title: Rate of beta-cell destruction in type 1 diabetes influences the development of diabetic retinopathy: protective effect of residual beta-cell function for more than 10 years.
abstract: BACKGROUND
  Although residual beta-cell function delays the onset and progression of diabetic retinopathy in patients with type 1 diabetes, the rate of beta-cell destruction is variable.
  
  
  OBJECTIVE
  The aim of the study was to clarify the influence of the rate of beta-cell destruction on the development and progression of diabetic retinopathy in type 1 diabetes.
  
  
  METHODS
  We performed a historical cohort study regarding residual beta-cell function and retinopathy.
  
  
  METHODS
  The study was conducted in the outpatient clinic of a general hospital.
  
  
  METHODS
  A total of 254 patients with type 1 diabetes participated.
  
  
  METHODS
  Serum C-peptide and fundus findings were evaluated longitudinally.
  
  
  RESULTS
  The cumulative incidence of mild nonproliferative diabetic retinopathy was higher in the patients without detectable beta-cell function than in those with residual beta-cell function at 20, 15, and 10 yr after the onset of diabetes (P = 0.013, P = 0.006, and P = 0.048, respectively), but not at 5 yr after the onset (P = 0.84). There were higher mean glycosylated hemoglobin values during the entire follow-up period in the patients without detectable beta-cell function at 20 and 15 yr after the onset of diabetes (P = 0.030 and P = 0.042, respectively). Positivity for HLA-A24 and -DQA1 03, as well as the acute onset of diabetes, was associated with early beta-cell loss and also with early development of diabetic retinopathy. Cox proportional hazards analysis showed that undetectable beta-cell function at 20, 15, or 10 yr after the onset of diabetes was an independent risk factor for the development of diabetic retinopathy.
  
  
  CONCLUSIONS
  Undetectable beta-cell function within 10 yr of the onset of type 1 diabetes is associated with the earlier occurrence of diabetic retinopathy.
authors.affiliation: Department of General Internal Medicine and Metabolism, Toranomon Hospital, 1-3-1 Kajigaya, Takatsu-ku, Kawasaki, Kanagawa 213-8587, Japan. koji01@toranomon.gr.jp
authors.forename: Koji
authors.initials: K
authors.lastname: Nakanishi
authors.forename: Chizuru
authors.initials: C
authors.lastname: Watanabe
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000473:pathology*; D003930:Diabetic Retinopathy / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D005654:Fundus Oculi; D006442:Glycated Hemoglobin / Q000378:metabolism; D006680:HLA Antigens / Q000032:analysis; D006801:Humans; D050417:Insulin-Secreting Cells / Q000473:pathology*; D008137:Longitudinal Studies; D008297:Male; D015999:Multivariate Analysis; D010186:Pancreatic Function Tests
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D006442:Glycated Hemoglobin; D006680:HLA Antigens