The differential diagnosis of iron deficiency anemia should take into account other microcytic hypochromic anemias and/or other conditions of altered iron tests.

Apart from lack of iron supply to erythropoiesis, microcytic erythrocytes may result from defective globin or heme production in thalassemia syndromes and congenital sideroblastic anemias respectively. Red blood cell abnormalities in iron deficiency are less severe than in thalassemia where typical target cells are present on the peripheral blood smear. MCV and MCH are less decreased and RCDW wider in iron deficiency than in thalassemia. Heterozygous carriers of β-thalassemia usually have mild or no anemia but severe MCV and MCH reduction and compensatory Hb A2 increase at hemoglobin electrophoresis. Carriers of deletion or non-deletion α-thalassemia may be silent or have microcytic red cells depending on the severity of the molecular defect. Only tests based on α-globin gene sequencing can establish the correct diagnosis.

Congenital sideroblastic anemia may be microcytic and hypo chromic especially in males with X-linked sideroblastic anemia due to delta-aminolevulinate synthase 2 (ALAS2) mutations and in recessive forms due to mutations in the glycine mitochondrial importer SLC25A38 gene. However, serum iron and ferritin are high, ringed sideroblasts are present at bone marrow Perls’ staining, and siderocytes may be observed in the peripheral blood smears (see Fig. 1). Precise molecular diagnosis of sideroblastic anemia requires genetic testing. Rare atypical microcytic anemias such as atransferrinemia, mutations of DMT1, and aceruloplasminemia are associated with increased body iron.

Fig2. IRON DEFICIENCY ANEMIA. Peripheral blood smear (A, B), bone marrow (BM) aspirate (C), and Prussian blue stain of BM aspirate (D) from a 16-year-old girl with hemoglobin 6.7 g/dL, hematocrit 22.6%, and mean corpuscular volume 59.2 fL. Peripheral smear shows hypochromic microcytic red blood cells (A), with widening of the central pallor and “pencil” cells (B). Polychromatophilic erythroid precursors in the aspirated specimen have scanty cytoplasm that is irregular and vacuolated (C). The Prussian blue-stained aspirate shows no iron stores in multiple spicules (D).

Anemia of inflammation is usually normocytic unless the underlying disorder is severe, longstanding, or complicated by absolute iron deficiency. As discussed above, transferrin saturation may be normal or decreased (100 μg/L) (see Table 1). The differential diagnosis relies on the discrepancy between low transferrin saturation and high ferritin. Usually the diagnosis is suggested by both the underlying disorder and elevated CRP or erythrocyte sedimentation rate.

Table1. Laboratory Tests for Differential Diagnosis of Iron Deficiency Anemia

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