Liver injury associated with high value of D-dimer plasmatic level in COVID-19 patients

Minerva Gastroenterol (Torino). 2023 Mar;69(1):141-148. doi: 10.23736/S2724-5985.22.03189-8. Epub 2022 Apr 26.

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

MeSH terms

  • COVID-19* / complications
  • Cross-Sectional Studies
  • Humans
  • Inflammation
  • Liver Diseases* / etiology
  • SARS-CoV-2

Substances

  • fibrin fragment D