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

Context: 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.

Design: We performed a historical cohort study regarding residual beta-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 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.