Published online Oct 16, 2021. doi: 10.12998/wjcc.v9.i29.8749
Peer-review started: January 29, 2021
First decision: May 2, 2021
Revised: May 20, 2021
Accepted: September 8, 2021
Article in press: September 8, 2021
Published online: October 16, 2021
Processing time: 259 Days and 5.1 Hours
There is little evidence about the association of pre-existing hepatitis C infection (HCV) with outcomes in patients with coronavirus disease 2019 (COVID-19).
To assess the prevalence of history of HCV among patients with COVID-19 and to study the relationship of in-hospital mortality in relation with other predictors of poor outcomes in the presence or absence of COVID-19 induced acute liver injury.
In a retrospective single-center study design, 1193 patients with COVID-19 infection were studied. Patients were then classified into those with and without a history of HCV, 50 (4.1%) and 1157 (95.9%) respectively.
Multivariate cox-regression models showed that age, HCV, D-Dimer, and ferritin were the only predictors of in-hospital mortality. Acute liver injury and fibrosis score (Fib-4 score) were not different between both groups. Multivariate cox-regression model for liver profile revealed that aspartate aminotransferase/ alanine aminotransferase ratio, Fib-4 score, and HCV were predictors of in-hospital mortality. After propensity score matching HCV was the only predictor of mortality in the multivariate cox-regression model. A model including HCV was found to add predictive value to clinical and laboratory parameters.
In patients with COVID-19, history of HCV infection leads to an accentuated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virulence, irres
Core Tip: In patients with coronavirus disease 2019 (COVID-19), history of hepatitis C infection accentuated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral virulence and is a strong predictor of in-hospital mortality irrespective of baseline comorbidities, laboratory parameters, or COVID-19-induced liver injury. History of hepatitis C infection (HCV) in these patients seems to add a cumulative mortality risk to any clinical or laboratory profile. The mechanisms involved may be related to extra hepatic effects of HCV leading to enhanced ACE-2/TMPRSS mechanisms of SARS-CoV-2 virus and subsequent endothelial dysfunction. The realization is important for better characterization of the disease and triage this sub-group as high risk for therapeutic or prophylactic measures like vaccines.
