Insulin-like growth factor binding protein-1 levels in the diagnosis of hypoglycemia caused by hyperinsulinism

• Published in: The Journal of pediatrics 1997-08, Vol.131 (2), p.193-199
• Main Authors: Levitt Katz, Lorraine E., Satin-Smith, Marta S., Collett-Solberg, Paulo, Thornton, Paul S., Baker, Lester, Stanley, Charles A., Cohen, Pinchas
• Format: Article
• Language: English
• Subjects: Adolescent; Biological and medical sciences; Biomarkers - blood; C-Peptide - blood; Child; Child, Preschool; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Fasting - physiology; Fatty Acids - metabolism; Female; Glycogen Storage Disease Type I - blood; Glycogen Storage Disease Type I - complications; Glycogen Storage Disease Type I - diagnosis; Human Growth Hormone - deficiency; Humans; Hyperinsulinism - complications; Hyperinsulinism - congenital; Hyperinsulinism - diagnosis; Hypoglycemia - blood; Hypoglycemia - diagnosis; Hypoglycemia - etiology; Hypopituitarism - blood; Hypopituitarism - complications; Hypopituitarism - diagnosis; Infant; Infant, Newborn; Insulin - blood; Insulin - physiology; Insulin-Like Growth Factor Binding Protein 1 - blood; Insulin-Like Growth Factor Binding Protein 1 - metabolism; Ketosis - blood; Ketosis - diagnosis; Lipid Metabolism, Inborn Errors - blood; Lipid Metabolism, Inborn Errors - complications; Lipid Metabolism, Inborn Errors - diagnosis; Male; Medical sciences; Tumors. Hypoglycemia
• ISSN: 0022-3476; 1097-6833
• DOI: 10.1016/S0022-3476(97)70153-7

The diagnosis of hypoglycemia caused by hyperinsulinism may be difficult because insulin levels are not uniformly elevated at the time of hypoglycemia. Insulin-like growth factor binding protein-1 (IGFBP-1) is a 28 kd protein whose secretion is acutely inhibited by insulin. We hypothesized that serum levels of IGFBP-1 would be a useful marker of hyperinsulinism. We measured IGFBP-1 levels during the course of standardized fasting studies in hospitalized children; 36 patients became hypoglycemic during the fasting studies, and samples obtained at the point of hypoglycemia were analyzed. On the basis of the currently used diagnostic criteria, 13 children had hyperinsulinism, 16 had ketotic hypoglycemia or no disorder, 3 had hypopituitarism or isolated growth hormone deficiency, 2 had glycogen storage disease type I, and 2 had fatty acid oxidation disorders. In control subjects (children with ketotic hypoglycemia or no disorder), IGFBP-1 levels rose during fasting to a mean of 343.8 ± 71.3 ng/ml in the sample drawn at the time of hypoglycemia. Mean IGFBP-1 levels at hypoglycemia for the entire group with hyperinsulinism were 52.4 ± 11.5 ng/ml, significantly different from levels seen in control subjects (p < 0.0001). In children with moderately controlled hyperinsulinism (fasting tolerance >4 hours), mean IGFBP-1 levels at the time of hypoglycemia were 71.5 ± 16.9 ng/ml. IGFBP-1 levels in the children with poorly controlled hyperinsulinism (fasting tolerance