Abstract：
:Most of the body iron is found within hemoglobin in red cells (the erythron), a smaller amount being distributed in other tissues such as muscles and in deposits. Iron homeostasis is a finely tuned process in which the most important regulators are probably the liver-derived hepcidin which blocks iron absorption and directs iron towards deposits and the recently discovered erythroblast-derived erythroferrone which inhibits hepcidin synthesis and therefore increases availability of iron for hemoglobin synthesis. Hepcidin secretion is increased by inflammatory cytokines and erythroferrone production increases when there is active, expanding erythropoiesis, for example after acute blood loss. We hypothesize that in pathological situations associated with erythroid precursor suppression (erythroblastopenia), anemia is the result of two major mechanisms: (1) direct erythroblast suppression leading to decreased production of red cells and (2) low iron availability due to high hepcidin levels arising as a result of low erythroferrone production. Additionally, infectious episodes and other inflammatory conditions that often complicate the course of these diseases may further promote hepcidin synthesis through increased cytokine production leading to even lower iron availability and a vicious circle of worsening anemia.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Cucuianu A,Patiu M,Trifa AP,Tomuleasa C,Dima Ddoi
10.1016/j.mehy.2014.09.008subject
Has Abstractpub_date
2014-11-01 00:00:00pages
530-2issue
5eissn
0306-9877issn
1532-2777pii
S0306-9877(14)00333-8journal_volume
83pub_type
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