By Gunter Weiss, Victor R. Gordeuk, Chaim Hershko
This e-book summarizes the most up-tp-date examine at the anemia of persistent sickness and identifies powerful diagnostic thoughts for this universal medical condition-covering key issues on the topic of the layout and choice of healing strategies together with the remedy of the underlying affliction, the biology of erythropoietin and the law of erythropoiesis, the disturbance of iron homeostasis, and the complicated nature of the systemic inflammatory reaction.
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Extra info for Anemia of Chronic Disease (Basic and Clinical Oncology)
This miniscule amount is required to compensate iron losses by cell desquamation, blood loss, or in sloughed mucosal cells. A dynamic pool of $3 mg iron remains constant in plasma, despite a high turnover rate of 30 mg=day. BIOMEDICAL ASPECTS OF IRON METABOLISM The tight control of iron metabolism is critical for health, because both iron deficiency as well as iron overload are associated with disease (15). Depletion of body iron stores due to insufficient dietary iron supply is linked to impaired erythropoiesis and iron deficiency anemia (IDA).
The molecular basis of HHCS will be discussed in the next section. Interestingly, Fthþ=À mice also display hyperferritinemia (7- to 10-fold increase in serum L-ferritin) in the absence of iron overload (151). The biomedical relevance of ferritin function is also evident from some recent findings. First, a misregulation in the expression of H-ferritin (it will also be discussed in the next section) has been associated with a dominantly inherited form of hemochromatosis (156). In addition, a frameshift mutation in L-ferritin gene, predicted to alter 22 residues at the C-terminus of the polypeptide and extend it by 4 additional amino acids, is a causative defect in a dominant adult-onset basal ganglia disease (157).
The most prominent example is hereditary hemochromatosis (HH), a genetically heterogeneous group of iron overload disorders, where a chronic imbalance in dietary iron absorption results in iron accumulation, primarily within tissue parenchymal cells. Several types of HH have been described, which vary in the clinical symptoms and the underlying molecular basis. The most common form (HH type 1) is characterized by adult onset and predominant manifestations of liver disease. The disease is transmitted in an autosomal recessive manner.