Hepatitis c and Vitamin D and Iron Status
Hepatitis c and Vitamin D and Iron Status
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.
Inclusion Criteria:

 • Naïve HCV Patients (>18Y) coming to National Committee for control of viral hepatitis to
 receive their treatment

 Exclusion Criteria:

 -  Age less than 18 years old or more than 70 years old.

 -  previously received treatment for HCV

 -  Manifestations or history of manifestations of liver cell failure and cirrhosis
 including ascites and hepatic encephalopathy.

 -  Patients co-infected by the hepatitis B (HBV), human immunodeficiency viruses (HIV).

 -  Hepatocellular carcinoma and other extra hepatic carcinoma.

 -  Renal disease.

 -  Patients receiving vitamin D, calcium therapy or iron supplementation for the last 3
 months will be excluded.

 -  Total serum bilirubin ≥ 3 mg/dl.

 -  Serum albumin < 2.8 g/dl

 -  international normalization ratio (INR)> 1.7

 -  Platelet count <50000/mm3

 -  Serum creatinine >2.5mg/l