|Morlese, John - BAYLOR COLLEGE OF MED|
|Forrester, Terrence - TROPICAL METAB RES UNIT|
|Badaloo, Asha - TROPICAL METAB RES UNIT|
|Del Rosario, Melanie - BAYLOR COLLEGE OF MED|
|Frazer, Margaret - BAYLOR COLLEGE OF MED|
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 9, 1996
Publication Date: N/A
Interpretive Summary: We wanted to determine the changes that cause hypoalbuminemia (a deficiency of a protein called albumin) and the relationship between hypoalbuminemia and edema (excess fluid in tissue spaces) in protein energy malnutrition(PEM), a severely malnourished condition manifested by growth retardation and muscle wasting. It has been accepted that in PEM patients, hypoalbuminemia causes edema, but it has been argued that infection (which usually accompanies PEM) is responsible. We used a stable isotope infusion to trace the albumin synthesis of 14 children with protein-energy malnutrition: 7 with edema and 7 without it. We measured blood albumin concentration and synthesis rates 2 days after admission (study 1), 8 days later when infections were clear (study 2) and at recovery (study 3). In study 1 there was no difference in albumin concentrations in the two groups. In both groups, albumin concentrations, but not synthesis rates, were lower in studies 1 and 2 than in study 3. The results suggest hypoalbuminemia may be due to an increased breakdown of albumin rather than decreased synthesis, that edema isn't solely due to hypoalbuminemia, that infection is a factor in the altered albumin activity in PEM, and the ability to synhesize albumin is not affected by nutritional state.
Technical Abstract: The kinetic changes responsible for decreased plasma albumin and the relationship between plasma albumin and the edema of protein-energy malnutrition (PEM), was investigated by measuring the plasma concentration, fractional (FSR) and absolute (ASR) synthesis rates of albumin in seven edematous and seven non-edematous children with PEM using constant intragastric infusions of 2H3-leucine. Studies were done 2 d post-admission (study 1), 8 d post-admission (study 2), and at recovery (study 3). At study 1 there was no difference in plasma albumin concentrations in non-edematous and edematous children. In both groups, albumin concentrations, but not FSRs, were lower in studies 1 and 2 than study 3. ASR was lower only in edematous patients. These results suggest that depletion and repletion of the albumin pool of children with PEM is not mediated by changes in FSR, and the edema of malnutrition is not solely due to hypoalbuminemia.