Iron deficiency develops in stages. In the first stage, iron requirement exceeds intake, causing progressive depletion of bone marrow iron stores. As stores decrease, absorption of dietary iron increases in compensation. During later stages, deficiency impairs RBC synthesis, ultimately causing anemia. Severe and prolonged iron deficiency also may cause dysfunction of iron-containing cellular enzymes.
Iron deficiency anemia is
classically described as a microcytic anemia. The differential diagnosis
includes thalassemia, sideroblastic anemias, some types of anemia of chronic
disease, and lead poisoning. Serum ferritin is the preferred initial diagnostic
test. Total iron-binding capacity, transferrin saturation, serum iron, and
serum transferrin receptor levels may be helpful if the ferritin level is
between 46 and 99 ng per mL (46 and 99 mcg per L); bone marrow biopsy may be
necessary in these patients for a definitive diagnosis.
The diagnosis of IDA requires that a patient be anemic and show laboratory evidence of iron deficiency. Red blood cells in IDA are usually described as being microcytic (i.e., mean corpuscular volume less than 80 μm3 [80 fL]) and hypochromic, however the manifestation of iron deficiency occurs in several stages. Patients with a serum ferritin concentration less than 25 ng per mL (25 mcg per L) have a very high probability of being iron deficient. The most accurate initial diagnostic test for IDA is the serum ferritin measurement. Serum ferritin values greater than 100 ng per mL (100 mcg per L) indicate adequate iron stores and a low likelihood of IDA
