Better education for better health care.

PIP: In India, all national nutrition programs and activities are carried out by staff at the primary health centers under the leadership of medical officers. A study of 114 of these officers from 80 primary health centers in rural districts of Andhra Pradesh State was undertaken to assess their knowledge and performance, particularly with regard to nutrition and related matters. Scores were expressed in percentages, with under 50% considered poor, 50-75% satisfactory, and over 75% good. The highest score 67.7% was obtained on knowledge of nutrition and related areas, and the lowest, 19.7% was for the participant's awareness of their own job responsibilities. Although overall theoretical knowledge on nutrition and related matters was satisfactory, significant gaps existed. A majority were ignorant as to how many people were covered by their centers and the numbers of staff in different categories, suggesting little attention was being given to planning and implementation of various services. Only 23% were aware of their own responsibilities regarding nutrition, and only 16% mentioned teaching nutrition during their training programs. The conclusion is that the medical education system must be better coordinated with the health care delivery infrastructure. Medical undergraduates need more exposure to Practical aspects of health care in rural communities, managerial aspects of work in primary health centers, and programs with a stronger nutrition component. In addition, refresher courses must be offered, and the problem of overburdening the medical officers must be dealt with.^ieng

Mejor educación para mejorar la atención de salud / Better education for better health care

A survey of medical officers in charge of primary health centres in rural districts of Andhra Pradesh, India has revealed significant deficiencies in their knowledge and performance. The situation could be improved by creating closer links between the medical education system and the machinery for health care delivery, organizing refresher courses, and introducing educational programmes with a stronger nutrition component

Effect of intramuscular vitamin A injection on plasma levels of vitamin A and retinol-binding protein in malnourished children.

1. Serum levels of retinol-binding protein (RBP), total vitamin A and retinyl ester were measured in twenty-four malnourished children with corneal lesions and nine normal children. 2. Initially, the RBP and vitamin A levels were significantly lower in malnourished children than in normal children. 3. After intramuscular injection of 30000 microgram of aqueous vitamin A, serum levels of total vitamin A were increased significantly at 24 h and tended to fall within 5 d of treatment in both groups. 4. Before treatment, retinyl ester accounted for less than 10% of the vitamin in circulation. After vitamin A injection, it increased to 30%, a level much lower than that reported in patients with hypervitaminosis A. 5. There was no significant difference between the two groups of children and none of them showed clinical signs of toxicity. These observations indicate that administration of massive doses of vitamin A over a short period will not produce toxic effects even in malnourished children.

Humoral immune response in vitamin A deficient children.

Humoral immune response was evaluated in children with vitamin A deficiency. The percentage of B lymphocytes and the initial levels of plasma IgA, IgG and IgM were normal. Two weeks after the immunisation with diphtheria and tetanus toxoids, there was a marked increase in the antibody titers. There were no significant differences between the deficient and the normal children. The results indicate that the antibody production is not altered in children with vitamin A deficiency.

Humoral immune response in children with iron-deficiency anaemia.

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 iron-deficient 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.

Effect of zinc supplementation on plasma levels of vitamin A and retinol-binding protein in malnourished children.

The relationship between plasma levels of vitamin A and zinc was studied in 45 children suffering from vitamin A deficiency and 20 children with protein-energy malnutrition. Thirty apparently normal children of the same age group were also studied for comparison. The mean levels of plasma vitamin A, retinol-binding protein and zinc were significantly lower in vitamin A-deficient children and in children with PEM, as compared to controls. Supplementation with 40 mg zinc daily for 5--10 days resulted in a significant increase in plasma vitamin A and RBP levels in children with PEM but not in the vitamin A-deficient group. There was, however, no correlation between plasma levels of vitamin A and zinc. The data suggest that in children with PEM, apart from deficiencies of protein and vitamin A, zinc deficiency may also contribute to the lowering of plasma vitamin A levels. They also suggest that in vitamin A-deficient children, without protein-energy malnutrition, zinc deficiency does not seem to have a role.

Serum retinol-binding protein and vitamin A levels in malnourished children.

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.

Hematopoietic studies in vitamin A deficiency.

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.

Alkaline ribonuclease activity in plasma and leucocytes of malnourished women.

Alkaline RNase activity was measured in plasma and leucocytes of pregnant and non-pregnant women belonging to low and high socio-economic groups. It was observed that the enzyme activities were significantly higher in pregnant as well as non-pregnant women of the low socio-economic group as compared to women of the high socio-economic group. There was no correlation between the enzyme activities in maternal or cord blood on the one hand and birth weight of the infants on the other. These results suggest that RNase activities in maternal blood reflect the nutritional status of the mother but not that of the fetus.

Ribonuclease activity in plasma and leucocytes of malnourished children.

RNAase activity was measured in plasma and leucocytes of manourished children. In subjects suffering from kwashiorkor, alk. RNAase levels in plasma and leucocytes were markedly raised and they returned to normal after therapy. However, the enzyme activity was not altered in undernourished children. These data indicate that circulating level of alkaline. RNAase is not a useful parameter for detecting milder grades of protein-calorie malnutrition (PCM).

Hematological studies in vitamin A deficient children.

Hematological studies were carried out in 110 children with varying levels of plasma retinol to investigate the relationship between vitamin A deficiency and anemia. In children with plasma retinol levels below 20 microgram/100 ml, the mean levels of hemoglobin and hematocrit were lower than those in children who had retinol levels above 20 microgram/100 ml. Following supplementation of vitamin A, there was a significant increase in the levels of hemoglobin, hematocrit and plasma iron. These findings suggest that apart from deficiency of iron, vitamin A deficiency may also have a contributory role in the development of anemia in children.

Vitamin A deficiency and the metabolism of glycosaminoglycans and ascorbic acid in the rat.

Weanling rats were fed diets with and without the addition of retinyl palmitate at 6,500 units/kg. The supplemented groups were fed either ad libitum or food was restricted daily to that amount consumed by the group of rats receiving the unsupplemented diet. After a 10 week experimental period, signs of vitamin A deficiency were observed (growth plateau, xerophthalmia) and liver values as retinol were only 1% of control values. Relative to the two control groups, vitamin A deficiency resulted in approximately 30% lower liver, 50% lower blood and 40% lower urinary ascorbic acid. Vitamin A deficiency did not appear to result in significant and direct impairment of GAG sulfate metabolism. Although the total amount of GAG in rat skin was increased, the composition of GAG fractions did not appear to be altered by vitamin A deficiency. Studies regarding the incorporation and disappearance of 35S-sulfate in vivo into GAG fractions obtained from skin indicated no serious impairment in GAG turnover with vitamin A deficiency. Twenty-four hour urine samples were also collected for estimation of 35SO4 excreted in GAG and non-GAG fractions. Likewise, little change was observed with respect to radioactivity associated with sulfate fractions excreted in urine. Although many previous studies have directly linked vitamin A with sulfation of GAG, the results reported here suggest that if there is an alteration in GAG sulfate metabolism, it is probably an indirect consequence of vitamin A status.

Ascorbic acid and tyrosine metabolism in preterm and small-for-dates infants.

Ascorbic acid levels in plasma and leucocytes and urinary excretion of tyrosyl derivatives (TD) were determined in 11 normal, 18 preterm, and 4 small-for-dates infants. Concentrations of ascorbic acid in both plasma and leucocytes were found to be similar in the 3 groups. There was no difference in the basal levels of TD between normal and small-for-dates infants, but preterms showed higher basal excretion of TD than the other two groups. After protein load the excretion of TD was higher than the basal level in preterms. It was concluded that the altered metabolism of tyrosine observed in preterms is not the result of poor ascorbic acid status; and that tyrosine metabolism is influenced by the period of gestation rather than the body weight of the infant.