Clinical, autoimmune, and genetic characteristics of very young children with type 1 diabetes

Citation
J. Komulainen et al., Clinical, autoimmune, and genetic characteristics of very young children with type 1 diabetes, DIABET CARE, 22(12), 1999, pp. 1950-1955
Citations number
30
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
DIABETES CARE
ISSN journal
01495992 → ACNP
Volume
22
Issue
12
Year of publication
1999
Pages
1950 - 1955
Database
ISI
SICI code
0149-5992(199912)22:12<1950:CAAGCO>2.0.ZU;2-C
Abstract
OBJECTIVE - To study the characteristics of type 1 diabetes in very young c hildren. RESEARCH DESIGN AND METHODS - Clinical outcome, islet cell antibodies (ICA) , insulin autoantibodies (IAA), antibodies against GAD (GADA), IA-2 antibod ies (IA-2A), and HLA-DQBI-defined genetic risk were analyzed in 35 children diagnosed with type 1 diabetes before 2 years of age and compared with tho se in 146 children who were diagnosed between 2.0 and 4.9 years of age and with those in 620 children diagnosed between 5.0 and 14.9 years of age. RESULTS - The youngest age-group had severer metabolic decompensation at cl inical onset, and their serum C-peptide levels, compared with those of olde r children, were lower at the time of diagnosis and during the first 2 year s after the diagnosis. The levels of ICA and IAA were highest in children < 2 years of age, but there were no differences in GADA levels among the thre e age-groups. The youngest age-group had the lowest IA-ZA levels. The HLA D QBI*02/*0302 genotype associated with strong genetic susceptibility was mor e frequent in children diagnosed <5 years of age, whereas the proportion of children carrying a genotype, which includes protective alleles, was highe r among those diagnosed at greater than or equal to 5 years of age. CONCLUSIONS - The clinical presentation of type 1 diabetes at a very young age is associated with severe metabolic decompensation, poorly preserved re sidual beta-cell function, strong humoral autoimmunity against islet cells and insulin, and strong HM-defined disease susceptibility.