Pathophysiology of critical illness hyperglycemia in children
Journal of Pediatric Endocrinology and Metabolism, cilt.26, sa.7-8, ss.715-720, 2013 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 26 Sayı: 7-8
- Basım Tarihi: 2013
- Doi Numarası: 10.1515/jpem-2012-0313
- Dergi Adı: Journal of Pediatric Endocrinology and Metabolism
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.715-720
- Anahtar Kelimeler: beta-cell dysfunction, children, critical illness hyperglycemia, pathophysiology
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Causes of hyperglycemia in critically ill nondiabetic 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. © 2013 by Walter de Gruyter.