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Blood Iron
Screening for Total-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:
- 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.
- 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.
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)
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TRUTH
(posted 13 October 1999 (1st update 6 Feb. 2000;
reviewed 1 December 2006)
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