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Pathophysiology of critical illness hyperglycemia in children

  • Bülent Hacıhamdioğlu EMAIL logo , Tanıl Kendirli , Gönül Öçal , Zeynep Şıklar , Şenay Savaş Erdeve , Erdal İnce and Merih Berberoğlu
Published/Copyright: May 3, 2013

Abstract

Causes of hyperglycemia in critically ill non-diabetic children may differ from those in adults. The objective of this study was to investigate the pathogenesis of critical illness hyperglycemia (CIH) in terms of insulin resistance and β-cell dysfunction. Critically ill children with blood glucose (BG) levels of >150 mg/dL (8.3 mmol/L) were enrolled in the study. Insulin sensitivity and β-cell function in the hyperglycemic and euglycemic periods were analyzed with BG/insulin and BG/C-peptide ratios, and utilizing homeostasis model assessment (HOMA). A total of 40 patients were enrolled in the study. BG/insulin and BG/C-peptide ratios were significantly higher in the hyperglycemic period. The HOMA-B and S scores for the hyperglycemic period revealed that out of all the patients who survived (n=30), 20 had β-cell dysfunction, while the remaining (n=11) had insulin resistance. β-cell dysfunction was significantly higher in the hyperglycemic period (p<0.001). As in adults, β-cell dysfunction may play a major role in the pathophysiology of CIH in children.


Corresponding author: Bülent Hacıhamdioğlu, MD, Department of Pediatric Endocrinology, Ankara University Faculty of Medicine, Ankara, Turkey, Phone: +90 03125956791, Fax: +90 0312 3191440

Conflict of interest statement

The authors declare that they have no competing interests.

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Received: 2012-10-7
Accepted: 2013-3-24
Published Online: 2013-05-03
Published in Print: 2013-08-01

©2013 by Walter de Gruyter Berlin Boston

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