Surgical and Medical Sciences, Magna Grecia University, Catanzaro, Italy.
Minerva Gastroenterol (Torino). 2023 Mar;69(1):141-148. doi: 10.23736/S2724-5985.22.03189-8. Epub 2022 Apr 26.
The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), causal agent of the coronavirus disease (COVID-19), has infected millions of people worldwide. Currently, the scientific community debates on the direct viral responsibility of liver damage or whether the observed changes are secondary manifestations of systemic inflammation triggered by COVID-19. The hepatic involvement is associated with worse clinical outcomes and higher risk of COVID-19 related morbidity and mortality. Furthermore, SARS-CoV-2 infection may predispose patients to thrombotic disease due to excessive inflammation, platelet activation, and endothelial dysfunction.
In this paper, we reported a cross-sectional analysis of five patients affected by a severe form of COVID-19, who died between April 11 and May 1, 2020. Each patient has been subjected to a medico-legal autopsy in which both gross and histological liver changes were evaluated, as well as the correlation with the related coagulation profile.
In three cases of our cohort, the thromboembolism was recognized as cause of death. Furthermore, a significant statistical difference between D-dimer values at hospital admission and death among enrolled patients (P=0.033), was evaluated. No patient has recorded a pre-existing liver disease.
Our results support the evidence that hepatic damage in subjects with severe form of COVID-19 is related to the changes in coagulative and fibrinolytic pathways. Hence, the evaluation of D-dimer blood levels may be useful in clinical practice to predict the involvement of the liver and the prognosis of these patients. This data highlights the fundamental role of coagulation balance in subjects with advanced form of COVID-19.
严重急性呼吸综合征冠状病毒2（SARS-CoV-2）是冠状病毒病（COVID-19）的病原体，已感染全球数百万人。目前，科学界正在争论肝损伤是否直接由病毒引起，或者所观察到的变化是否是由COVID-19引发的全身炎症的继发表现。肝脏受累与更差的临床结果以及更高的COVID-19相关发病率和死亡率风险相关。此外，由于过度炎症、血小板活化和内皮功能障碍，SARS-CoV-2感染可能使患者易患血栓性疾病。
在本文中，我们报告了对2020年4月11日至5月1日期间死亡的5例重症COVID-19患者的横断面分析。每位患者均接受了法医尸检，评估了肝脏的大体和组织学变化以及与相关凝血指标的相关性。
在我们队列中的3例病例中，血栓栓塞被确认为死亡原因。此外，评估了入组患者入院时和死亡时D-二聚体值之间的显著统计学差异（P=0.033）。没有患者有既往肝病记录。
我们的结果支持了重症COVID-19患者肝损伤与凝血和纤溶途径变化相关的证据。因此，评估D-二聚体血水平在临床实践中可能有助于预测这些患者的肝脏受累情况和预后。该数据突出了凝血平衡在重症COVID-19患者中的重要作用。
