Anemia (a decrease in the number of RBCs, Hb content, or Hct) can result from decreased RBC production (erythropoiesis), increased RBC destruction, or blood loss. Anemias due to decreased erythropoiesis are recognized by reticulocytopenia, which is usually evident on the peripheral smear (see Testing). The RBC indices, mainly the MCV, narrow the differential diagnosis of deficient erythropoiesis and determine what further testing is necessary.
Microcytic anemias result from deficient or defective heme or globin synthesis. Microcytic anemias include iron deficiency anemias, iron-transport deficiency anemias, iron-utilization anemias (including some sideroblastic anemias and lead poisoning), and thalassemias (which also cause hemolysis—see Thalassemias). Patients with microcytic anemias typically require testing of iron stores (see Iron Deficiency Anemia).
Normocytic anemias result from primary bone marrow failure. They are usually characterized by a normal RBC distribution width (RDW) and normochromic indices. The mechanisms involved are hypoproliferation (deficiency of or inadequate response to erythropoietin [EPO]), hypoplasia (in aplastic anemia), myelophthisis, and myelodysplasia.
Macrocytic anemias result most often from impaired DNA synthesis, as occurs with deficiencies of vitamin B12 or folate.
Some anemias have variable findings on the peripheral smear. Anemia of chronic disease may be microcytic or normocytic. Anemias due to myelodysplastic syndromes may be microcytic, normocytic, or macrocytic. Treatment of deficient RBC production depends on the cause; however, stimulation of erythropoiesis with human recombinant EPO often is helpful in the anemia due to renal failure. Because erythropoiesis increases the iron requirement, supplemental iron is helpful when administering any treatment that aims to increase erythropoiesis.
Last full review/revision May 2013 by Alan E. Lichtin, MD
Content last modified September 2013