Submitted to: Journal of Burn Care and Rehabilitation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/19/1999
Publication Date: 3/20/2000
Citation: GORE, D.C., JAHOOR, F. DEFICIENCY IN PERIPHERAL GLUTAMINE PRODUCTION IN PEDIATRIC PATIENTS WITH BURNS. Journal of Burn Care and Rehabilitation. 2000. v. 21(2). p. 172-177. Interpretive Summary: Glutamine is the most abundant free amino acid in plasma and muscle and is an integral substrate in numerous metabolic functions. For example, glutamine is a primary fuel source for the gut and for aminogenesis by the kidney. Glutamine is also essential for the nucleic acid synthesis. An inherent acceleration of many of these same metabolic processes is associated with sever trauma. Furthermore, the increased turnover and replication of numerous cell populations, such as those connected with inflammation and wound healing require an increased synthesis of nucleic acid. Thus, on many fronts, glutamine consumption is greatly increased after a severe injury. The skeletal muscle breakdown and overall catabolism that accompany trauma release large quantities of glutamine soon after the injury to fuel these accelerated metabolic functions. Unfortunately with protracted illness, glutamine concentrations decrease precipitously in both plasma and muscle; this finding raises concern about a possible deficiency of glutamine in patients who are critically ill for an extended time. In support of this concept of a stress-induced deficiency, Ziegler et al parenterally supplemented glutamine to patients who underwent bone marrow transplants and found a significant reduction in infectious complications. More recently, Houdijk et al observed a reduced incidence of infections in patients with trauma who were given a glutamine-enriched diet. Other studies have shown the efficacy of glutamine supplementation in the maintenance of mucosal height and gut integrity in catabolic states. These findings suggest that glutamine may become a conditionally essential amino acid during severe illness. Because virtually none of these clinical studies have examined the possibility of a deficit in glutamine availability in children, we undertook this study to quantitate glutamine kinetics in both healthy children and children with severe injuries. Furthermore, we used isolated limb studies to determine any variations in peripheral efflux of glutamine in relationship to whole body measurements. We hope that insight into conditions that foster glutamine deficiency can be elucidated through assessment of any kinetic differences between healthy children and critically ill children.
Technical Abstract: Plasma glutamine levels decrease in association with severe injury, which suggests that the consumption of glutamine exceeds the production of glutamine or possibly represents a deficit in the release of glutamine from skeletal muscle. The goal of this study was to assess the peripheral glutamine kinetic response to prolonged stress in children with critical injuries. To accomplish this purpose, we quantitated peripheral glutamine kinetics in vivo with the use of 5N15 glutamine in 5 children with severe burns (total body surface area, 74% ± 14%; mean ± SEM) and 3 children who underwent elective scar reconstruction. In the children with severe burns, leg blood flow was significantly elevated (16.2 ± 2.1 vs 7.5 ± 0.3 mL/min/100 mL leg volume, P < .02) and the arterial concentration of glutamine was significantly reduced (0.31 ± 0.04 vs 0.84 ± 0.05 mmol/L, P < .001). The rate of glutamine turnover within the leg was significantly reduced in the patients with accurate burns, whereas the net efflux of glutamine was similar between the 2 groups. These findings suggest that plasma glutamine concentrations decrease during severe stress as a result of a deficit in peripheral glutamine release in conjunction with an increased central consumption. This preliminary study supports the notion that exogenous glutamine supplementation in pediatric patients with severe injuries may be needed because of this inadequate skeletal muscle response.