Serum iron is increased in
hemosiderosis, hemolytic anemias especially thalassemia, sideroachrestic
anemias, hepatitis, acute hepatic necrosis, hemochromatosis, and with
inappropriate iron therapy. Iron may reach high levels with iron
poisoning. Some patients who receive multiple transfusions (eg, some
hemolytic anemias, thalassemia, renal dialysis patients) will have
increased serum iron levels.
Serum iron is decreased
with insufficient dietary iron, chronic blood loss (including the
hemolytic anemias paroxysmal nocturnal hemoglobinuria), inadequate
absorption of iron and impaired release of iron stores as in
inflammation, infection and chronic diseases. The combination of low
iron, high TIBC and/or transferrin and low saturation indicates iron
deficiency. Without all of these findings together, iron deficiency is
unproven.2 Low ferritin supports the diagnosis of iron deficiency.
Detection of iron deficiency may lead to detection of adenocarcinoma of
gastrointestinal tract, a point which cannot be overemphasized. In recovery from pernicious anemia, especially just after B12
dose, iron levels are low. In fact, the drop in serum iron 1 to several
days after the Schilling test flushing dose of vitamin B12
may be more useful in diagnosis than the radioactivity of the 24-hour
urine collection. Serum iron is reported to drop with acute infarct of
myocardium.
TIBC is increased in iron-deficiency, use of oral contraceptives, and in pregnancy.
TIBC is decreased in hypoproteinemia due to many causes, and is decreased in a number of inflammatory states.
Increased saturation
occurs with HLA-related (classical) hemochromatosis before ferritin is
greatly increased, and also with iron overload (eg, cirrhosis and
portacaval shunt), in hemolytic anemias and with iron therapy.
Saturation >70% in females, >80% in males is described as
prerequisite for parenchymal loading; however, sample contamination and
the vagaries of fluctuation in serum iron levels can make such criteria
misleading on occasion.2
The serum ferritin is a more sensitive test than the serum iron or TIBC for iron deficiency and for iron overload.2
When all these tests are used together, as is often necessary, they
usually can distinguish between iron deficiency anemia and the anemia of
chronic disease. The best and most reliable evaluation of total body
iron stores is by bone marrow aspiration and biopsy. The best evaluation
of iron deficiency in childhood (unless lead toxicity is suspected) is
free erythrocyte porphyrins.
With recombinant erythropoietin
therapy serum iron, transferrin saturation, and ferritin levels decline
due to rapid utilization by stimulated erythropoiesis with resultant
decrease in storage iron.3,5
While iron is usually
considered in relation to hematopoiesis and oxygen transport functions
of red cells, it is also of prime import to the lymphomyeloid systems.6
