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  • This type of anemia is prevalent in school children in several underdeveloped African countries (eg, Malawi).

  • Anemia is characterized by reduced mean (red) cell volume (MCV), mean (red) cell hemoglobin concentration, and anisocytosis and poikilocytosis.

  • Unlike iron deficiency, but similar to the anemia of chronic disease, serum iron concentration is decreased, serum total iron-binding capacity is normal or low, and iron stores, reflected in serum ferritin levels, are increased. The anemia fails to respond to treatment with medicinal iron.

  • The condition responds to vitamin A repletion.

  • Coupling vitamin A with iron administration may lead to a faster response because of the evidence that vitamin A deficiency impairs iron utilization.


Vitamin B6 includes pyridoxal, pyridoxine, and pyridoxamine.

  • Deficiency may lead to hypochromic microcytic anemia.

  • Microcytic anemia may occur in patients taking isoniazid, which interferes with vitamin B6 metabolism. Such an anemia may be corrected with large doses of pyridoxine.

  • A small fraction of patients (5%–10%) who are not vitamin B6 deficient may have sideroblastic anemia that will respond partially to high doses of pyridoxine (see Chap. 11).

  • Malabsorptive states and renal dialysis may result in vitamin B6 deficiency.


  • Volunteers receiving a riboflavin-deficient diet plus a riboflavin antagonist (galactoflavin) develop vacuolated erythroid precursors, followed by pure red cell aplasia—all reversed by administration of riboflavin.

  • Reduced erythrocyte glutathione reductase activity occurs in riboflavin deficiency but is not associated with hemolysis or oxidant-induced injury.


  • Rare childhood syndrome is marked by diabetes mellitus, sensorineural deafness, and megaloblastic anemia and occasionally thrombocytopenia.

  • It is observed in children of Asian descent and results from mutation in SLC19A2 gene on chromosome 1q23.3.

  • It responds to lifelong administration of thiamine (25–100 mg/day).


  • Anemia in humans with scurvy may be macrocytic, normocytic, or microcytic, and the marrow may be hypocellular, normocellular, or hypercellular. In approximately 10% of patients, the marrow hematopoiesis is megaloblastic.

  • Macrocytic (megaloblastic) anemia may develop with vitamin C deficiency because vitamin C interacts with folic acid in the generation of tetrahydrofolic acid.

  • Microcytic anemia may develop because vitamin C facilitates the absorption of iron and because of the bleeding manifestation of scurvy.

  • Iron deficiency in children is often associated with dietary vitamin C deficiency.

  • Normocytic normochromic anemia with a reticulocytosis of 5% to 10% also can develop as a manifestation of scurvy, perhaps from compromised cellular antioxidant defense mechanisms.

  • The anemia of vitamin C deficiency responds promptly to administration of vitamin C. Sufficient folic acid and iron is required for the response to occur.

  • If the anemia is macrocytic (megaloblastic), folate should be administered with vitamin C to obtain a timely response.



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