Although residual β-cell function delays the onset and progression of diabetic retinopathy in patients with type 1 diabetes, the rate of β-cell destruction is variable.Objective:
The aim of the study was to clarify the influence of the rate of β-cell destruction on the development and progression of diabetic retinopathy in type 1 diabetes.Design:
We performed a historical cohort study regarding residual β-cell function and retinopathy.Setting:
The study was conducted in the outpatient clinic of a general hospital.Patients:
A total of 254 patients with type 1 diabetes participated.Main Outcome Measures:
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 β-cell function than in those with residual β-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 β-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 β-cell loss and also with early development of diabetic retinopathy. Cox proportional hazards analysis showed that undetectable β-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 β-cell function within 10 yr of the onset of type 1 diabetes is associated with the earlier occurrence of diabetic retinopathy.