Serum and Ascitic Fluid Hepcidin in HCV Positive Liver Cirrhosis with and without HCC

Abstract

Background & Aim: Chronic HCV infection suppresses hepatic hepcidin expression which may enhance iron toxicity and lead to disease progression and HCC development. The aim of the study is to investigate the role of hepcidin in HCV+ve liver cirrhosis patients in relation to disease progression and HCC development. Patients and methods: The study population consists of: 20 HCV+ve patients without HCC (HCV patients), 20 HCV+ve patients with HCC (HCV-HCC patients) and 10 controls. In addition to comprehensive clinical examination, they were subjected to laboratory check-up for albumin, bilirubin, PT %, ferritin, AFP and hepcidin. Ascitic fluid hepcidin was done for all patients. Results: There was a significant difference among HCV and HCV-HCC patients and controls with regard serum ferritin and hepcidin (P = 0.001 & 0.0001 respectively). Serum hepcidin of HCV and HCV-HCC patients were significantly lower than controls (P = 0.0001). Serum and ascitic fluid hepcidin of HCV-HCC patients was significantly lower than HCV patients (P = 0.01 & 0.02 respectively). Serum ferritin was significantly higher in HCV and HCV-HCC patients than controls (P = 0.001). Serum ferritin of HCV-HCC patients was significantly higher than HCV patients (P = 0.02). Ascitic fluid hepcidin was negatively correlated with Child-Pugh score in HCV (r=-0.55 & P=0.01) and HCV-HCC patients (r = -0.53 & P = 0.02). Ascitic fluid hepcidin was negatively correlated with bilirubin in HCV (r = -0.43 & P=0.04) and HCV-HCC patients (r = -0.47 & P=0.04). Ascitic fluid hepcidin was positively correlated with serum albumin in HCV (r = +0.44 & P=0.04) but there was no correlation in HCV-HCC patients (r =-0.1 & P=0.7). Conclusion: Low levels of hepcidin may be involved in the pathophysiologic mechanism of iron overload in patients with chronic HCV with and without HCC. Moreover, there is a positive relationship between hepcidin levels and synthetic liver function suggesting that uniform suppression of hepcidin may be linked to disease progression and HCC development. Further analysis is still required to evaluate its usefulness as a marker for early detection of HCC by serial measurement of hepcidin in blood and ascitic fluid.