FREE iron / labile iron / heart / BAD

Discussion in 'Food and nutrition' started by Ironjustice, Sep 13, 2003.

  1. Ironjustice

    Ironjustice Guest

    When the upper limit has been reached in iron stores .. generally 35% saturation of transferrin ..
    'free' iron / leaked iron appears .. NTBI - non transferrin bound iron .. NPBI - non protein bound
    iron .. which forms what is known as the 'labile iron pool' / LIP. Transfusional iron toxicity is
    the SAME as simple secondary induced iron toxicity .. elevated iron levels in the body.

    <<snip>> This further supports the concept of the labile iron pool as the compartment directly
    involved in transfusional iron toxicity. <<snip>>

    Blood 2003 Feb 6;

    Evaluation of myocardial iron by magnetic resonance imaging during iron chelation therapy with
    desferrioxamine. Indication of close relation between myocardial iron content and chelatable
    iron pool.

    Jensen PD, Jensen FT, Christensen T, Eiskjaer H, Baandrup U, Nielsen JL Department of Hematology,
    Aarhus University Hospital, Aarhus, Denmark.

    [Record supplied by publisher]

    Evaluation of myocardial iron during iron chelation therapy is not feasible by repeated
    endomyocardial biopsies owing to the heterogeneity of iron distribution and the risk of
    complications. Recently, we described a non-invasive method based on magnetic resonance imaging.
    Here the method is used for repeated estimation of the myocardial iron content during iron chelation
    with desferrioxamine in 14 adult non-thalassemic patients with transfusional iron overload. We
    investigated the repeatability of the method and the relation between the myocardial iron estimates
    and iron status. The repeatability coefficient (2xSD) was 2.8 micro mol/g in the controls
    (day-to-day) and 4.0 micro mol/g in the patients (within-day). Myocardial iron estimates were
    elevated in 10 of all 14 patients at first examination, but normalized in six after 6 to 18 months
    of treatment. If liver iron declined below 350 micro mol/g all but one of the myocardial iron
    estimates were normal or nearly normal. At start (R(2)=0.69, P=.0014) and still after 6 months of
    iron chelation (R(2)=0.76, P=.001), the estimates were significantly and more closely related to the
    urinary iron excretion than to liver iron or serum ferritin levels. In conclusion, our preliminary
    data, which may only pertain to patients with acquired anemias, suggest the existence of a critical
    liver iron concentration, above which elevated myocardial iron is present, but its extent seems
    related to the size of the chelatable iron pool, as reflected by the urinary iron excretion. This
    further supports the concept of the labile iron pool as the compartment directly involved in
    transfusional iron toxicity.

    PMID: 12576333

    J Lab Clin Med 2003 Feb;141(2):121-30

    Deferoxamine promotes survival and prevents electrocardiographic abnormalities in the gerbil model
    of iron-overload cardiomyopathy.

    Obejero-Paz CA, Yang T, Dong WQ, Levy MN, Brittenham GM, Kuryshev YA, Brown AM Rammelkamp Center for
    Education and Research, MetroHealth Campus, and the Department of Physiology and Biophysics, School
    of Medicine, Case Western Reserve University; and the Department of Pediatrics, Columbia University.

    [Medline record in process]

    We investigated the time course of electrocardiographic (ECG) changes in the Mongolian gerbil
    model of iron overload and the effects of the iron chelator deferoxamine (DFO) on these changes.
    Iron overload was produced with weekly subcutaneous injections of low doses (200 mg/kg/wk) or high
    doses (800
    mg/kg/wk) of iron-dextran. DFO was administered subcutaneously at a dose of 200 mg/kg/day to
    high-dose animals. Our results show that (1) survival of iron-overloaded gerbils is
    dose-dependent, with median survival times of 68 and 14 weeks for low- and high-dose animals,
    respectively; (2) both low and high doses produce prolongation of the PR interval and bradycardia
    in early stages and prolongation of the QT interval, premature ventricular contractions, variable
    degrees of atrioventricular block, changes in the ST segment, and T-wave inversion at later
    stages coinciding with the development of heart failure; (3) DFO prevented death during 20 weeks
    of high-dose iron-dextran; (4) DFO prevented ECG changes, although delayed prolongation of PR
    intervals and QRS complexes occurred; and (5) despite marked prolongation of survival and
    prevention of ECG changes, DFO had modest effects on total cardiac iron content. We speculate
    that DFO chelates a small iron pool located within the cytoplasm of iron-overloaded
    cardiomyocytes.

    PMID: 12577048, UI: 22464621

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