Serum markers of iron metabolism in chronic hepatitis C virus infections

Abstract

Background Hepatitis C virus (HCV) infection is a common cause of chronic hepatitis, which leads to cirrhosis of the liver and hepatocellular carcinoma. Chronic hepatitis can cause iron buildup in the liver and result in liver injury. The major iron metabolism regulator, the hepatic hormone hepcidin, inhibits iron absorption and recycling, and as hepcidin is suppressed by the virus, it contributes to the pathogenesis of the liver. Aim To assess serum iron markers in patients with chronic hepatitis C (CHC) as opposed to people who are healthy and a summary of interactions of HCV and iron overload. Patients and methods This case–control study was performed on 30 hepatitis C-infected Egyptian patients (group I) and 15 apparently healthy control (group II). Routine laboratory investigations, as well as serum hepcidin and iron marker assessments were performed. Results Throughout this study, the serum hepcidin level in patients significantly decreased relative to the control group (P<0.001). The patients showed significantly higher serum iron, transferrin saturation, alanine aminotransferase, and aspartate aminotransferase compared with the control group (P<0.001). Serum albumin in patients’ group was considerably decreased in comparison with the control (P<0.05). There was a highly statistically significant lower platelet count value in patients compared with the control group (P<0.001). The interaction between hepcidin and iron, transferrin, and alanine aminotransferase is significantly negative. Conclusion Hepatic iron deposition is a joint feature in patients with CHC. Chronic HCV infection may reduce serum hepcidin, which may lead to iron overload in these patients. So hepcidin is a surrogate marker for evaluation of iron overload in patients with CHC.