Vitamin A, E and carotenoid status in Jamaica children with sickle cell disease

Nutritional deficiencies would appear to be an important determinant of morbidity in homozygous sickle cell (SS) disease. This is evidenced by the growth and development deficits which are observed in children with SS disease. In a study of the nutritional status of Jamaican children with SS disease aged 3 to 6 years, serum samples from blood taken after an overnight fast in the SS children and children of the same age with normal haemoglobin (AA) were collected. Micro-nutrient analyses of these serum samples for vitamin A (retinol) and vitamins E (alpha and gamma tocopherol) and the carotenoids, beta-carotene and lycopene were carried out using high performance liquid chromatography (HPLC). The results suggest that in children with SS disease several of the micro-nutrients which are essential for maintaining optimal antioxidant status are found in decreased amounts in serum. The confirmation of these micronutrients deficiencies in SS children provide the basis fo further exploration of their interrelationshipo with the growth and development deficits in this population. (AU)

Vitamin E status in oedematous and non-oedematous malnourished children - abstract

The antioxidant function of vitamin E is essential for maintaining the integrity of cell membranes. During the early phase of recovery from severe malnutrition, we measured the plasma levels of Vitamin E in 58 children on admission (A), and after metabolic recovery (B). A total of 19 marasmic children, and 34 with oedematous malnutrition (19 with marasmic-kwashiorkor and 15 with kwashiorkor) were studied. A further group of 5 oedematous children who were clinically assessed as extremely sick received daily vitamin E supplements. The children were all fed on the same dietary regimen. The results indicated that although vitamin E intake was greater in the non-oedematous (marasmic) children, the rate of change of concentration in the plasma did not differ between the two groups. This could possibly be attributed to a difference in the absorption or utilization of the vitamin between the groups. In the group receiving supplements, there was a significant increase in plasma vitamin E concentration between A and B. However, the rate of increase and the concentration at B did not differ from that in the two groups of unsupplemented children. We conclude that in malnourished children: (1) plasma viatmin E levels are low on admission, (2) values normalize by time B, and (3) supplementation with alpha-tocopherol in oil did not affect the rate of increase in plasma vitamin E. The supplement did not seem to be bioavailable (AU)

Vitamin E in malnutrition - abstract

Free radical generation in vivo occurs through the normal activity of some oxidative enzymes, through food contaminants, microbial products and during infections. The manifestations of oxidant damage are fatty liver, increased membrane permeability and haemolysis - all features of severe malnutrition. The major antioxidant that prevents free radical-induced peroxidation in lipids is Vitamin E. We have therefore measured Vit. E concentration in the plasma of 52 severely malnourished children on admission and again at discharge. Thus of the oedematous children, 83 percent had biochemical Vit. E deficiency. Two of these children died: they had 1.0 and 2.4 mg/l Vit. E and at post mortem grossly fatty livers. Low Vit. E status occurred in about half the marasmic children. Two who died had Vit. E levels of 3.7 mg/l with fatty liver and 5.5 mg/l without fatty liver. At recovery, most of the children had normal Vit. E levels. They remained low in 6 children (5 boys and 1 girl). The only 2 children with the sex-linked disorder G-6-PD deficiency (45 were tested) failed to show an increase in Vit. E with recovery. A third boy had a very low activity of 6-PGAD - the second enzyme in the hexose monophosphate shunt. Two boys were not tested. The girl had normal G-6-PD and 6-PGAD but developed osteomyelitis during recovery. Thus, it is likely that each of these children failed to achieve normal levels of Vit. E during recovery because of increased oxidant stress. We conclude that biochemical Vit. E deficiency is common in malnutrition, particularly oedematous malnutrition, and that Vit. E deficiency may play a role (together with deficiencies of other antioxidants) in the fatty liver and membrane cation leak seen in malnutrition. Vit. E status should be assessed in a larger series of children with G-6-PD deficiency (AU)