title: Poor beta-cell function after the clinical manifestation of type 1 diabetes in children initially positive for islet cell specific autoantibodies. The Childhood Diabetes in Finland Study Group.
abstract: The prognostic significance of islet cell specific autoantibodies at the diagnosis of Type 1 (insulin-dependent) diabetes mellitus for the persistence of residual beta-cell function over the first 2 years of clinical disease was evaluated in a prospective population-based study. Seven hundred and eighty probands, aged 0.8-14.9 years, were examined for islet cell antibodies (ICA) and insulin autoantibodies (IAA), while 769 probands were studied for antibodies to glutamic acid decarboxylase (GAD65A). They were subsequently observed for 2 years. Lower serum C-peptide concentrations and higher requirement of exogenous insulin during the follow-up period were observed in the group of probands positive for at least one of the antibodies, especially for ICA or IAA. We conclude that the residual beta-cell function after the presentation of Type 1 diabetes is less in children initially positive for islet cell specific autoantibodies than in those testing negative at diagnosis. This might reflect possible heterogeneity in the pathogenesis of childhood diabetes. It also demonstrates that ICA and IAA negativity at the diagnosis of Type 1 diabetes is not associated with a smaller amount of functioning beta-cell mass, but the absence of antibodies probably reflects a slower beta-cell destructive process and a longer duration of preclinical disease.
authors.affiliation: Department of Pediatrics, Kuopio University Hospital, Finland.
authors.forename: J
authors.initials: J
authors.lastname: Komulainen
authors.forename: M
authors.initials: M
authors.lastname: Knip
authors.forename: R
authors.initials: R
authors.lastname: Lounamaa
authors.forename: P
authors.initials: P
authors.lastname: Vähäsalo
authors.forename: J
authors.initials: J
authors.lastname: Karjalainen
authors.forename: E
authors.initials: E
authors.lastname: Sabbah
authors.forename: H K
authors.initials: HK
authors.lastname: Akerblom
mesh_terms: D000293:Adolescent; D000367:Age Factors; D000704:Analysis of Variance; D000918:Antibody Specificity; D001323:Autoantibodies / Q000097:blood*; D002096:C-Peptide / Q000097:blood / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology / Q000276:immunology* / Q000473:pathology*; D016883:Diabetic Ketoacidosis / Q000276:immunology / Q000473:pathology; D005260:Female; D005387:Finland / Q000453:epidemiology; D005500:Follow-Up Studies; D005968:Glutamate Decarboxylase / Q000097:blood; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000276:immunology / Q000627:therapeutic use; D007223:Infant; D007328:Insulin / Q000008:administration & dosage / Q000276:immunology / Q000627:therapeutic use; D007330:Insulin Antibodies / Q000097:blood; D007515:Islets of Langerhans / Q000276:immunology / Q000503:physiopathology*; D008297:Male; D011446:Prospective Studies; D012737:Sex Factors
chemical_list: D001323:Autoantibodies; D002096:C-Peptide; D007004:Hypoglycemic Agents; D007328:Insulin; D007330:Insulin Antibodies; C024211:islet cell antibody; D005968:Glutamate Decarboxylase