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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, acting through the retinoic acid receptors on erythroid progenitor cells.

  • 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. Anemia is, at least in part, due to the effect of riboflavin on iron absorption.

  • 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 biallelic mutation of the gene encoding the thiamine transporter, SLC19A2, on chromosome 1q23.3.

  • The anemia responds to lifelong administration of thiamine (25–100 mg/d).


  • 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 are required for ...

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