Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With Chronic Hepatitis C

Overview

The aim of this study is to address questions regarding the link among hepcidin, hematological iron markers, inflammation and hepatitis C in HD patients. In attempt to address this issue, we planned to measure serum levels of hepcidin prohormone (pro-hepcidin), inflammatory and iron parameters.

Hepatitis C virus (HCV) infection is the most common cause of chronic liver disease in the world and also common among chronic hemodialysis (HD) patients. Patients with chronic HCV often have increased liver iron, a condition associated with reduced sustained response to antiviral therapy, more rapid progression to cirrhosis, and development of hepatocellular carcinoma; however, little is known about the mechanism of iron accumulation in the liver. Recently identified hepcidin, a 25-amino acid peptide hormone exclusively synthesized in the liver, is thought to be a key regulator for iron homeostasis and is induced by infection and inflammation. Hepcidin expression is modulated by iron stores, so that it decreases in iron deficiency to facilitate iron absorption while it increases in iron repletion to prevent pathological overload. Interleukin (IL)-6 has been proposed as a major inducer of hepcidin, via direct transcriptional activation of hepatic hepcidin expression by binding to its receptor complex containing gp130 to activate janus kinase (JAK) and activator of transcription 3 (STAT 3).

Conditions

Eligibility

Locations (1)

Outcomes