Pathophysiology of critical illness hyperglycemia in children

• Published in: Journal of pediatric endocrinology & metabolism : JPEM Vol. 26; no. 7-8; p. 715
• Main Authors: Hacıhamdioğlu, Bülent, Kendirli, Tanıl, Oçal, Gönül, Sıklar, Zeynep, Savaş Erdeve, Senay, Ince, Erdal, Berberoğlu, Merih
• Format: Journal Article
• Language: English
• Published: Germany 2013
• Subjects: Adolescent; Blood Glucose - analysis; C-Peptide - blood; Child; Child, Preschool; Critical Illness; Female; Humans; Hyperglycemia - blood; Hyperglycemia - etiology; Hyperglycemia - physiopathology; Infant; Insulin Resistance; Insulin-Secreting Cells - physiology; Male
• ISSN: 0334-018X
• DOI: 10.1515/jpem-2012-0313

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.