Evaluation of the pancreas reserve in siblings of type I diabetic children

• Published in: Pediatrics international 1999-02, Vol.41 (1), p.42-45
• Main Authors: Berberoğlu, MERIH, Öcal, GÖNÜL, İkincioğullar?, AYDAN, Ad?yaman, PELIN, Çetinkaya, ERGUN, Tutar, ERCAN, Babacan, EMEL
• Format: Article
• Language: English
• Subjects: Adolescent; Antibodies - blood; C-Peptide - blood; Case-Control Studies; Child; Child, Preschool; Diabetes Mellitus, Type 1 - genetics; Diabetes Mellitus, Type 1 - immunology; Diabetes Mellitus, Type 1 - metabolism; Female; Humans; Insulin - blood; Insulin - immunology; Islets of Langerhans - immunology; Killer Cells, Natural - immunology; Male; Pancreas - immunology; pancreas reserve; Pedigree; sibling; T-Lymphocyte Subsets - immunology; type I diabetes mellitus
• ISSN: 1328-8067; 1442-200X
• DOI: 10.1046/j.1442-200x.1999.01010.x

The purpose of this study was to determine the pancreas reserve in siblings of diabetic patients by screening islet cell antibodies (ICA), insulin auto antibodies (IAA), reduced C-peptide levels, first-phase insulin release and the derangement of cellular immunity (reduction of natural killer cells, abnormality of the T cell subpopulations). Twelve siblings (aged 9.3 +/- 2.8 years) of diabetic children were evaluated and results were compared with the control group (12.1 +/- 3.5 years). For siblings of the diabetic children, fasting, post-prandial and glucagon response C-peptide mean values were 2.2 +/- 1.2, 7.2 +/- 7.1 and 5.3 +/- 3.6 ng/mL, respectively, while in the control group they were 1.5 +/- 0.8, 3.6 +/- 2.0 and 5.1 +/- 2.9 ng/mL, respectively. There were no differences between the two groups. In 33%, postprandial C-peptide, and in 11% of the siblings, glucagon response C-peptide values were exaggerated. In siblings the first phase insulin release (FPIR) during an intravenous glucose tolerance test was 128.5 +/- 96.6 (above the 50th percentile) and stimulated insulin release (SIR) was 103.8 +/- 92.5 (above 25th percentile). Sibling values were significantly lower than the control group (FPIR 152.4 +/- 42.5, P = 0.01; SIR 134.9 +/- 38.2, P = 0.01). Values for FPIR (in two children) and SIR (three cases) were below the 5th percentile. In one, FPIR and SIR levels were both below the 1st percentile. Islet cell antibodies and IAA were also present in this subject. Treatment with nicotinamide was started in the cases with FPIR and SIR below the 5th percentile. We did not observe overt diabetic symptoms during the follow-up period of more than 3 years. We recommend that borderline insulin secretion be tested annually in siblings who show insufficient FPIR.