[The diagnosis of anemia caused by a deficiency of vitamin B 12 or of folic acid].
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The fetus, the neonate, and the pregnant woman have a greater requirement for folic acid and vitamin B12 and are more likely to suffer from a deficiency of these vitamins. This article reviews the source, requirement, absorption, and metabolism of these vitamins and discusses the problems attributed to their deficiency in pregnancy and in the neonatal period.
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Folate deficiency is a relatively uncommon disorder in central Iran. In order to explain this finding; the acid content of various Iranian breads was determined, since bread is the staple food in Iran. Tanok, the village wholemeal bread, has an average "free" folate content (without conjugase incubation) of 0.34 mug/g. Sangask and Bazari, leavened breads made from flours of high extraction rates and widely consumed in towns and cities, have aberage "free" folate contents of 0.38 and 0.71 mug/g, respectively. The folate content of these breads are significantly higher than that of white bread from refined flour (0.13 mug/g) or oatmeal bread (0.09 mug/g). Iranian breads also have a high content of indigestible fiber (1.6 to 4.2% of dry weight). Since substances within the bread, such as fiber, may interfere with folate absorption by the small intestine, sequential folate absorption tests (tritiated pterolymonoglutamic acid) were performed in four subjects with meals of increasing fiber content and fasting. No interference with folate absorption was found. Furthermore, in vitro studies did not demonstrate the formation of insoluble complexes between bread fiber and folic acid, which might indicate decreased availability.
Megalocytic anemia of alcoholics is due to the deficiency of folic acid: the proof is the serum hypofolemia. The mechanism is complex and due to : a dietary deficiency; a malabsorption; an insufficiency of conversion of polyglutamate to monoglutamate; a liver deficiency; a specific effect of alcohol on the folate absorption. Alcohol has a toxic effect on the marrow and inhibits the folic acid.
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The nutritional status (assessed by anthropometric indices, and biochemical and hematological variables in blood) of three groups of elderly women (aged > or = 65 years) was evaluated within the framework of the Dutch Nutrition Surveillance System. The groups were composed of women living in a nursing home (n = 51), women living in service flats and receiving their dinners from the nursing home kitchen (n = 29), and women living independently (n = 52). Mean blood levels of folate, pyridoxal 5'-phosphate, 25-hydroxyvitamin D, alpha-tocopherol, vitamin C, albumin, selenium and total cholesterol were significantly (p < 0.05) lower among nursing home women. Among these women a biochemical deficiency was frequently found for 25-hydroxyvitamin D (73%), pyridoxal 5'-phosphate (57%), vitamin C (38%), selenium (30%) and folate (28%). These nutritional risks were largely independent of each other. Since folate and pyridoxal 5'-phosphate were associated with several clinicochemical indicators, health status may be an important determining factor for this unfavorable situation. Low 25-hydroxyvitamin D concentrations were associated with limited exposure to ultraviolet radiation and nonusage of vitamin D supplements. We conclude that dietary intake variables are not the only determinants of a marginal nutritional status among nursing home women. Use of foods with a high nutrient density should be encouraged, whereas other preventive measures are needed to improve vitamin D status.
Serum vitamin levels of 40 patients undergoing parenteral nutrition over a 5-to 42-day period were studied while the subjects received daily water-soluble and once weekly fat soluble vitamin formulations intravenously. Initial serum deficiencies of vitamins A, C, and folate were noted in a large portion of the severely malnourished population. At the replacement levels used in this study a small number of patients developed subnormal levels of vitamins A and D. Improvement in levels for vitamin C and folate were noted for most patients. Vitamin B12 deficiencies were not noted in any patient. Currently available commercial vitamin preparations can be used with safety in the parenterally nourished population and recommended guidelines for weekly infusion of both water and fat soluble vitamins are presented.
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Dietary deficiencies of specific nutrients profoundly alter cell-mediated immune responses in man and experimental animals. Both moderate and severe deficiencies are associated with significant changes in immunocompetence. Diets with inadequate levels of protein, calories, vitamin A, pyridoxine, biotin and zinc result in loss of thymic cellularity. Secondary to thymic atrophy, the production of thymic hormones critical for the differentiation of T lymphocytes is reduced, especially in protein-calorie malnutrition and zinc deficiency. Confirmation of a T cell maturational defect in nutritional deprivation comes from the observations of decreased total (T3 and rosette-forming) T cells in the peripheral blood of children with kwashiorkor and marasmus, with preferential loss of helper/inducer (T4) T cell subsets. Reduced number and in vitro function of T cells have also been reported in experimental deficiencies of iron, zinc, copper, and vitamins A and E. Loss of cutaneous hypersensitivity to mitogens and antigens is a consistent sequela of dietary deficiencies of protein, vitamins A and C, pyridoxine, iron and zinc. Cell-mediated immunity directed against allogeneic histocompatibility antigens (e.g. mixed leukocyte cultures, graft versus host, skin graft rejection) may actually be enhanced by experimental protein and polyunsaturated fat deficiencies. Alternatively, pyridoxine, ascorbate and biotin deficiencies resulted in delayed rejection of skin allografts. Cytotoxic T lymphocyte (CTL) activity is impaired in zinc-, iron- and copper-deficient mice, as well as in scorbutic guinea pigs. Natural killer (NK) cell function may be either enhanced or depressed, depending upon the nutrient and its effects on interferon production. Several authors have demonstrated normal or enhanced macrophage activity in a variety of experimental deficiencies. The extrapolation of these observations to infectious disease resistance is not straightforward, and depends upon the nature of the microbe, its own nutrient needs, and the relative importance of innate, as opposed to immunologic, defense mechanisms.
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