Chapter 10: Anemia Resulting from Other Nutritional Deficiencies

VITAMIN A DEFICIENCY

• 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 DEFICIENCY

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.

RIBOFLAVIN 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.

THIAMINE DEFICIENCY

• 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).

VITAMIN C (ASCORBIC ACID) DEFICIENCY

• 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.

VITAMIN E (α-TOCOPHEROL) DEFICIENCY