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Blood Iron Screening for Body Iron Status

 

Public screening efforts in search of iron overloaded patients are currently popular. About 4% of those screened are found to have too much or too little. Interestingly, we tend to find 5 whose iron is too low for every 1 whose level is too high.

Only fairly small amounts of iron consumption and intestinal absorption are needed to balance daily iron loss...when all is normal and healthy. Most of the iron in us cycles back and forth between removal from worn-out red blood cells and incorporation into new red blood cells.

WHAT IS THE BIG DEAL?

Most of the time, the below diseases sneak up on a person. Low blood iron often results in chronic fatigue (patient is tired and lacking "energy"..."iron poor, tired blood"). When causing ANEMIA [IDA...iron-deficiency anemia], it may reflect hidden bleeding things such as ulcers or cancer. When iron is too high, this also often results in chronic fatigue; and its accumulation can poison organs and result in liver, pancreas, and/or heart failure. All of the common situations can be managed, treated, and maybe cured; rarer disorders can be treated and managed.

Here are the two abnormal situations:

  1. IRON TOO LOW:

    Blood loss (often not obvious):

    benign or cancerous bleeding: from airway (hemoptysis) or nose (epistaxis); from mouth/gums, esophagus, stomach, or intestines (includes both bleeding and loss to an overload of parasites...parasitosis); from kidneys or bladder; from uterus/vagina; or from hemorrhoids.

    intravascular red blood cell destruction (heart valve problems; intense jogging trauma; red cell membrane/enzyme defects...such as PNH): the loss of iron is in urine.


    trauma with bleeding.


    excessive blood sample draws or donations.


    insufficient dietary intake: especially milk-fed infants

    insufficient/defective intestinal absorption:

    dietary iron blocked/tied up by eaten stuff:

    > antacids at/after meals (may block acid levels needed for cell brush-border ferrireductase to
       convert  ferric to ferrous iron)

    > clay eaters ("pica")
    > starch eaters ("pica")
    > excessive tea or coffee (tannins excess)
    > excessive phytic acid intake (a fiber in seeds and bran)
    > steatorrhea (fat) malabsorption (any cause)


    absorption "nearly turned off": myeloproliferative syndrome (producing too many red cells)


    intestine cell-membrane iron-binding protein deficiency (this DMT1 protein moves ferrous iron through the gut-lining enterocyte cell apical membrane into cell's cytoplasm where it can stay in reserve as ferritin or be moved by a protein through the basolateral cell membrane of the enterocyte out and into blood plasma & then to marrow).


    absent/insufficient (because of antacids or loss of ability to produce) stomach acid (acid to convert ferric iron to absorbable ferrous iron).


    absorption normal but insufficient modulation mechanisms for natural or tumorous growth spurts.


    chronic immune interference by the intraepithelial lymphocytic (IEL) T cell infiltrate in such as non-diarrhea manifesting gluten sensitive enteropathy (GSE) (and see generic enteric lymphocytic exocytosis)


    disease-defective, too little, or absent intestinal absorption site: sites bypassed by intestinal defects/fistulae or sites absent due to surgical bypass or removal.


    chronic renal failure.

  2. IRON TOO HIGH:
     
    Primary iron overload (primary siderosis):


    hemochromatosis (genetic penetrance may vary)

     
         autosomal recessive HFE gene...the common type. [check out the genetics]

     
      > homozygous: C282Y/C282Y (the classical pathological genotype) and indirect
         (elevated transferrin saturation) or direct (elevated liver iron content) evidence of actual
         overload (the correct phenotype).

     
      > heterozygous (carrier) varieties with phenotype evidence.

      
         non-HFE-associated types.

         > familial, genetic defect unknown (genetic penetrance may vary).
         > autosomal dominant (Solomon Islands).
         > non-hereditary, non-familial, presumed genetic, sporadic.
         > persons being phlebotomized for the condition but maintaining elevated biochemical
            markers due to unawareness of constant medical iron intake related to some other
            co-morbidity (as in iron replacement in chronic renal dialysis).

    neonatal hemochromatosis: bad disease with liver failure in perinatal life.

    juvenile hemochromatosis: often die before age 30 of heart failure.

    African siderosis (sub-Saharan siderosis; Bantu siderosis) is peculiar in that the screening test, transferrin saturation, is often not elevated (though the serum ferritin is elevated); black descendents in USA can have it.


    Secondary iron overload (secondary siderosis):

    parenteral (via IV's, multiple chronic blood transfusions, or other non-natural intake).

    increased dietary/nutritional -supplement intake (whether you realize it or not).

    things increasing iron absorption: anemia of "ineffective erythropoiesis" ; acutely poor oxygen intake (hypoxia); chronically reduced plasma iron levels (even growth spurts); increased levels of unsaturated transferrin; excessive vitamin C (an acid which promotes iron absorption by ferric to ferrous conversion) intake.

    iron workers (welding and/or grinding)...increases iron trapped in lungs (lung overload).


    "anemia of chronic disease" [a common diagnosis] (blockade of iron release from storage cells to the cells making red blood cells...the body's storage cells become overloaded...serum iron usually not increased, serum ferritin may be normal or increased, bone marrow iron increased but marrow sideroblasts decreased).


    "sideroblastic anemia": iron overload of the red blood cell system.


           > acquired: vitamin B6 deficient; medication-related; toxin-related.


           > hereditary.


           > myelodysplastic syndrome (MDS): "refractory anemia with ringed sideroblasts" variant.


    thalassemia (and other chronic hemolytic anemias): serum iron may be normal; absorption increased



    Porphyria cutanea tarda: a chronic blistering skin disease



    aceruloplasminemia (deprives cells of ferroxidase activity and iron can't be released from cells).


    congenital dyserythropoietic anemia (iron absorption increased).


    after porta-caval shunt surgery.


    in association with liver cirrhosis of various types.


    a-transferrinemia/hypotransferrinemia: severe iron deficiency anemia but with body iron overload.


The Screening Process for Body Iron Status:


Our health screening "fairs" use a blood test, the iron profile, which uses a fasting [haven't eaten in 6-8 hours] blood specimen and determines serum iron, TIBC (total serum iron binding capacity), and percent transferrin saturation [this last being the most sensitive phenotypic expression for hemochromatosis when 45-55% or higher].

Lexington Medical Center, West Columbia, S. C.


Lexington Medical Center (LMC) has had a hemochromatosis registry (coordinated treatment program) for years, willing to take treatment referrals (803-791-2409) from any doctor. And LMC's doctors and facilities are ready to deal with all of the above, locally or by referral to experts. The above information is taken from a number of medical references and journals. An outstanding review article with detail and graphics is: Nancy C. Andrews, M. D., Ph. D., Review Article: Medical Progress: "Disorders of Iron Metabolism" The New England Journal of Medicine 341(26): 1986-1995, 23 Dec. 1999. Patients in central South Carolina may find additional information in the LMC Community Health Information Library (803-739-3884).

 

The following links are for your further interest:

Iron Disorders Institute, Greenville, S. C.

The Hemochromatosis Foundation, Inc., Albany, N. Y.
and a list of interesting link topics by way of American Hemochromatosis Society, Delray Beach, Fla.
National Organization for Rare Disease (NORD)
Support Group Links: Midlands Area Support Group Network

 

 

 

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(posted 13 October 1999 (1st update 6 Feb. 2000; reviewed 1 December 2006)