09-07-2008

Dergi Hakkında
Yayın Kurulu
Uluslararası Danışmanlar
İstatistik ve Epidemiyoloji Danışmanları
Ulusal Danışmanlar
Yazım Kuralları
Yayın Hakları Devir Formu
Online Makale İşlemleri
İletişim
Tıp Bilimleri Dergisi
ISSN: 1300-0292
İndekslendiği Dizinler: SCIENCE CITATION INDEX EXPANDED
CINAHL, Index Copernicus,
Chemical Abstracts (CA),
Excerpta Medica / EMBASE
Dil: Türkçe, İngilizce
İçerik: Orijinal Araştırma, Derleme, Editöre Mektup, Olgu Sunumu, Tıp Eğitimi, Tıbbi Kitap İncelemeleri

 

REVIEW ARTICLES


Anemia Of Chronic Disease And Hepcidin: Review

Dr. Mustafa KAPLAN,a Dr. Emrullah SOLMAZGÜL,a Dr. Selim NALBANTa

aİç Hastalıkları Servisi, GATA Haydarpaşa, İSTANBUL



Anemia of chronic disease is the second most prevalent type after anemia due to iron deficiency und occurs in conditions of acute or chronic immune activation. It is also called anemia of inflammation. Anemia of chronic disease is immune driven; cytokines and cells of the reticuloendothelial system induce changes in iron homeostasis, the proliferation of erythroid progenitor cells, the production of erythropoietin, and life span of red cells, all of which contribute to the pathogenesis of anemia. Recent evidence shows that deficient hepcidin response to iron loading may contribute to iron overload even in the much milder common form of hemochromatosis. In anemia of inflammation, hepcidin production is increased up to 100-fold and this may account for the defining feature of this condition, sequestration of iron in macrophages. The discovery of hepcidin and its role in iron metabolism seems to be promising in the development of new treatment approaches for hemochromatosis and anemia of inflammation. Advances in our understanding of the pathophysiology of anemia of chronic disease-including disturbances of iron homeostasis, impaired proliferation of erythroid progenitor cells, and a blunted erythropoietin response to anemia- have made possible the emergence of new therapeutic strategies. These include treatment of the underlying disease and the use of erythropoietic agents, iron, or blood transfusions. In the case of hepsidin having an effect similar to that of peptide hormones or cytokines, it may be activated by the stimulation of superficial receptors. Future strategies may include the use of hepcidin antagonists that overcome iron retention within the reticuloendothelial system, and hormones or cytokines that may effectively stimulate erythropoiesis under inflammatory conditions. Elucidation of the receptor and its transduction pathways should lead to the development of hepcidin antagonists, some of which may be useful in the treatment of anemia of inflammation, a condition often resistant to erythropoetin therapy.

Keywords: Hepcidin, anemia, inflammation

Turkiye Klinikleri J Med Sci 2006, 26:538-544

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