|Reid, Marvin - BAYLOR COL OF MED|
|Badaloo, Asha - U WEST INDIES JAMAICA|
|Forrester, Terrence - U WEST INDIES JAMAICA|
|Morlese, John - U WEST INDIES JAMAICA|
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 8, 2002
Publication Date: December 20, 2002
Citation: REID, M., BADALOO, A., FORRESTER, T., MORLESE, J.F., HEIRD, W.C., JAHOOR, F. 2002. THE ACUTE-PHASE PROTEIN RESPONSE TO INFECTION IN EDEMATOUS AND NONEDEMATOUS PROTEIN-ENERGY MALNUTRITION. AMERICAN JOURNAL OF CLINICAL NUTRITION. 76(6):1409-1415. Interpretive Summary: Severely malnourished children who also have leakage of water into their tissues, a condition called edema, are usually sicker and more difficult to treat than severely malnourished children who do not have edema. It is believed that this is due to the fact that they cannot fight infections very well because their livers are not making sufficient quantities of proteins called acute phase proteins. These proteins help the body fight infections. To find out whether this is indeed the case we measured the rate at which five of these proteins were being made by two groups of severely malnourished children, one group with edema and another group without. We made these measurements two times, first when all the children had infections and second when their infections were cured. We found that both groups made larger quantities of 4 out of the five proteins when they had the infections. However, the children without edema made more of the proteins than the children with edema. These findings suggest that although all severely malnourished children can make most of the acute phase proteins, those with edema make less than those without edema. This may be one reason why they cannot fight infections effectively.
Technical Abstract: BACKGROUND: Immune structure and function are more compromised in edematous protein-energy malnutrition (PEM) than in nonedematous PEM. Whether the positive acute-phase protein (APP) response to infection is affected remains unknown. OBJECTIVE: We assessed whether children with edematous PEM can mount a general APP response and compared the kinetic mechanisms of the response in children with edematous PEM with those in children with nonedematous PEM. DESIGN: Plasma C-reactive protein, alpha(1)-acid glycoprotein, alpha(1)-antitrypsin, haptoglobin, and fibrinogen concentrations and the fractional and absolute synthesis rates of alpha(1)-antitrypsin, haptoglobin, and fibrinogen were measured in 14 children with edematous PEM, aged 11.4 +/- 2 mo, and 9 children with nonedematous PEM, aged 10.1 +/- 1.4 mo, at 3 times: approximately 2 d after hospital admission (period 1), when they were malnourished and infected; approximately 8 d after admission (period 2), when they were malnourished but free of infection; and approximately 54 d after admission (period 3), when they had recovered. RESULTS: Children with edematous and nonedematous PEM had higher plasma concentrations of 4 of 5 APPs in period 1 than in period 3. The magnitude of the difference in concentration and in the rate of synthesis of the individual APPs was less in the children with edematous PEM than in those with nonedematous PEM. The kinetic data show that the characteristics of the APP response were different in the 2 groups. CONCLUSIONS: These results suggest that severely malnourished children can mount only a partial APP response to the stress of infection and that the magnitude of this response is less in those with edema.