Subject: iron/supplementation/bacteria

   
   Haematologia (Budap) 1993;25(2):69-84
   
Adequate iron stores and the 'Nil nocere' principle.

    Hollan S, Johansen KS
    
   National Institute of Haematology, Blood Transfusion and Immunology,
   Budapest.
   
   There is a need to change the policy of unselective iron
   supplementation during periods of life with physiologically increased
   cell proliferation. Levels of iron stores to be regarded as adequate
   during infancy and pregnancy are still not well established. Recent
   data support the view that it is not justified to interfere with
   physiological adaptations developed through millions of years by
   sophisticated and precisely coordinated regulation of iron absorption,
   utilization and storage. Recent data suggest that the chelatable
   intracellular iron pool regulates the expression of proteins with
   central importance in cellular iron metabolism (TfR, ferritin, and
   erythroid 5-aminolevulinic synthetase) in a coordinately controlled
   way through an iron dependent cytosolic mRNA binding protein, the iron
   regulating factor (IRF). This factor is simultaneously a sensor and a
   regulator of iron levels. The reduction of ferritin levels during
   highly increased cell proliferation is a mirror of the increased
   density of TfRs. An abundance of data support the vigorous competition
   for growth-essential iron between microbial pathogens and their
   vertebrate hosts. The highly coordinated regulation of iron metabolism
   is probably crucial in achieving a balance between the blockade of
   readily accessible iron to invading organisms and yet providing
   sufficient iron for the immune system of the host. The most evident
   adverse clinical effects of excess iron have been observed in
   immunodeficient patients in tropical countries and in AIDS patients.
   Excess iron also increases the risk of initiation and promotion of
   malignant processes by iron binding to DNA and by the iron-catalysed
   release of free radicals. Oxygen radicals were shown to damage
   critical biomolecules leading, apart from cancer, to a variety of
   human disease states, including inflammation and atherosclerosis. They
   are also involved in processes of aging and thrombosis. Recent
   clinical trials have suggested that the use of iron-chelators, natural
   and synthetic antioxidants, and anti-TfR monoclonal antibodies can
   contribute in retarding malignant cell proliferation. Hypoferraemia
   during pregnancy is--like haemodilution--an adaptation to the risks
   involved in the natural hypercoagulable state of pregnancy. It may
   also serve to prevent the risk of infections and mutagenicity in the
   highly proliferating tissues of the foetus. Blunted erythropoiesis has
   been revealed during the first 30 weeks of pregnancy by the use of the
   newly developed method of determining the soluble serum transferrin
   receptor. The lack of increase in erythropoietin levels proves that
   there is no hypoxia. Decreases in Hb and iron levels are parts of a
   physiological adaptation. As a consequence they should neither be
   treated nor prevented. It is stressed that whenever a widespread and
   ingrained routine medical intervention has to be changed it is
   essential to first monitor the potential health effects of the
   recommended change in a national policy.
   
   Publication Types:
     * Review
     * Review, tutorial
       
   PMID: 8244202, UI: 94063698
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