Physiological basis
Plasma iron concentration is determined by absorption from the intestine; storage in the
intestine, liver, spleen, bone marrow, rate of breakdown or loss of hemoglobin, and rate of
synthesis of new hemoglobin.
Interpretation for Iron (Fe), serum or plasma
| Increased |
Decreased |
| Hemosiderosis (eg, multiple transfusions,
excess iron administration), acute Fe poisoning (children), hemolytic anemia, pernicious
anemia, aplastic or hypoplastic anemia, viral hepatitis, lead poisoning, thalassemia,
hemochromatosis. Drugs: estrogens, ethanol, oral contraceptives. |
Iron deficiency, nephrotic
syndrome, chronic renal failure, many infections, active hematopoiesis, remission of
pernicious anemia, hypothyroidism, malignancy (carcinoma), postoperative state, kwashiorkor.
|
TIBC correlates with serum transferrin, but the relationship is not linear over a
wide range of transferrin values and is disrupted in diseases affecting transferrin-binding capacity
or other iron-binding proteins.
Increased
in: Iron deficiency anemia, late pregnancy, infancy, acute hepatitis. Drugs: oral
contraceptives.
Decreased
in: Hypoproteinemic states (eg, nephrotic syndrome, starvation, malnutrition, cancer),
hemochromatosis, thalassemia, hyperthyroidism, chronic infections, chronic inflammatory disorders,
chronic liver disease, and other chronic diseases.
Increased % transferrin saturation with iron is seen in iron overload (iron
poisoning, hemolytic anemia, sideroblastic anemia, thalassemia, hemochromatosis, pyridoxine
deficiency, aplastic anemia, RBC transfusions).
Decreased % transferrin saturation with iron is seen in iron deficiency (usually
saturation < 16%). It can also be used to assess nutritional status.