Study of serum hepcidin in patients with chronic hepatitis C

Abstract

Objective The aim of the present work was to study serum hepcidin in patients with chronic hepatitis C (CHC) as an iron homoeostasis-regulating hormone. Background Persistent infection with hepatitis C virus (HCV) is a major cause of chronic liver disease. Many experimental and clinical studies suggest that excessive iron in CHC is a cofactor promoting the progression of liver damage and increasing the risk for fibrosis. Patients and methods In all, 40 patients with CHC (group 1) and 20 healthy individuals (group 2) who served as a control group were included in this study. All patients were subjected to the following: full and detailed history taking, complete clinical examinations, routine laboratory investigations such as complete blood count, liver function tests, prothrombin time, serum creatinine, antinuclear antibody, thyroid-stimulating hormone, α-fetoprotein, viral markers, PCR for hepatitis C, serum hepcidin (ng/ml), serum iron (μg/dl), serum ferritin (ng/ml) and serum total iron-binding capacity (TIBC) (μg/dl), abdominal ultrasound and liver biopsy for CHC patients only for histopathological examination according Metavir scoring. Results Serum hepcidin (ng/ml) was highly significantly lower in CHC patients than in controls (7.95 ± 1.72 and 17.09 ± 1.19, respectively; P Conclusion Hepcidin levels (ng/ml) in patients with CHC were significantly lower than that in HCV-negative individuals. It is an important factor in iron abnormalities and is detected in such cases in which serum iron (μg/dl) levels are significantly low. However, serum ferritin (ng/ml) and serum TIBC (μg/dl) were significantly high in CHC patients compared with HCV-negative individuals.