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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 blood smear (see Approach to the Patient With Anemia: 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 Anemias Caused by Hemolysis: Thalassemias).
Normocytic anemias result from primary bone marrow failure. They are characterized by a normal RBC distribution width (RDW) and usually 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 do deficiencies of vitamin B12 or folate. Anemia of chronic disease may be microcytic or normocytic. Anemias due to myelodysplastic syndromes may be microcytic, normocytic, or macrocytic. Patients with microcytic anemias require testing of iron stores (see Iron Deficiency Anemia, below).
Treatment of deficient RBC production depends on the cause; however, stimulation of erythropoiesis with human recombinant EPO often is helpful. Because erythropoiesis increases the iron requirement, supplemental iron is helpful when administering any type of treatment that aims to increase erythropoiesis.
Last full review/revision November 2005
Content last modified November 2005
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