Recent studies of experimental vitamin A deficiency in man led the authors to conclude that anemia may result from lack of vitamin A. A review of numerous nutrition surveys in underdeveloped countries enhanced the suspicion that deficiency of vitamin A does contribute to the prevalence of anemia. Preliminary studies of vitamin A-deficient rats confirmed previous observations that anemia may result from lack of this vitamin. The livers of these animals had very low concentrations of vitamin A but normal or increased concentrations of iron. The finding of anemia is in contrast with other reports that vitamin A deficiency may cause elevated values for hemoglobin and hematocrit. The authors suggest that loss of taste and smell as a result of deficiency may account for refusal of experimental animals to eat and drink enough to prevent inanitation and dehydration. The resulting hemoconcentration may mask the true hematological picture, which is one of anemia.
of mortality in middle and early old age in the county boroughs of England and Wales. Br J Prev Soc Med 1969 ;23:133-40. 6 Roberts CJ, Lloyd S. Association between mortality from ischaemic heart disease and rainfall The humoral immune response (as shown by plasma immunoglobulin concentrations and antibody response to diphtheria and tetanus toxoids) was evaluated in 14 children with iron-deficiency anaemia and in 24 normal controls. Mean concentrations of haemoglobin and serum iron and mean transferrin saturation were significantly lower in children with iron-deficiency anaemia than in controls. Serum immunoglobulin concentrations were within the normal range in both groups. Two weeks after immunisation with diphtheria and tetanus toxoids the concentrations of IgG increased significantly in both groups. Antibody titres in irondeficient children were similar to those of controls before and after immunisation. The mean T-lymphocyte count was significantly lower in iron-deficient children than that in controls, but the mean B-lymphocyte counts were similar in the two groups. These observations suggest that humoral immunity in children is not affected by iron deficiency and that conventional immunisation programmes would be effective in children with iron-deficiency anaemia.
Serum levels of vitamin A and retinol-binding protein (RBP) were measured in children with vitamin A deficiency, in children with protein-energy malnutrition (PEM) and in normal children, before and after administration of 100 000 IU of water-miscible vitamin A. Serum vitamin A and RBP levels were significantly low in children with vitamin A deficiency and in children with severe PEM, whereas the values in milder grades of PEM were similar to those of normal subjects. In severely malnourished children with corneal lesions, serum vitamin A concentration was reduced to a much greater extent than the level of serum RBP. Administration of vitamin A resulted in a significant increase in serum levels of both the components within 4 hours in all the 3 groups of children. The increase in RBP concentration observed in children with PEM was similar to that in vitamin A deficient children. These results indicate that in malnourished children, particularly in those who are at risk of developing keratomalacia, vitamin A is the main limiting factor. It is, therefore, recommended that children with PEM should be treated with vitamin A in addition to dietary protein and calories.
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