Fibroblast Growth Factor 21 in Chronic Hepatitis C: A Potential Non-Invasive Biomarker of Liver Status upon Viral Eradication
Filippo Biagi,
Francesco Carlomagno,
Martina Carbone,
Roberta Veralli,
Umberto Vespasiani-Gentilucci,
Elisabetta Riva,
Silvia Manfrini,
Dario Tuccinardi,
Adriano De Santis,
Lucio Gnessi,
Mikiko Watanabe
Affiliations
Filippo Biagi
Department of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy
Francesco Carlomagno
Department of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy
Martina Carbone
Department of Translational and Precision Medicine, Sapienza University of Rome, 00185 Rome, Italy
Unit of Clinical Medicine and Hepatology, Area of Medicine, Campus Bio-Medico University of Rome, 00128 Rome, Italy
Elisabetta Riva
Unit of Virology, Fondazione Policlinico Universitario Campus Bio-Medico, 00128 Rome, Italy
Silvia Manfrini
Department of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, 00128 Rome, Italy
Dario Tuccinardi
Department of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, 00128 Rome, Italy
Adriano De Santis
Department of Translational and Precision Medicine, Sapienza University of Rome, 00185 Rome, Italy
Lucio Gnessi
Department of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy
Mikiko Watanabe
Department of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy
Fibroblast growth factor 21 (FGF-21), previously recognized as a marker of liver damage and a potential drug target in non-alcoholic fatty liver disease (NAFLD), has unclear implications in hepatitis C virus (HCV) infections. This study aimed to investigate the relationship between FGF-21 levels and liver health in patients with HCV undergoing direct-acting antiviral (DAA) treatment. Forty-five patients were assessed for liver stiffness, blood chemistry, and other relevant metrics before and after achieving sustained viral response (SVR), defined as the absence of detectable HCV-RNA after 24 weeks of treatment. Post-treatment, all patients showed a decrease in liver stiffness and improved liver enzyme levels (AST and ALT), alongside an increase in FGF-21 levels. Interestingly, the increase in FGF-21 correlated negatively with liver stiffness but showed no correlation with hepatic steatosis. The observed elevation in FGF-21 levels at SVR following DAA therapy for chronic HCV infection can be attributed to the restoration of hepatic function, including its synthetic capabilities. Specifically, the mitigation of liver fibrosis post-HCV eradication is expected to lead to improvements in liver function, such as enhanced albumin and FGF-21 production. This improvement in synthetic function likely drives the increase in FGF-21 levels, rather than changes in liver fat content. We suggest a potential role of FGF-21 as a marker of fibrosis and hepatic cytotoxicity and as a drug target beyond NAFLD, to be confirmed by additional studies.
