الفهرس 
Review of literatureOnly 14 pages are availabe for public view
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Abstract
The discovery of hepcidin and the role that it plays as a negative regulator of intestinal iron absorption and macrophage iron release has significantly progressed our understanding of iron metabolism.
Further research towards understanding hepcidin’s molecular control, physiology and pharmacodynamics, is needed prior to the development of a reliable laboratory immunoassay. Such an assay may have potential clinical utility in the future in both the diagnosis and classification of iron storage disorders such as HH, IDA and ACD.
The development of hepcidin analogues may have future therapeutic applications. A hepcidin agonist may be useful in the management of patients with HH, although the majority of these patients are generally well controlled on simple venesection programmes. A hepcidin agonist may also have utility in reducing the iron overload in patients with inappropriately suppressed hepcidin, secondary to a hypoxic or anaemic stimulus, such as patients with thalassaemia.
Patients with ACD in whom the underlying condition is not reversible may traditionally not have had anaemia severe enough to warrant a packed cell transfusion, given the risk and inconvenience involved in this treatment. This group of patients may gain significant symptomatic benefit from the development of a hepcidin antagonist and potential reversal of the iron restricted erythropoiesis contributing to the anaemia.
Our conclusion is that hepcidin decreases but not sufficiently to correct anaemia of renal failure in some patients. Elevated hepcidin levels in haemodialyzed patients may be due to functional iron deficiency and anemia. Liver plays an important role in the synthesis of hepcidin. Low-grade inflammation, frequently found in haemodialyzed patients, might also contribute to elevated hepcidin concentration. The hypothesis that hepcidin might link anemia, inflammation and liver function in kidney disease should be further evaluated.
Lowering hepcidin in CRF patients by antihepcidin therapy might decrease the need for iron therapy and erythropoietin therapy with all their potential hazards .Lowering hepcidin may be associated with a better control .of anaemia