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    RussianJoo's Avatar
    RussianJoo is offline Ultimate Member
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    TIBC levels and Different Iron Diseases.

    I have a problem understanding TIBC levels in different iron disease. I think I have it figured out but I could use some feedback to see if my thinking is correct.

    TIBC is an indirect measure of Transferrin so in hemochromatosis, Iron storage pools are high thus the liver isn't making Transferrin because it doesn't need to transport the iron to any tissue, thus TIBC is low.

    In iron deficiency anemia iron storage pools are drained thus in an effort to transport more iron to the tissues that need it, the liver produces more Transferrin and thus TIBC is high.

    In anemia of chronic disease, the body traps the iron so that the infective agent can't use the iron for it's own needs, thus Iron stores are high and transferrin is low because the stores are high, and thus TIBC is low.

    So is it correct to look at the Iron stores to predict the levels of TIBC? I also know that TIBC depends on liver function as well since transferrin is made in the liver.

    Please let me know if my rational is correct.

    thank you.
    Last edited by RussianJoo; 02-26-2008 at 06:02 PM.
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    Sree Cheruku is offline Super Moderator 533 points
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    TIBC is an indirect measure of Transferrin so in hemochromatosis, Iron storage pools are high thus the liver isn't making Transferrin because it doesn't need to transport the iron to any tissue, thus TIBC is low.

    In iron deficiency anemia iron storage pools are drained thus in an effort to transport more iron to the tissues that need it, the liver produces more Transferrin and thus TIBC is high.

    In anemia of chronic disease, the body traps the iron so that the infective agent can't use the iron for it's own needs, thus Iron stores are high and transferrin is low because the stores are high, and thus TIBC is low.
    All of the above is correct, as far as I know.

    So is it correct to look at the Iron stores to predict the levels of TIBC? I also know that TIBC depends on liver function as well since transferrin is made in the liver.
    Yeah, synthesis of transferrin is dependent on ferritin level ( = iron stores) in the absence of liver pathology. Decreased ferritin = iron deficiency. Increased ferritin = increased iron sequestration by bone marrow macrophages or hemochromatosis/hemosiderosis.
    Last edited by Sree Cheruku; 02-26-2008 at 07:57 PM.
    PGY-4 Anesthesiology

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    RussianJoo's Avatar
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    ok so my rational is correct? cool thanks Sree
    Hollywood Upstairs School of Medicology, Class of 2010
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