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Department of Pediatrics (D.A.v.W., G.D.V.), Research Institute Nutrim, University Hospital Maastricht, 6202 AZ Maastricht, The Netherlands; Department of Intensive Care (T.C.J.), Erasmus MC University Medical Center, 3000 CA Rotterdam, The Netherlands; and Department of Surgery (W.A.B.), Research Institute Nutrim, Maastricht University, 6200 MD Maastricht, The Netherlands
Address all correspondence and requests for reprints to: D. A. van Waardenburg, Department of Pediatrics, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands. E-mail: dvwa{at}paed.azm.nl.
Context: Hyperglycemia and insulin resistance are common findings in critically ill adult patients and are associated with increased morbidity and mortality.
Objectives: The objective of this study was to investigate the hyperglycemic response to critical illness in children.
Design: The study was designed as an observational cohort study.
Setting: The study was set in a university-affiliated pediatric intensive care unit.
Patients: Six children with meningococcal sepsis (MS) without shock and 10 children with meningococcal septic shock (MSS) were patients.
Main Outcome Measures: Differences in blood glucose levels (measured during 72 h after admission) and differences in plasma levels of glucoregulatory hormones (insulin, GH, IGF-I, cortisol, glucagons, leptin), soluble cytokine receptors (sTNF-R55, R75, sIL-1R2), and IL-6 (measured on d 3) between MS and MSS patients were assessed.
Results: Blood glucose levels on d 2 and 3 were higher in MSS patients than in MS patients [7.5 (3.913.0) vs. 5.1 (4.06.0) and 6.5 (4.09.9) vs. 5.5 (4.86.8) mmol/liter, both P < 0.05]. Maximum blood glucose values recorded in individual patients were higher in MSS patients [9.3 (6.513) vs. 7.2 (6.29.9), P < 0.05] and correlated with severity of illness (r = 0.833, P < 0.001). Insulin levels in MSS patients were significantly lower (7.2 vs. 19.0 mU/liter, P < 0.001), compatible with insufficient insulin response to hyperglycemia, whereas MS patients showed insulin resistance. Insulin levels correlated inversely with levels of sTNF-R55 and R75 (r = 0.814 and 0.878, both P < 0.001), suggesting suppression of the proinflammatory response on insulin secretion.
Conclusion: Hyperglycemia associated with hypoinsulinemia rather than insulin resistance may be the normal pathophysiological response in acute MSS in children. Our study emphasizes that application of intensive insulin therapy in critically ill children demands further investigation.
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