Abstract
Compared to healthy infants, over 80 per cent of infants with protein malnutrition excreted excessive quantities of urocanic acid and formiminoglutamic acid (FIGLU) after administration of a relatively large loading dose of histidine. Excessive urinary urocanic acid excretion decreased on refeeding, irrespective of folic acid or vitamin B12supplementation. High urinary urocanic excretion correlated with elevated serum vitamin B12, levels, suggesting that both were associated with hepatocellular damage. All infants with clinical folate deficiency excreted excessive quantities of formiminoglutamic acid after histidine loading, but this excessive excretion could be eliminated by folic acid therapy in only one third of the infants. Many infants with excessive urinary FIGLU had normal serum Lactobacillus casei folate levels and normoblastic bone marrows. Excessive urinary excretion of histidine derivatives by infants with protein malnutrition apparently is dependent on the interaction of a number of factors including folate deficiency, utilization of histidine for protein synthesis and the integrity of the various hepatic enzymes controlling the histidine-glutamic acid pathway.
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