(P19) Plasma CD163 and FABP4 are biomarkers associated with residual liver disease and fibrosis recovery during DAA treatment of chronic HCV infection
Författare/Medförfattare
Jean-Baptiste Gorin [1], David F. G. Malone [1], Benedikt Strunz [1], Tony Carlsson [2], Soo Aleman [2], [3], Niklas K. Björkström [1], Karolin Falconer [2], and Johan K. Sandberg [1]
Affiliates
1 Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden. 2 Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden. 3 Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
Abstract
Direct-acting antiviral (DAA) drugs have dramatically improved the management of chronic hepatitis C (CHC). The effects of hepatitis C virus (HCV) clearance on immune parameters, inflammation and residual liver disease remain relatively little studied. Here, we identified an inflammatory plasma protein profile associated with CHC, which was not shared with alcohol-induced non-viral liver disease. DAA therapy rapidly normalized the plasma inflammatory milieu, with the exception of soluble (s)CD163, which remained elevated and segregated patients with different levels of cirrhosis. DAA-treated patients experienced durable improvement in liver fibrosis measurements. Interestingly, our data identified pre-treatment levels of fatty acid-binding protein 4 (FABP4) as a candidate biomarker of fibrosis reduction during DAA treatment. Together, these results support the notion of rapid restoration of the inflammatory state in CHC in response to DAA therapy and identify sCD163 and FABP4 as potential plasma biomarkers of residual liver disease and fibrosis improvement.