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VITAMIN A DEFICIENCY

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  • Prevalent in school children in several underdeveloped African countries (e.g., Malawi).

  • Anemia is characterized by reduced MCV, MCHC, and anisocytosis and poikilocytosis.

  • Similar to the anemia of chronic disease with reduced serum iron concentration, normal or low serum total iron-binding capacity and increased liver and marrow iron stores (increased serum ferritin), and failure to respond to treatment with medicinal iron.

  • Responds to vitamin A repletion.

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VITAMIN B6 DEFICIENCY

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  • Vitamin B6 includes pyridoxal, pyridoxine, and pyridoxamine.

  • May lead to hypochromic microcytic anemia.

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

  • Some patients who are not vitamin B6 deficient may have sideroblastic anemia that will partially respond to high doses of pyridoxine (see Chap. 14).

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RIBOFLAVIN DEFICIENCY

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  • Volunteers receiving a riboflavin-deficient diet plus a riboflavin antagonist (galactoflavin) developed 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.

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VITAMIN C (ASCORBIC ACID) DEFICIENCY

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

  • Macrocytic 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 percent also develops in 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.

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VITAMIN E (α-TOCOPHEROL) DEFICIENCY

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  • The vitamin E requirement varies with polyunsaturated fatty acid content of diet and the content of lipids that can peroxidize in tissues.

  • Perinatal period: Low-birth-weight infants have low serum and tissue concentrations of vitamin E.

  • A diet rich in polyunsaturated fatty acids and adequate in iron but inadequate in vitamin E may lead to hemolytic anemia by 4 to 6 weeks of age.

  • Anemia is often associated with altered red cell morphology, thrombocytosis, and edema of the dorsum of the feet and pretibial area.

  • These abnormalities are reversed promptly by treatment with vitamin E.

  • Chronic fat malabsorption, such as is common in cystic fibrosis, can lead to vitamin E deficiency, if daily supplements of the water-soluble form of this vitamin are not given. In such patients, the red cell life span is mildly reduced and anemia may develop.

  • Patients with sickle cell disease often have low ...

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