Insulin treatment improves the systemic inflammatory reaction to severe trauma

MG Jeschke, D Klein, DN Herndon - Annals of surgery, 2004 - journals.lww.com
MG Jeschke, D Klein, DN Herndon
Annals of surgery, 2004journals.lww.com
Objective: Determine the effect of insulin on the systemic inflammatory response, pro-and
anti-inflammatory cytokines and hepatic acute-phase-response in severely burned pediatric
patients. Summary Background Data: The systemic inflammatory and hepatic acute-phase-
response contribute to hypermetabolism, multi-organ failure, and mortality. Insulin has been
recently shown to decrease mortality and to prevent the incidence of multi-organ failure in
critically ill patients; however, the underlying mechanisms have not been defined. Methods …
Objective:
Determine the effect of insulin on the systemic inflammatory response, pro-and anti-inflammatory cytokines and hepatic acute-phase-response in severely burned pediatric patients.
Summary Background Data:
The systemic inflammatory and hepatic acute-phase-response contribute to hypermetabolism, multi-organ failure, and mortality. Insulin has been recently shown to decrease mortality and to prevent the incidence of multi-organ failure in critically ill patients; however, the underlying mechanisms have not been defined.
Methods:
Thirteen thermally injured children received insulin to maintain blood glucose at a range from 120 to 180 mg/dl, 15 children received no insulin with blood glucose levels also at range from 120 to 180 mg/dl and served as controls. Our outcome measures encompassed the effect of insulin on pro-inflammatory mediators, the hepatic acute-phase-response, fat, and the IGF-I system.
Results:
Insulin administration decreased pro-inflammatory cytokines and proteins, while increasing constitutive-hepatic proteins (P< 0.05). Burned children receiving insulin required significantly less albumin substitution to maintain normal levels compared with control (P< 0.05). Insulin decreased free fatty acids and serum triglycerides when compared with controls (P< 0.05). Serum IGF-I and IGFBP-3 significantly increased with insulin administration (P< 0.05).
Conclusion:
Insulin attenuates the inflammatory response by decreasing the pro-inflammatory and increasing the anti-inflammatory cascade, thus restoring systemic homeostasis, which has been shown critical for organ function and survival in critically ill patients.
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