RESUMO
The liver is the main body site for iron stores and central in the regulation of iron homeostasis. Elevated serum ferritin and hepatic iron concentrations are frequently observed in chronic hepatitis C [CHC], and may be associated with more aggressive disease and decreased responsiveness to interferon therapy. It is now established that hepcidin, a peptide hormone made in the liver, is the principal regulator of systemic iron homeostasis. Because the role of hepcidin in CHC remains unclear, we aimed in this study to generate more information about it and its role in CHC and cirrhosis caused by CHC. This work was carried out on 20 chronic liver patients with HCV infection divided into two groups: Group 1: 10 patients with chronic hepatitis C [CHC], and Group 2: 10 patients with post hepatitis C liver cirrhosis A control group of 10 age and sex matched individuals undergoing emergency abdominal surgery was also included. Hepcidin mRNA from liver biopsy samples was extracted and quantified. Hepcidin mRNA levels were then correlated with haemoglobin, serum iron, ferritin, aspartate aminotransferase, alanine aminotransferase, prothrombin time, serum albumin, bilirubin, hepatic necroinflammatory activity and fibrosis. Liver Hepcidin mRNA expression correlated significantly with serum ferritin, serum albumin, prothrombin time, and liver fibrosis staging. However it did not correlate with haemoglobin, serum iron, transferrin receptor ALT, AST or hepatic necroinflammatory scoring. Hepcidin plays a unique role in hepatitis C infection. In CHC hepcidin gene expression shows no correlation with hepatic inflammatory activity contrary to other inflammatory conditions. Hepcidin gene expression correlates with serum albumin levels and hepatic fibrosis and could therefore be considered a marker for progression of fibrosis and hepatic dysfunction. Liver hepcidin gene expression correlates with ferritin levels indicating that its increase may be in response to increased iron stores with the purpose of down regulating iron absorption. Further studies could lead to improved understanding of the pathophysiology of systemic and hepatic iron disorders, and result in improved therapy for hepatitis C