Chronic hepatitis-C infection in COVID-19 patients is associated with in-hospital mortality

Diana Ronderos1, Alaa Mabrouk Salem Omar2, Hafsa Abbas3

  • 1Department of Internal Medicine, BronxCare Hospital Center, Bronx, NY 10457, United States.

Insights

Pre-existing hepatitis C infection (HCV) significantly increases mortality risk in COVID-19 patients. This association persists regardless of liver injury, suggesting extrahepatic effects of HCV worsen COVID-19 outcomes.

Area of Science:

  • Hepatology
  • Infectious Diseases
  • Critical Care Medicine

Background:

  • Limited evidence exists on the impact of pre-existing hepatitis C virus (HCV) infection on outcomes for patients with coronavirus disease 2019 (COVID-19).
  • Understanding this association is crucial for managing COVID-19 patients with a history of HCV.

Purpose of the Study:

  • To determine the prevalence of HCV history in COVID-19 patients.
  • To investigate the relationship between HCV and in-hospital mortality, considering COVID-19-induced liver injury and other risk factors.

Main Methods:

  • A retrospective single-center study included 1193 patients with COVID-19.
  • Patients were categorized into those with (4.1%) and without (95.9%) a history of HCV.
  • Multivariate Cox-regression and propensity score matching were employed to analyze mortality predictors.

Main Results:

  • HCV, age, D-Dimer, and ferritin were identified as independent predictors of in-hospital mortality.
  • No significant difference in acute liver injury or Fib-4 scores was observed between groups.
  • HCV independently predicted mortality after propensity score matching, adding predictive value to clinical and laboratory parameters.

Conclusions:

  • A history of HCV infection exacerbates severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virulence in COVID-19 patients.
  • This effect is independent of comorbidities, admission variables, or COVID-19-induced liver injury.
  • Potential mechanisms include HCV's extrahepatic effects on viral entry, inflammation, and endothelial function.
Abstract

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