title: Islet autoantibody status in a multi-ethnic UK clinic cohort of children presenting with diabetes.
abstract: OBJECTIVE
  We prospectively determined islet autoantibody status in children presenting with diabetes to a single UK region in relation to ethnicity.
  
  
  METHODS
  316 (68.0% non-white) children presenting with diabetes between 2006 and 2013 were tested centrally for islet cell autoantibodies (ICA) and glutamic acid decarboxylase autoantibodies (GAD-65) at diagnosis, and if negative for both, tested for insulin autoantibodies (IAA). The assay used to measure GAD-65 autoantibodies changed from an in-house to a standardised ELISA method during the study.
  
  
  RESULTS
  Even with use of the standardised ELISA method, 25.8% of children assigned a diagnosis of type 1 diabetes still tested negative for all three autoantibodies. 30% of children assigned a diagnosis of type 2 diabetes were autoantibody positive, and these had the highest glycated haemoglobin (HbA1c) levels at 12 months follow-up compared with other groups (p value for analysis of variance <0.001), although the sample size was small. Autoantibody positivity was similar between non-white and white children regardless of assay used (60.0% (n=129) vs 56.4% (n=57), χ(2)=0.9, p=0.35), as was mean GAD-65 autoantibody levels, but fewer non-white children had two or more autoantibodies detectable (13% (n=28) vs 27.7% (n=28), χ(2)=12.1, p=0.001).
  
  
  CONCLUSIONS
  Islet autoantibody positivity was associated with a more severe phenotype, as demonstrated by poorer glycaemic control, regardless of assigned diabetes subtype. Positivity did not differ by ethnic group.
authors.affiliation: Department of Paediatrics, Royal London Hospital, London, UK Department of Paediatrics, Queens Hospital, Romford, UK.
authors.forename: R
authors.initials: R
authors.lastname: Perchard
authors.affiliation: Department of Immunology, Royal London Hospital, London, UK.
authors.forename: D
authors.initials: D
authors.lastname: MacDonald
authors.affiliation: Department of Paediatrics, Royal London Hospital, London, UK.
authors.forename: J
authors.initials: J
authors.lastname: Say
authors.affiliation: Department of Paediatrics, Queens Hospital, Romford, UK.
authors.forename: J
authors.initials: J
authors.lastname: Pitts
authors.affiliation: Department of Immunology, Royal London Hospital, London, UK.
authors.forename: S
authors.initials: S
authors.lastname: Pye
authors.affiliation: Department of Paediatrics, Royal London Hospital, London, UK.
authors.forename: J
authors.initials: J
authors.lastname: Allgrove
authors.affiliation: Department of Paediatrics, Queens Hospital, Romford, UK.
authors.forename: K
authors.initials: K
authors.lastname: Banerjee
authors.affiliation: Clinical & Molecular Genetics Unit, UCL Institute of Child Health, London, UK.
authors.forename: R
authors.initials: R
authors.lastname: Amin
mesh_terms: D000293:Adolescent; D000704:Analysis of Variance; D001323:Autoantibodies / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D003924:Diabetes Mellitus, Type 2 / Q000208:ethnology / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007515:Islets of Langerhans / Q000276:immunology*; D008297:Male; D010641:Phenotype; D011446:Prospective Studies
chemical_list: D001323:Autoantibodies
keywords: Endocrinology; Race and Health