http://www.medrants.com/archives/5100 Internal medicine, American health care, and especially medical education Sat, 11 Feb 2012 15:15:48 +0000 hourly 1 http://wordpress.org/?v=3.3.1 http://www.medrants.com/archives/5100/comment-page-1#comment-530811 Stalwart Hospitalist Sun, 20 Dec 2009 23:29:24 +0000 http://www.medrants.com/?p=5100#comment-530811 This patient has anemia secondary to chronic inflammation.  Chronic active hepatitis C can be a chronically inflammatory condition (sometimes resulting in cryoglobulinemia, vasculitis, inflammatory arthritis, etc.). Persistent inflammation, manifested by elevated levels of IL-6, result in higher levels of a short peptide called hepcidin.  Hepcidin acts to sequester iron in the reticuloendothelial system (through downregulating ferroportin synthesis), making less iron available in the circulation and less iron mobilizable for erythrocytosis. The typical iron studies and bone marrow evaluation in chronic inflammation anemia shows a low iron saturation (since iron is sequestered out of circulation), an elevated ferritin (as an acute phase reactant to inflammatory cytokines) and normal to high iron stores in the bone marrow (since hepcidin promotes iron storage rather than use). Hepcidin is probably part of the innate immune system -- sequestering iron was probably an evolutionary move to slow bacterial growth in bacteremia, since all organisms need iron to replicate and grow. Treating this can be challenging -- the body often has enough iron and erythropoietin, but the building blocks are prevented from being used.  Hepcidin receptor antagonists and anti-hepcidin biologics are under investigation currently. This patient has anemia secondary to chronic inflammation.  Chronic active hepatitis C can be a chronically inflammatory condition (sometimes resulting in cryoglobulinemia, vasculitis, inflammatory arthritis, etc.).
Persistent inflammation, manifested by elevated levels of IL-6, result in higher levels of a short peptide called hepcidin.  Hepcidin acts to sequester iron in the reticuloendothelial system (through downregulating ferroportin synthesis), making less iron available in the circulation and less iron mobilizable for erythrocytosis.
The typical iron studies and bone marrow evaluation in chronic inflammation anemia shows a low iron saturation (since iron is sequestered out of circulation), an elevated ferritin (as an acute phase reactant to inflammatory cytokines) and normal to high iron stores in the bone marrow (since hepcidin promotes iron storage rather than use).
Hepcidin is probably part of the innate immune system — sequestering iron was probably an evolutionary move to slow bacterial growth in bacteremia, since all organisms need iron to replicate and grow.
Treating this can be challenging — the body often has enough iron and erythropoietin, but the building blocks are prevented from being used.  Hepcidin receptor antagonists and anti-hepcidin biologics are under investigation currently.

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