Abstract

Objectives To investigate the changes in hepcidin regulation in anemic chronic hepatitis C virus (HCV) patients with and without bleeding and the role of hepcidin in ameliorating the development of iron deficiency in anemic HCV bleeders. Background Chronic liver disease is frequently associated with anemia in about 75% of patients which is usually multifactorial. One of the causes of anemia in chronic liver disease is acute or chronic blood loss into the gastrointestinal tract, resulting in iron deficiency anemia. Hepcidin, the key regulator of iron homeostasis, has a relatively low expression level in the liver in chronic HCV patients; however, the changes in hepcidin regulation have not been examined previously in anemic chronic HCV bleeders compared with nonbleeders. Patients and methods This case–control study was carried out at the Faculty of Medicine and National Liver Institute, Menoufia University, in the duration between February 2016 and February 2017. The study included 70 individuals: 50 treatment-naive compensated chronic hepatitis C patients (25 anemic nonbleeders and 25 anemic bleeders) and 20 age-matched and sex-matched healthy individuals. Complete blood counts, iron profile, prothrombin, and serum hepcidin using enzyme-linked immunosorbent assay were done. Results Serum hepcidin levels were significantly lower in anemic nonbleeder patients (70.08 ± 13.40) and anemic bleeders (68.91 ± 10.66) than in controls (78.52 ± 7.46). P value is 0.017. There was no significant difference between the patient groups compared with each other. No statistically significant differences between the studied groups were found regarding serum iron, total iron binding capacity, transferrin saturation, and serum ferritin. Conclusion Chronic HCV bleeders do not develop iron deficiency.

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