Sections View Full Chapter Figures Tables Videos Full Chapter Figures Tables Videos Supplementary Content ++ VITAMIN A DEFICIENCY ++ 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. ++ VITAMIN B6 DEFICIENCY ++ 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). ++ RIBOFLAVIN DEFICIENCY ++ 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. ++ 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 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. ++ VITAMIN E (α-TOCOPHEROL) DEFICIENCY ++ 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 ... GET ACCESS TO THIS RESOURCE Sign In Username Error: Please enter User Name Password Error: Please enter Password Forgot Username? Forgot Password? Sign in via OpenAthens Sign in via Shibboleth Get Free Access Through Your Institution Contact your institution's library to ask if they subscribe to McGraw-Hill Medical Products. What is MyAccess? Create a FREE MyAccess profile to: Use this site remotely Bookmark your favorite content Track your self-assessment progress and more!