BackgroundPatients with chronic hepatitis C (CHC) often have increased liver iron, a condition associated with reduced sustained response to antiviral therapy, more rapid progression to cirrhosis, and development of hepatocellular carcinoma. The hepatic hormone hepcidin is the major regulator of iron metabolism and inhibits iron absorption and recycling from erythrophagocytosis. Hepcidin decrease is a possible pathophysiological mechanism of iron overload in CHC, but studies in humans have been hampered so far by the lack of reliable quantitative assays for the 25-amino acid bioactive peptide in serum (s-hepcidin).AimsTo determine the clinical relevance of hepatic producing iron regulatory hormone-hepcidin, on iron overload in patients with chronic hepatitis C (CHC). And To detect the effect of interferon based therapy on hepcidin level correlating it with early virological response (This may be later used as a predictor of response to interferon therapy according to hepcidin levels). Patient&MethodsSerum hepcidin measured in 30 CHC patients by surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS), and compared to those of healthy controls and analyzed their relationship to the clinical, hematological, and histological findings. The sequential changes of hepcidin were investigated in CHC patients treated with a 24 weeks-course of pegylated-interferon (PEG-IFN) plus ribavirin therapy.ResultsSerum hepcidin was significantly lower in CHC patients compared to the control group Serum hepcidin was positively correlated with serum ferritin. Serum hepcidin-to-ferritin ratios were significantly lower in HCV positive patients than in HCV negative controls . This relative impairment of hepcidin production was fully reversible after 24 weeks courseby PEG-IFN plus ribavirin. ConclusionsThe consequences of dysregulation of the hepcidin expressionby HCV may be an important mechanism underlying the iron overload seen in CHC and may have significant implications for the management of chronic HCV infection. Improvement for its regulation or supplementation of hepcidin may be beneficial for CHCpatients with iron overload.