Anemia diet therapy

Pernicious anemia—Lifetime therapy is necessary. Eat a balanced diet tiiat includes seafood, eggs, meats, and dairy products. Avoid contact with infections, and report any signs of infection to the primary health care provider immediately because an increase in dosage may be necessary. 

Other than transfusion, nonpharmacologic therapy plays a limited role in the management of anemia. Certainly, some causes of anemia can be attributed to diets poor in iron, folic acid, or vitamin B12. However, in the United States, nutrient-poor diets are rarely the sole cause of anemia in a patient. Therefore, ingesting a diet that is rich in iron, folic acid, or vitamin B12 should be encouraged but should not be the only... 

Common precipitating factors that may cause a previously compensated patient to decompensate include noncompliance with diet or drug therapy, coronary ischemia, inappropriate medication use, cardiac events (e.g., MI, atrial fibrillation), pulmonary infections, and anemia. 

Vitamin E may be indicated in some rare forms of anemia such as macrocytic, megaloblastic anemia observed in children with severe malnutrition and the hemolytic anemia seen in premature infants on a diet rich in polyunsaturated fatty acids. Also anemia s in malabsorption syndromes have shown to be responsive to vitamin E treatment. Finally, hemolysis in patients with the acanthocytosis syndrome, a rare genetic disorder where there is a lack of plasma jS-lipoprotein and consequently no circulating alpha tocopherol, responds to vitamin E treatment. In neonates requiring oxygen therapy vitamin E has been used for its antioxidant properties to prevent the development retrolental fibroplasia. It should be noted that high dose vitamin E supplements are associated with an increased risk in allcause mortality. 

Acute heart failure occurs frequently in patients with chronic failure. Such episodes are usually associated with increased exertion, emotion, salt in the diet, noncompliance with medical therapy, or increased metabolic demand occasioned by fever, anemia, etc. A particularly common and important cause of acute failure—with or without chronic failure—is acute myocardial infarction. 

Cobalt must be supplied in the diet in its physiologically active form, vitamin B12. GI absorption of cobalt is about 25%, with wide individual variation excretion occurs mainly via the urine. The major part is excreted within days and the rest has a biological half-life of about two years. Originally, the therapy for pernicious anemia was to have patients eat large amounts of liver. The most reliable treatment now is monthly injections of cobalamin. 

The duration of treatment is governed by the rate of recovery ofHb and the desire to create iron stores. The former deperuls on the severity of the anemia. With a daily rate of repair of 0.2 g of Hb/dL of whole blood the red cell mass usually is reconstituted within 1—2 months. Thus, an individual with an Hb of 5 g/dL may achieve a normal complement of 15 g/dL in about 50 days, whereas an individual with an Hb of 10 g/dL may take only half that time. The creation of stores of iron requires many months of oral iron administration. The rate of absorption decreases rapidly after recovery from anemia, and after 3—4 months of treatment, stores may increase at a rate of not much more than 100 mg/month. Much of the strategy of continued therapy depends on the estimated future iron balance. Patients with an inadequate diet may require continued therapy with low doses of iron. If the bleeding has stopped, no further therapy is required after the Hb has returned to normal. With continued bleeding, long-term therapy clearly is indicated. 

FOLATE DEFICIENCY Folate deficiency is a common complication of diseases of the small intestine, which interfere with the absorption of dietary folate and the recirculation of folate through the enterohepatic cycle. In acute or chronic alcohohsm, daily intake of dietary folate may be severely restricted, and the enterohepatic cycle of the vitamin may be impaired by toxic effects of alcohol on hepatic parenchymal cells this is the most common cause of folate-deficient megaloblastic erythropoiesis. However, it also is the most amenable to therapy, inasmuch as the reinstitution of a normal diet is sufficient to overcome the effect of alcohol. Disease states characterized by a high rate of cell turnover, such as hemolytic anemias, also may be complicated by folate deficiency. Additionally, drugs that inhibit dihydrofolate reductase (e.g., methotrexate and trimethoprim) or that interfere with the absorption and storage of folate in tissues (e.g., certain anticonvulsants and oral contraceptives) can lower the concentration of folate in plasma and may cause a megaloblastic anemia. 

No definite evidence for the occurrence of copper deficiency in man has been presented, and human requirement is unknown. The diet usually furnishes 2 to 4 mg. of copper daily.Studies in man indicate that 2 mg. daily will maintain an adult in balance. The Food and Nutrition Board suggests a daily allowance of 1 to 2 mg. of copper for an adult, and 0.05 mg. per kilogram of body weight for infants and children. The copper content of whole blood is between 90 and 150 /xg- per 100 ml., equally divided between cells and plasma. There is little evidence that the administration of copper is of assistance in the therapy of hypochromic microcytic anemia. 

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