Immune Response and Risk of Decompensation following SARS-CoV-2 Infection in Outpatients with Advanced Chronic Liver Disease

Author:

Brujats Anna12,Huerta Anna1,Osuna-Gómez Rubén3ORCID,Guinart-Cuadra Albert3ORCID,Ferrero-Gregori Andreu1ORCID,Pujol Clàudia1,Soriano German124ORCID,Poca Maria14,Fajardo Javier1,Escorsell Angels124ORCID,Gallego Adolfo1,Vidal Silvia3ORCID,Villanueva Càndid124,Alvarado-Tapias Edilmar124ORCID

Affiliation:

1. Department of Gastroenterology and Hepatology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Insitute Sant Pau (IIB Sant Pau), 08041 Barcelona, Spain

2. Departament Medicina UAB, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain

3. Inflammatory Diseases Department, Institut Recerca Hospital de la Santa Creu i Sant Pau (IR Sant Pau), 08041 Barcelona, Spain

4. Centre for Biomedical Research in Liver and Digestive Diseases Network (CIBERehd), Instituto de Salud Carlos III, 28029 Madrid, Spain

Abstract

Advanced chronic liver disease (ACLD) is associated with a wide spectrum of immune dysfunction. The clinical impact of SARS-CoV-2 on the development of decompensation and immune response in unvaccinated outpatients has not as yet been clearly defined. This study aimed to evaluate the clinical and immunological impact of SARS-CoV-2 on outpatients with ACLD. This is an observational case–control study, in which ACLD outpatients were included prospectively and consecutively and classified into two groups: SARS-CoV-2 infected and non-infected. Patients’ baseline characteristics and infection data were collected and analyzed. Immunoglobulin G (IgG) levels against Spike 1 were evaluated. The primary endpoint was risk of liver decompensation during follow-up, assessed after propensity score matching and adjusted by Cox regression. Between October 2020 and July 2021, ACLD outpatients (n = 580) were identified, and 174 patients with clinical follow-up were included. SARS-CoV-2 infection incidence was 7.6% (n = 44). Risk of liver decompensation was significantly higher after infection (HR = 2.43 [1.01–5.86], p = 0.048) vs. non-infection. The time of IgG evaluation was similar in all patients (n = 74); IgG concentrations were significantly higher in compensated vs. decompensated patients (1.02 ± 0.35 pg/mL vs. 0.34 ± 0.16 pg/mL, p < 0.0001) and correlated with hemoglobin levels. The dysregulation of the innate immune response in patients with decompensated liver disease increased the risk of further decompensation following SARS-CoV-2, mainly due to a worsening of ascites.

Funder

Instituto de Salud Carlos III

ISCIII and Fondos Feder

Publisher

MDPI AG

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