By Gunter Weiss, Victor R. Gordeuk, Chaim Hershko
This publication summarizes the most up-tp-date learn at the anemia of persistent affliction and identifies potent diagnostic innovations for this universal scientific condition-covering key themes on the topic of the layout and choice of healing recommendations together with the remedy of the underlying affliction, the biology of erythropoietin and the rules of erythropoiesis, the disturbance of iron homeostasis, and the complicated nature of the systemic inflammatory reaction.
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Additional info for Anemia of Chronic Disease (Basic and Clinical Oncology)
Regulation of Iron Metabolism 15 The Role of Hepcidin It has long been proposed that the pathway for iron absorption is regulated by sensing body iron stores and the requirement of iron for erythropoiesis (90). The nature of the so-called ‘‘stores’’ and ‘‘erythroid’’ regulator has remained elusive, but a growing body of evidence suggests that the antimicrobial peptide hepcidin is a very good candidate to fulfill such functions (91,92). Hepcidin is a cysteine-rich peptide (Fig. 5) synthesized predominantly in the liver and secreted in the plasma.
5) synthesized predominantly in the liver and secreted in the plasma. It was first isolated from human blood ultrafiltrate (93) and urine (94) and studied for its bacteriostatic properties. In an independent screen for hepatic genes related to iron metabolism, hepcidin was found overexpressed in response to iron overload (95). Recent genetic data, initiated by a serendipitous observation, have provided strong evidence that hepcidin is an important regulator of iron metabolism. The targeted disruption of the gene for murine transcription factor Usf2 (upstream stimulatory factor 2) resulted in the silencing of the downstream hepcidin gene.
Under physiological conditions, the concentration of plasma iron is $18 mM and of Tf $56 mM. Thus, only one-third of Tf is saturated with iron, of which $10% is in the diferric form. However, in most types of hemochromatosis (exceptions are discussed below), Tf saturation gradually reaches almost maximum capacity, and this leads to accumulation of redox active low molecular weight iron in plasma and in tissues. Loading of Tf with iron very likely requires the Regulation of Iron Metabolism 11 Figure 4 A model for iron export from macrophages.