Alan A Jackson

ZINC AND IMMUNOCOMPETENCE IN PROTEIN-ENERGY MALNUTRITION

Malnourished children have thymic atrophy which is reversed by zinc supplementation. To see if their defect in cell-mediated immunity was also associated with zinc deficiency ten children were skin-tested with Candida antigen on both arms. One test site was covered with local zinc sulphate and the other with placebo ointment. There was a highly significant increase in the typical delayed-hypersensitivity reaction at the site covered with zinc. The magnitude of the difference between the supplemented and unsupplemented arms correlated negatively with the plasma-zinc concentration. These data show that zinc deficiency is a cause of the immunoincompetence seen in malnutrition. The normal reactions of the zinc-supplemented side indicate that, of the many nutritional deficits of malnourished children, zinc deficiency specifically impairs the cell-mediated immune system. Local skin-testing with and without zinc may provide a measure of zinc status. Local application of zinc may enhance the reliability of tests to diagnose diseases such as tuberculosis in malnourished patients.

EFFECT OF ZINC ON THYMUS OF RECENTLY MALNOURISHED CHILDREN

Zinc-deficient animals and children have thymic atrophy and an increased susceptibility to infections. Children with protein-energy malnutrition similarly have thymic atrophy, zinc deficiency, and increased susceptibility to infections. 8 children, recently malnourished, who were supplemented with zinc, showed an increase in thymic size as judged radiographically. It is suggested that zinc deficiency may play a part in the thymic atrophy and infections associated with malnutrition.

Blood glutathione in severe malnutrition in childhood

The blood glutathione (GSH) concentration was measured in 25 severely malnourished children and compared with a group of normal adults. In children with marasmus GSH (3.3 +/- 0.7 mg/gHb) was not different from normal (2.9 +/- 0.4 mg/gHb). However there was a highly significant decrease in all forms of oedematous malnutrition, kwashiorkor (1.5 +/- 0.4 mg/gHb) and marasmic kwashiorkor (1.7 +/- 0.7 mg/gHb). There was no relationship between wasting or stunting and blood GSH.

ALBUMIN AND NUTRITIONAL ŒDEMA

Abstract The nature of the association between plasma albumin and nutritional œdema has been examined by observing the changes in albumin during loss of œdema in patients on a restricted diet. Since there was no difference in the concentration of plasma albumin before and after loss of œdema, the association is not causal. These results provide no support for the assertion that nutritional œdema should be treated with a high-protein diet or an albumin infusion.

The effect of the level of dietary protein, carbohydrate and fat on urea kinetics in young children during rapid catch-up weight gain

The kinetics of urea metabolism were measured in children recovering from severe malnutrition. For a period of up to 10 d they received one of four diets which provided 711 kJ (170 kcal)/kg per d. Two groups received a diet with a high protein:energy (P:E) ratio of 10-6% (HP), enriched with either fat (HP/F) or maize starch and sucrose (HP/C). Two groups received a diet with a low P:E ratio of 8.8% (LP), enriched with either fat (LP/F) or maize starch and sucrose (LP/C). The rate of weight gain on the HP diets was significantly greater than on the LP diets. There was no difference in urea production between any of the four diets: HP/F 1.23 (SE 0.12), HP/C 1.37 (SE 0.14), LP/F 1.64 (SE 0.22), LP/C 1.15 (SE 0.15) mmol nitrogen/kg per h. On the HP diets urea excretion was 0.77 (SE 0.07) mmol N/kg per h, 61% of production. There was significantly less urea excreted in the urine on diet LP/C than on LP/F (0.36 (SE 0.05) and 0.64 (SE 0.04) mmol N/kg per h respectively). A significantly greater percentage of the urea production was hydrolysed on the LP diets (61%) compared with the HP diets (39%), with the consequence that 50% of urea-N produced was available for synthetic activity on the LP diets compared with 30% on the HP diets. The increase in the urea hydrolysed on the LP diets was equivalent in magnitude to the decreased intake of N, so that overall intake plus hydrolysis did not differ between the LP and the HP diets. Crude N balance was similar on diets HP/F, HP/C and LP/C, but was significantly reduced on diet LP/F. These results show that there is an accommodation in urea kinetics during rapid catch-up weight gain, which becomes evident when the P:E ratio of the diet falls to 8.8%. It is proposed that, for a P:E ratio of 8.8%, protein is limiting for catch-up growth. When the intake has a P:E ratio of 8.8% the pattern of urea kinetics can be modified by the relative proportions of fat and carbohydrate in the diet. The measurement of urea kinetics provides a useful approach to the definition of the adequacy of the protein in the diet.

The excretion of 5‐oxoproline in urine, as an index of glycine status, during normal pregnancy

The urinary excretion of 5‐oxoproline, which may be used as an index of glycine status, was investigated in 30 normal pregnant women during different stages of pregnancy and in 18 non‐pregnant female volunteers. During an 18‐h study there was little variation in the 5‐oxoproline/creatinine index, and a single sample gave a representative value. The excretion of 5‐oxoproline/creatinine (μmol/mmol) rose progressively as pregnancy advanced (non‐pregnant mean 10, SD5, first trimester mean 46, SD 12, second trimester mean 150, SD 180, and third trimester mean 280, SD 320) and by the third trimester was over 20 times greater than in non‐pregnant women. The data suggest that as pregnancy advances the endogenous production of glycine may be insufficient to satisfy the increasing demands.

Severe Undernutrition in Jamaica Kwashiorkor and Marasmus: the Disease of the Weanling

ABSTRACT. The syndromes of severe undernutrition, marasmus and kwashiorkor, have causes related to the interplay of social and medical considerations in the society. Kwashiorkor supervenes when the individual is exposed to a level of stress that exceeds the bodys ability to cope. One final common pathway, through which a variety of environmental factors exert an effect, may be associated with oxidant damage to cells. In kwashiorkor there is a severe decrease in the level of both oxidised and reduced glutathione in the red cell. This could be caused by a decreased production, increased consumption or a combination of the two. This is discussed with specific reference to the metabolism of glycine and the possible causal relationship to the pathophysiology of the disease process.

Thiamin status in normal and malnourished children in Jamaica

Thiamin status has been measured using the erythrocyte transketolase (EC 2.2.1.1) assay in twenty-eight normal children and in twenty-five severely-malnourished children throughout the course of recovery. Subclinical thiamin deficiency was found in 7% of the normal children and 36% of the malnourished children on admission. There was no significant association between thiamin status and oedema, stunting or wasting, history of breast-feeding, pattern of weaning, age or sex. Five malnourished children, who died, all had a normal thiamin status on admission; however, two developed biochemical evidence of thiamin deficiency preterminally.

Total body water in malnutrition: the possible role of energy intake.

1. Total body water (TBW) was measured using tritiated water in sixty-five children. The measurements were distributed throughout rehabilitation in order to define the effect of changing energy intakes. 2. Oedematous children had a high TBW which decreased to the normal range during loss of oedema providing they were not receiving more than maintenance amounts of energy during this period. 3. Marasmic children who had not received greater than maintenance amounts of energy had a normal TBW. 4. Treatment with a high-energy diet was associated with an initial increase in TBW. 5. The possible mechanisms for this phenomenon are discussed.

In vivo Metabolism of Nitrogen Precursors for Urea Synthesis in the Postprandial Rat

(1) Adult postprandial rats were given a continuous, intravenous infusion of 15N-labelled glutamate, alanine, ammonium chloride and glutamine amide for 6 h. The enrichment in the free hepatic pool was measured for ammonia, glutamine amide, urea, aspartate, glutamate and alanine. (2) Glutamine and glutamate supplied significantly more nitrogen to urea than ammonium chloride or alanine. (3) Glutamate was not a significant source of hepatic ammonia, hence in this situation it is not necessary to impute a major role to glutamate dehydrogenase in hepatic ammoniagenesis for urea synthesis. (4) Glutamine and ammonia, mostly of intestinal origin in the postprandial state, were major precursors of hepatic ammonia. (5) The nitrogen of glutamate and alanine moved to urea primarily through aspartic acid.