title: Autoimmune markers in slow type 1 diabetes: confrontation to type 1 diabetes.
abstract: Slow onset type 1 diabetes is an heterogeneous entity. Its clinical features may mimick type 2 diabetes but its pathophysiological mechanisms are close to type 1 diabetes.
  
  
  OBJECTIVE
  To find out the frequencies, levels and associations of ICA, GADab and IA-2ab in type 2 diabetic patients with atypical phenotype. To compare it to type 1 diabetes.
  
  
  METHODS
  ICA, GADab and IA-2ab were determined in: - 61 patients (age at diagnosis 48.2 +/- 10, range 36-73 years) with an initial diagnosis of type 2 diabetes but having at least one symptom suggesting a slow type 1 diabetes (loss of weight, absence of obesity at diagnosis or secondary failure of oral hypoglycaemic agents). - 70 patients with type 1 diabetes (age 18 +/- 8.9, range 2-35 years). Clinical data evaluated in slow type 1 were maximal BMI, BMI and loss of weight at diagnosis and autoimmune disease. Fasting C-peptide and insulinemia were also assessed.
  
  
  RESULTS
  (Slow type 1 diabetes versus type 1 diabetes). ICA (43% vs 70%; p <0.01) and IA-2ab (16% vs 75%; p <0.01) were more frequent in type 1. GADab were as frequent (62% vs 74%). Association of the three antibodies (15.7% vs 58.5%; p <0.05) were more frequent in type 1. Prevalence of GADab alone (27.5% vs 7.5%; p <0.05) was higher in slow type 1 diabetes and with higher levels (median 55.5 UI/ml vs 17 UI/ml; p <0.01). There was no difference for levels of ICA (25.5 UJDF/ml vs 28 UJDF/ml) or IA-2ab (11.5 UI/ml vs 38.5 UI/ml). BMI of GADab positive patients was lower. Delay of insulinotherapy was shorter in GADab or ICA positive patients. We did not find any relationship between antibodies presence and fasting C-peptide or insulinemia.
  
  
  CONCLUSIONS
  Slow type 1 diabetes should be evoked in atypical type 2 diabetes. Slow onset type 1 diabetic patients have different autoimmune patterns suggesting a different pathophysiological process. GADab and ICA are useful markers to predict future insulinopenia.
authors: Service d'Endocrinologie et de Diabétologie, Clinique Marc Linquette, Centre Hospitalier Régional et Universitaire de Lille.
authors: R
authors: R
authors: Desailloud
authors: I
authors: I
authors: Fajardy
authors: A
authors: A
authors: Vambergue
authors: G
authors: G
authors: Prevost
authors: P
authors: P
authors: Pigny
authors: P
authors: P
authors: Fontaine
mesh_terms: D000328:Adult; D017668:Age of Onset; D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000276:immunology* / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D008875:Middle Aged; D015431:Weight Loss
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; C096322:ICA512 autoantibody; C024211:islet cell antibody; D005968:Glutamate Decarboxylase