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Published on: November 16, 2011
Abnormal insulin sensitivity persists up to three years in pediatric patients post-burn
Gerd G Gauglitz1, David N Herndon, Gabriela A Kulp
1Shriners Hospitals for Children, Galveston, Texas 77550, USA.
Insights
Severe burns cause long-lasting insulin resistance in children, persisting for up to three years post-injury. This study tracked metabolic changes and insulin sensitivity in pediatric burn survivors.
Area of Science:
- Pediatric endocrinology
- Metabolic disorders
- Burn injury research
Background:
- The acute hypermetabolic response following severe burns leads to insulin resistance and hyperglycemia, negatively impacting patient outcomes.
- Understanding the long-term metabolic sequelae is crucial for managing pediatric burn survivors.
Purpose of the Study:
- To investigate the persistence of insulin resistance and related metabolic abnormalities in severely burned children for up to three years post-burn.
- To assess changes in clinical parameters used to evaluate insulin sensitivity over time.
Main Methods:
- A prospective study involving 194 severely burned children compared to 95 non-burned controls.
- Measurements included urinary cortisol, catecholamines, serum cytokines, resting energy expenditure, and oral glucose tolerance tests with insulin sensitivity index calculations at multiple time points up to 36 months post-burn.
Main Results:
- Elevated urinary cortisol, catecholamines, specific cytokines, and resting energy requirements persisted for up to 36 months.
- Hyperglycemia was noted for 6 months, with elevated serum C-peptide and insulin persisting for 36 months.
- Insulin sensitivity indices (ISI Matsuda, HOMA, QISSI) remained abnormal throughout the 3-year study period, confirming persistent insulin resistance.
Conclusions:
- Severe burn injury induces stress-related insulin resistance in children.
- This insulin resistance is not confined to the acute phase but persists for as long as three years post-burn, highlighting the need for long-term metabolic monitoring.
Context:
The acute hypermetabolic response post-burn is associated with insulin resistance and hyperglycemia, significantly contributing to adverse outcome of these patients.
Objective:
The aim of the study was to examine the persistence of abnormalities of various clinical parameters commonly utilized to assess the degree of insulin resistance in severely burned children for up to 3 yr after the burn injury.
Design, Setting And Patients:
A total of 194 severely burned pediatric patients, admitted to our institute between 2002 and 2007, were enrolled in this prospective study and compared to a cohort of 95 nonburned, noninjured children.
Main Outcome Measures:
Urinary cortisol, epinephrine, and norepinephrine, serum cytokines, and resting energy requirements were determined at admission and 1, 2, 6, 9, 12, 18, 24, and 36 months post-burn. A 75-g oral glucose tolerance test was performed at similar time points; serum glucose, insulin, and C-peptide were measured; and insulin sensitivity indices, such as ISI Matsuda, homeostasis model assessment, quantitative insulin sensitivity check index, and ISI Cederholm, were calculated. Statistical analysis was performed by ANOVA with Bonferroni correction with significance accepted at P < 0.05.
Results:
Urinary cortisol and catecholamines, serum IL-7, IL-10, IL-12, macrophage inflammatory protein-1b, monocyte chemoattractant protein-1, and resting energy requirements were significantly increased for up to 36 months post-burn (P < 0.05). Glucose values were significantly augmented for 6 months post-burn (P < 0.05), associated with significant increases in serum C-peptide and insulin that remained significantly increased for 36 months compared to nonburned children (P < 0.05). Insulin sensitivity indices, ISI Matsuda, ISI quantitative insulin sensitivity check index, and homeostasis model assessment were abnormal throughout the whole study period, indicating peripheral and whole body insulin resistance. The insulinogenic index displayed physiological values, indicating normal pancreatic beta-cell function.
Conclusions:
A severe burn is associated with stress-induced insulin resistance that persists not only during the acute phase but also for up to 3 yr post-burn.
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