title: Glutamic acid decarboxylase antibodies (GADA) is the most important factor for prediction of insulin therapy within 3 years in young adult diabetic patients not classified as Type 1 diabetes on clinical grounds.
abstract: BACKGROUND
  Differentiation between Type 1 and Type 2 diabetes in adults is difficult at diagnosis. In this study we tested the hypothesis that autoantibodies at diagnosis are predictive for insulin treatment within 3 years in patients initially not classified as Type 1 diabetes.
  
  
  METHODS
  In a nationwide population-based study, blood samples were obtained from 764 patients, all diagnosed with diabetes during a 2-year period. At diagnosis, 583 (76%) were classified as Type 1, 110 (14%) as Type 2 and 71 (9.3%) could not be classified.
  
  
  RESULTS
  Among patients not classified as Type 1 diabetes, 52 (47%) of Type 2 and 42 (59%) of unclassified patients were positive for islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GADA) or tyrosine phosphatase antibodies (IA-2A). These patients (n=94) had lower body mass index (BMI) (p<0.001) and lower C-peptide (p<0.001) compared to the autoantibody negative patients (n=87). Compared to clinically classified Type 1 diabetes patients positive for autoantibodies (n=477), they have higher BMI (p<0.001), higher C-peptide (p<0.001) and the same levels of ICA, GADA and IA-2A. After 3 years, 93% of autoantibody positive patients initially not classified as Type 1 were on insulin. When ICA, GADA, IA-2A, BMI and C-peptide were tested in a multiple logistic regression, only GADA was significant for insulin treatment within 3 years (OR=18.8; 95% CI 1.8-191) in patients treated with diet or oral drugs at diagnosis.
  
  
  CONCLUSIONS
  A correct classification is difficult in adult diabetic patients. The presence of pancreatic autoantibodies, especially GADA, at diagnosis of diabetes are highly predictive for insulin therapy within 3 years from diagnosis.
authors: Department of Medicine, University Hospital, Lund, Sweden. Carina.Torn@med.lu.se
authors: C
authors: C
authors: Törn
authors: M
authors: M
authors: Landin-Olsson
authors: J
authors: J
authors: Ostman
authors: B
authors: B
authors: Scherstén
authors: H
authors: H
authors: Arnqvist
authors: G
authors: G
authors: Blohmé
authors: E
authors: E
authors: Björk
authors: J
authors: J
authors: Bolinder
authors: J
authors: J
authors: Eriksson
authors: B
authors: B
authors: Littorin
authors: L
authors: L
authors: Nyström
authors: G
authors: G
authors: Sundkvist
authors: A
authors: A
authors: Lernmark
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000145:classification* / Q000188:drug therapy*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000145:classification* / Q000188:drug therapy*; D003937:Diagnosis, Differential; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D007515:Islets of Langerhans / Q000276:immunology; D007527:Isoenzymes / Q000276:immunology*; D011237:Predictive Value of Tests; D013548:Sweden
chemical_list: D001323:Autoantibodies; D002096:C-Peptide; D007004:Hypoglycemic Agents; C096322:ICA512 autoantibody; D007328:Insulin; D007527:Isoenzymes; C024211:islet cell antibody; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2