Laboratory tests to detect iron deficiency anemia are grouped into 3 categories i.e., screening, diagnostic and specialised.
Screening tests for iron deficiency anemia
Complete blood picture
Shows anisocytosis, microcytosis and hypochromia
Red cell distribution width (RDW) – greater than 15%
Mean cell volume (MCV) – decreases
Mean corpuscular haemoglobin (MCH) – decreases
Mean corpuscular haemoglobin concentration (MCHC) – decreases
RBC count-decreases
Reticulocyte count –decreased as the rate of erythropoiesis is reduced.
Poikilocytosis-showing ellipocytes and target cells
WBC-Normal in morphology and number
Hematocrit – decreases
Iron deficiency anemia should be suspected if there is hypochromic microcytic anemia with an elevated RDW, but no consistent shape changes in RBC.
Diagnostic tests for iron deficiency anemia
Iron studies like assay of
Serum iron – Measure of the amount of iron bound to transferring in serum.
Total iron binding capacity (TIBC) – Indirect measure of transferrin and the available binding sites for iron in the plasma.
Transferrin saturation – Transferrin saturation can be calculated by
% of transferrin saturation = serum iron (µg/dl)X100 TIBC (µg/dl)
Serum ferritin – reflects the levels of iron stored with cell.
Amount of haemoglobin in reticulocytes can be assessed by some automated analyzers .This helps in detection of iron restricted erythropoiesis within days as the first iron deficiency cells leave the bone marrow.
Specialised test:
Tests for accumulated porphyrin precursors to heme are elevated.
Free erythrocyte protoporphyrin (FEP) accumulates when iron is unavailable. In the absence of iron, free erythrocyte protoporphyrin may be preferentially elevated with zinc to form zinc protoporphyrin
FEP and zinc chelate can be assayed fluorometrically.
Soluble transferrin receptors can be assayed using immunoassay which increases as the disease progresses.
Bone marrow is not indicated in iron deficiency anemia. But if the bone marrow sample is available iron stores can be assessed.
Bone marrow in iron deficiency anemia
Hyperplastic in early stages with decreased myeloid to erythroid ratio as a result of increase in erythropoiesis.
As disease progresses hyperplasia subsides and the profound deficiency of iron leads to slowed RBC production.
Late normoblasts show characteristics “Shaggy” blue cytoplasm due to asynchrony in maturation with cytoplasmic maturation lagging behind nuclear maturation.
References
Elaine M. Keohane, Larry J Smith, Jeanine M. Walenga. Rodaks Haematology: Clinical Principles and Applications. Fifth edition
Vinay kumar, Abul K.Abbas, Jon C. Aster. Robbins and Cotran. Pathologic Basis of Disease. 9th edition
Shirish M.Kawthalkar. Essentials of Haematology. Second edition
