الفهرس 
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Abstract
Iron is an essential element used by living organisms in redox enzymes, oxygen carriers, and oxygen-storage proteins The human iron economy is based on iron conservation and recycling as the excretion of iron is poorly regulated and there is no specific mechanism of its removal
The amount of iron that enters the body through enterocytes is the key determinant in the maintenance of iron homeostasis. This quantity is upregulated in conditions of iron deficiency and anaemia, and can be reduced in conditions of excess iron
a fundamental mechanism for controlling iron metabolism occurs post-transcriptionally through iron regulatory proteins (IRPs) and iron responsive elements (IREs).
Hepcidin is a small peptide hormone secreted by hepatocytes, circulating in blood plasma and excreted in urine. Hepcidin expression is inversely related to body iron demand, being increased in times of iron defficiency and decreased when iron requirements are high.
The phagocytic process secondary to chronic necro-inflammatory hepatocytic damage may result in iron redistribution toward Kupffer cells, but hepatic iron excess remains usually slight
Suppression of hepcidin expression by HCV has been linked to virally induced reactive oxygen species (ROS) that reduce hepcidin gene transcription
In end-stage liver cirrhosis, additional and sometimes massive parenchymal iron-overload may occur in relation to decreased transferrin and hepcidin synthesis secondary to hepatic insufficiency
The down-regulation of FP-1 mRNA in enterocytes and hepatocytes, both of which correlated with body mass index and tumor necrosis factor α concentrations, suggests that this occurs via a similar mechanism in the liver and the duodenum linked to visceral adipose tissue and associated inflammation.
It is known that free iron promotes generation of oxygen radicals by catalysing the Fenton reaction in which Fe2 reacts with H2O2 to generate highly reactive hdroxyl radicals, which can cause nucleic acid damage and 8-OHdG adducts. Therefore, iron may cause liver tissue injury by increasing the formation of toxic hydroxyl radicals leading to progression of liver inflammation, fibrosis, and increased risk for developing liver cancer during chronic liver disease.
MRI allows both the recognition of excessive iron accumulation in liver tissue and the evaluation of the level of iron overload In the recent studies a good correlation between MR technique and biopsy results with liver iron concentration measurement was observed.
The identification of hepcidin as the central regulator of iron homeostasis immediately raised the possibility of diagnostic applications. Recently, immunochemical assays for hepcidin-25 have also been developed, which comprise of competitive radioimmunoassay and enzyme-linked immunosorbent assays
therapeutic phlebotomy remains the standard treatment for iron overload in chronic liver diseases. Recently, Alexander et al found that iron depletion in chronic HCV was associated with a biochemical response in 22% of patients who did not respond to IFN monotherapy and that, among patients with serum ALT normalization, there was a significant reduction of serum markers of liver fibrosis (procollagen III peptide).