microcytic anemia

Microcytic anemias result from defects in hemoglobin synthesis, which requires adequate iron, globin chains, and heme synthesis. Reduced hemoglobin production leads to smaller-than-normal erythrocytes as cells undergo extra divisions to maintain hemoglobin concentration.

Key etiologies: 1. **Iron deficiency anemia** - most common cause globally; due to chronic blood loss (GI bleeding, menorrhagia), poor intake, or malabsorption. Labs: low ferritin, low serum iron, high TIBC, high RDW, low transferrin saturation. 2. **Thalassemia** - genetic defect in alpha or beta globin chain synthesis. Labs: normal/high RBC count, normal RDW, target cells on smear, requires hemoglobin electrophoresis for diagnosis (elevated HbA2/HbF in beta-thal). 3. **Anemia of chronic disease (ACD)** - due to chronic inflammation (hepcidin-mediated iron sequestration); can be normocytic or mildly microcytic. Labs: low serum iron, low TIBC, elevated/normal ferritin (acute phase reactant). 4. **Sideroblastic anemia** - defective heme synthesis (e.g., due to lead poisoning, alcohol, isoniazid, myelodysplasia). Labs: elevated ferritin, ringed sideroblasts on bone marrow biopsy (iron-laden mitochondria). 5. **Lead poisoning** - inhibits ferrochelatase and ALA dehydratase, causing microcytic anemia with basophilic stippling.

Diagnostic approach: Start with CBC and peripheral smear. Check ferritin, iron studies (serum iron, TIBC, transferrin saturation), and RDW. High RDW suggests iron deficiency (variable cell size); normal RDW favors thalassemia (uniformly small cells). If iron studies are normal/high, consider thalassemia or sideroblastic anemia.

Clinical significance: Distinguishing between these causes is critical because iron supplementation is appropriate for iron deficiency but harmful in thalassemia or sideroblastic anemia (risk of iron overload). Identifying underlying cause of iron deficiency (e.g., occult GI malignancy) is essential, especially in older patients.