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American Journal of Clinical Nutrition, Vol 65, 1005-1010, Copyright © 1997 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Protein metabolism in children with edematous malnutrition and acute lower respiratory infection

MJ Manary, DR Brewster, RL Broadhead, JR Crowley, CR Fjeld and KE Yarasheski
Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA. manary@kidsA1.wustl.edu

This study tested the hypothesis that wholebody protein kinetics remain low in children with edematous malnutrition and acute infection. Thirteen children with edematous malnutrition and acute infection (subjects) were compared with 14 uninfected children with edematous malnutrition early in recovery (control children). Protein kinetics were determined by using a primed, constant intravenous infusion of [13C]leucine and [15N2]urea in the postabsorptive state. Calculations of rates of whole-body protein synthesis and breakdown were based on the rate of leucine appearance; the rate of leucine oxidation was estimated from the rate of urea appearance. Protein synthesis and breakdown rates were lower in subjects than in control children (97 +/- 30 compared with 153 +/- 67, P < 0.01, and 103 +/- 30 compared with 160 +/- 67 mumol leucine.kg-1.h-1, P < 0.01). No difference was found between the two groups in the rate of urea appearance, but this analysis only had a statistical power of 54%. The absence of the expected increase in the rate of protein turnover during acute infection in edematous malnutrition implies that acute phase proteins are made with a corresponding depletion of muscle, hepatic, and other body proteins such as albumin, and that there may also be a blunting of the acute phase response.


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Copyright © 1997 by The American Society for Nutrition