Purpose: Liver iron is frequently elevated in chronic hepatitis C and may con tribute to liver injury. The pathophysiology behind this phenomenon may involve hepcidin, a gene that is up- regulated in the liver by inflammation and iron. I nappropriately low hepcidin is important to the pathophysiology of hereditary he mochromatosis. However, the role of hepcidin in the iron loading of patients wit h hepatitis C is unknown. Subjects and Methods: To determine whether liver hepci din mRNA correlates with markers of hepatic inflammation and iron status in pati ents with hepatitis C, we extracted total RNA from liver biopsy specimens of pat ients with chronic hepatitis C and quantified hepcidin mRNA. Liver hepcidin mRNA levels were then correlated with aspartate aminotransferase, alanine aminotrans ferase, ferritin, viral load, fibrosis, hepatic iron concentration, and Hepatic Activity Index (HAI). Results: Among patients with hepatitis C, there was a sign ificant correlation of hepcidin mRNA expression in the liver with hepatic iron c oncentration and serum ferritin (r = 0.72, P = 0.006, and r = 0.60, P = 0.01, re spectively). Hepcidin mRNA expression in the liver did not correlate with aspart ate aminotransferase, alanine aminotransferase, HAI, or viral load. No differenc es in hepcidin mRNA were found based on viral genotype or the presence of fibros is. Conclusion: In contrast to other inflammatory states, hepcidin mRNA expressi on in the liver was independent of markers of inflammation in hepatitis C. Inste ad, our results suggest that iron stores in patients with hepatitis C regulate h epcidin expression and that iron loading in chronic hepatitis C is not due to in appropriate hepcidin expression. Purpose: Liver iron is frequently elevated in chronic hepatitis C and may con tribute to liver injury. The pathophysiology behind this phenomenon may involve hepcidin, a gene that is up-regulated in the liver by inflammation and iron. I nappropriately low hepcidin is important to the pathophysiology of hereditary he mochromatosis. However, the role of hepcidin in the iron loading of patients wit h hepatitis C is unknown. Subjects and Methods: To determine whether liver hepci din mRNA correlates with markers of hepatic inflammation and iron status in pati ents with Liver C, we extracted total RNA from liver biopsy specimens of patients with chronic hepatitis C and quantified hepcidin mRNA. Liver hepcidin mRNA levels were then correlated with aspartate aminotransferase, alanine aminotrans ferase, ferritin, viral load, fibrosis, hepatic iron concentration, and Hepatic Activity Index (HAI). Results: Among patients with hepatitis C, there was a signatureificant correlation of hepcidin mRN A expression in the liver with hepatic iron c oncentration and serum ferritin (r = 0.72, P = 0.006, and r = 0.60, P = 0.01, re spectively). Hepcidin mRNA expression in the liver did not correlate with aspart ate aminotransferase, alanine No differenc es in hepcidin mRNA were found based on viral genotype or the presence of fibros is. Conclusion: In contrast to other inflammatory states, hepcidin mRNA expressi on in the liver was independent of markers of inflammation in hepatitis C. Inste ad, our results suggest that iron stores in patients with hepatitis C regulate h epcidin expression and that iron loading in chronic hepatitis C is not due to inappropriate hepcidin expression.