Anemia macrocytic, nutritional

Spies, T. D., Lopez, G. G., Milanes, F., Toca, R. L., Reboredo, A., and Stone, R. E., The response of patients with pernicious anemia, with nutritional macrocytic anemia and with tropical sprue to folinic acid or citrovorum factor. Southern Med. J. 43, 1076-1082 (1950). 

Citrovorum factor stimulates hematologic improvement, similar to that induced by folic acid, in sprue, nutritional macrocytic anemia, macrocytic anemia of pregnancy, pernicious anemia and megaloblastic anemia of infancy. Whether this factor is more active than folic acid has not been determined. Neither folic acid nor citrovorum factor will prevent hematologic relapse or the development of neurologic lesions in pernicious anemia. Folic acid is helpful at times in the therapy of macrocytic anemia associated with cirrhosis of the liver. 

Cya n ocobalamin (Bir) Homocysteine methyltransferase Methylmalonyi CoA mutase Methionine, SAM Odd-carbon fatty acids, Val, Met, He, Thr MCC pernicious anemia. Also in aging, especially with poor nutrition, bacterial overgrowth of terminal ileum, resection of the terminal ileum secondary to Crohn disease, chronic pancreatitis, and, rarely, vegans, or infection with D. latum Megaloblastic (macrocytic) anemia Progressive peripheral neuropathy. ... 

Dietary. Cp deficiency is due to nutritional copper deficiency, with secondarily low levels of Cp, and is associated with neutropenia, thrombocytopenia, low serum iron, and hypochromic, normocytic, or macrocytic anemia unresponsive to iron therapy. The deficiency may be due to inadequate dietary intake, long-term parenteral nutrition without copper supplementation, malabsorption of any cause, penicillamine therapy, or combinations of these. Therapy includes dietary change or copper supplementation, plus treatment of the primary cause of malabsorption if present. 

Summary 47-year-old alcoholic white female has fatigue, malaise, nausea, vomiting, and poor nutritional intake with macrocytic anemia and no evidence of pancreatitis, liver disease, or peptic ulcer disease. 

Importance of thiamine An important water-soluble vitamin used as a cofactor in enzymatic reactions involving the transfer of an aldehyde group. Without thiamine, individuals can develop dementia, macrocytic anemia (folate deficiency), gastritis, peptic ulcer disease, liver disease, depression, nutritional deficiencies, cardiomyopathy, and pancreatitis. 

Certain aspects of the pathology of vitamin E deficiency suggest that nucleic acid metabolism may be deranged. In tissues severely affected by the deficiency one sees various nuclear changes. These include an increase in numbers of nuclei in rabbit skeletal muscle, appearance of giant multi-nucleated cells in rat testes (Mason, 1933), and the appearance of many multinucleated erythroid precursors in vitamin E-deficient monkey bone marrow (Porter et al., 1962). It is of course well known that these tissues are dramatically affected by vitamin E deficiency in the various species. In the rabbit one sees nutritional muscular dystrophy, in the male rat sterility, and in the monkey macrocytic anemia (Dinning and Day, 1957a). 

In Cuba and the southern United States, nutritional megaloblastic anemias, with or without sprue, seem usually to respond to vitamin B12, according to Suarez et al. (1949) and Spies et al. (1949). Orally administered vitamin B12 was not usually effective. On the other hand. Goldsmith (1951), also working in the southern United States, remarked that daily oral doses of only 5 /ig. of B12 frequently induced satisfactory hemopoiesis in sprue and in nutritional macrocytic anemia. 

In Macedonia, Fairley et al. (1938) saw nutritional macrocytic anemias which sometimes responded to refined liver extracts. 

The folic acid group of vitamins was recognized by various effects on several test organisms. The simplest active member may be considered to be pteroylglutamic acid or folacin. This may be combined with extra molecules of glutamic acid. Experimental production of a deficiency of these factors has not been reported in man, but the anemia of certain diseases of man responds to folacin therapy. These diseases include sprue, megaloblastic anemia of infancy, nutritional macrocytic anemia, and the pernicious anemia of pregnancy. Folic acid is involved in some way with the metabolism of amino acids. 

Loss of weight and its concomitants, loss of strength, performance, and growth, are not the only effects of parasites on their hosts that can be related to nutrition. At least two parasites cause anemia of a characteristic kind. Hookworms, both in men and some animals, cause a microcytic, hypochromic anemia of the iron-deficiency type the tapeworm Diphyllobothrium latum causes in man a macrocytic, megaloblastic anemia. The plasmodia of malaria are probably the most widespread parasites that cause anemia, but it is very doubtful if this type of anemia can be regarded as nutritional. There is also some evidence suggesting that some infestations may at least contribute to the production of vitamin deficiencies. 

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