By Gunter Weiss, Victor R. Gordeuk, Chaim Hershko
This booklet summarizes the most up-tp-date learn at the anemia of persistent sickness and identifies powerful diagnostic recommendations for this universal scientific condition-covering key issues relating to the layout and choice of healing techniques together with the therapy of the underlying ailment, the biology of erythropoietin and the law of erythropoiesis, the disturbance of iron homeostasis, and the advanced nature of the systemic inflammatory reaction.
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Additional resources for Anemia of Chronic Disease (Basic and Clinical Oncology)
Plasma iron is immediately scavenged by transferrin (Tf). activity of ceruloplasmin, a plasma blue copper ferroxidase of 1065 amino acids, despite the fact that Tf has intrinsic ferroxidase activity. Ceruloplasmin’s membrane-bound homologue hephaestin (56), which is expressed in enterocytes, very likely facilitates the basolateral transport of dietary iron. Functional inactivation of genes involved in dietary iron absorption or in iron delivery to the erythron is associated with disease. This is evident in microcytic anemia (mk) mice (49) and in Belgrade (b) rats (57), where a G185R mutation within a predicted transmembrane domain of DMT1 impairs iron absorption (58) due to improper targeting to the apical membrane of enterocytes (59).
Point mutations in the lower stem. Type (i) and (ii) mutations are associated with the most acute phenotypes; serum L-ferritin 1200–2700 mg=L and severe cataract (178). Type (iii) mutations correlate with slightly lower levels of L-ferritin (950–1900 mg=L) and milder cataract, while type (iv) lead to only a moderate increase in L-ferritin levels (350–650 mg=L) and asymptomatic cataract (178). Analysis of different mutants suggested a correlation between the degree of inhibition of IRP1 and IRP2 binding and the severity of HHCS (179), but a clinical variability among individuals sharing the same mutation suggests the involvement of additional factors (155).
The quantitative differences in the degree of regulation may reflect differences in IRE sequences and structure. The function of DMT1 and ferroportin IREs is as yet ill defined. Divalent metal transporter 1 mRNA contains a single IRE in its 30 UTR (an alternatively spliced variant has no IRE). The levels of the IRE-containing isoform are Regulation of Iron Metabolism 27 profoundly increased in the iron deficient duodenum (48), suggesting the involvement of an IRE=IRP mediated mechanism. Experiments in cultured cells suggest that the IREdependent regulation of DMT1 expression may be cell-type specific and restricted to intestinal cells (172–174).