Hepatitis c and Vitamin D and Iron Status

Overview

HCV is associated with vitamin D deficiency. Iron overload is frequently occurred in chronic hepatitis C patients; more than one third of HCV positive patients have elevated serum iron, ferritin, and transferrin which were linked to bad prognosis. Hepcidin is a regulatory peptide that is mainly synthesized by the liver cells and plays an important role in iron homeostasis. There is an interaction between iron metabolism and vitamin D metabolism. Iron is essential for vitamin D activation and vitamin D deficiency is associated with elevated hepcidin level, which partly accounts for anemia associated with vitamin D deficiency. Up to our knowledge, little is known about the association between vitamin D status and iron metabolism in HCV patients.

Hepatitis C virus (HCV) is one of the global public health problems. World Health Organization (WHO) reported that more than 80 million people all over the world are infected with HCV. Approximately 700000 persons die every year from hepatitis C-related complications. Egypt is one of the highest prevalence rates of HCV, worldwide. Vitamin D possesses anti-inflammatory, anti-oxidant, anti-fibrotic and immunomodulatory effects. HCV is associated with vitamin D deficiency. Liver plays an important role in vitamin D hydroxylation and iron metabolism. It stores iron, synthesizes iron transporting protein (transferrin), iron storage protein (ferritin) and an iron regulatory peptide (hepcidin). Iron overload is frequently occurred in chronic hepatitis C patients. More than one third of HCV positive patients have elevated serum iron, ferritin, and transferrin which were linked to bad prognosis. Excess iron is catalyzed by the rapid Fenton reaction producing hydroxyl radicals from hydrogen peroxide and superoxide (10), which induces lipid peroxidation and cellular damage. Hepcidin is a regulatory peptide that is mainly synthesized by the liver cells and plays an important role in iron homeostasis via inhibiting iron absorption and preventing iron efflux from macrophages and thus prevents normal recycling of the iron needed for erythropoiesis. In addition, hepcidin inhibits HCV replication via activation of STAT3. A reduced serum hepcidin has been reported in chronic HCV patients which was correlated to the severity of liver histopathological changes and related to iron overload in these patients. There is an interaction between iron metabolism and vitamin D metabolism. Iron is essential for vitamin D activation and vitamin D deficiency is associated with elevated hepcidin level, which partly accounts for anemia associated with vitamin D deficiency. Up to our knowledge, little is known about the association between vitamin D status and iron metabolism in HCV patients.