Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003969 (vitamin C deficiency)
 625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leucocyte ascorbic acid (LAA) levels were estimated in 26 Nigerian infants and preschool children with protein energy malnutrition (PEM) in order to ascertain their ascorbic acid status. The children included eight with kwashiorkor, 12 with marasmus and six with marasmic kwashiorkor. The mean (SD) LAA level of 13.7 (8.2) micrograms/10(8) leucocytes in the malnourished children did not vary significantly from the mean level of 14.4 (8.8) micrograms/10(8) leucocytes found in 26 age-matched controls, and the values were unrelated to the presence or absence of megaloblastic change in the 14 bone marrows examined. It was concluded that ascorbic acid deficiency was not prevalent amongst children with PEM in Lagos, and was therefore not usually contributory to the anaemia, megaloblastic changes or other features of the syndrome seen in Nigerian children in Lagos.
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PMID:Leucocyte ascorbic acid levels in Nigerian children with protein-energy malnutrition. 619 23

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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PMID:Cell-mediated immunity in nutritional deficiency. 639 15