title: Onset features and subsequent clinical evolution of childhood diabetes over several years.
abstract: OBJECTIVE
  To explore whether it is possible to predict a child's eventual diabetes phenotype using characteristics at initial presentation, we reassessed 111 young patients on average 7.8 ± 4.2 (2.2-19.7) [mean ± SD (range)] years after diagnosis.
  
  
  METHODS
  Medical records at diagnosis for 111 patients, aged 0-17, were compared with their follow-up characteristics including stimulated C-peptide (CP) and islet autoantibodies (AB).
  
  
  RESULTS
  Initially, 18 patients were obese; 9 displayed other type 2 diabetes (T2DM) features (polycystic ovary syndrome, acanthosis, diagnosed T2DM); the remaining 84 had a classic type 1 diabetes (T1DM) presentation. At follow-up, 83 patients (75%) with no measured CP were classified as T1DM; 17 (15%) were CP+ and AB- and thus considered T2DM. Eleven patients with both T1DM and T2DM features were classified as having mixed diabetes phenotype (MDM). One-fifth (22 subjects) changed presumed phenotype at follow-up. In multivariable models, T1DM patients were younger at diagnosis, had higher initial glucose values, were more likely to have experienced ketoacidosis, and less likely to be obese or of African American ethnicity.
  
  
  CONCLUSIONS
  Ten percent of subjects had MDM and 15% had T2DM at ∼8 years' duration. Although no onset feature was completely reliable, ketoacidosis and hyperglycemia were more likely to predict T1DM; obesity and African American ethnicity made T2DM more likely. At diagnosis, features of T2DM in addition to obesity were strongly predictive of eventual T2DM phenotype. Given the significant percentage who changed or had mixed phenotype, careful tracking of all young people with diabetes is essential to correctly determine eventual disease type.
authors.affiliation: Biological Sciences Division, University of Chicago, Chicago, IL, USA. lipton@uchicago.edu
authors.forename: Rebecca B
authors.initials: RB
authors.lastname: Lipton
authors.forename: Melinda L
authors.initials: ML
authors.lastname: Drum
authors.forename: Kirstie K
authors.initials: KK
authors.lastname: Danielson
authors.forename: Siri Aw
authors.initials: SA
authors.lastname: Greeley
authors.forename: Graeme I
authors.initials: GI
authors.lastname: Bell
authors.forename: William A
authors.initials: WA
authors.lastname: Hagopian
mesh_terms: D000293:Adolescent; D000328:Adult; D001741:Black or African American; D001323:Autoantibodies / Q000097:blood; D002096:C-Peptide / Q000097:blood; D002641:Chicago; D002648:Child; D003920:Diabetes Mellitus / Q000145:classification* / Q000208:ethnology; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis*; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis*; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D050417:Insulin-Secreting Cells / Q000502:physiology; D008137:Longitudinal Studies; D008297:Male; D009765:Obesity / Q000150:complications; D010641:Phenotype
chemical_list: D001323:Autoantibodies; D002096:C-Peptide; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2