Koji Nakanishi1, Chizuru Watanabe. 1. Department of General Internal Medicine and Metabolism, Toranomon Hospital, 1-3-1 Kajigaya, Takatsu-ku, Kawasaki, Kanagawa 213-8587, Japan. koji01@toranomon.gr.jp
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.
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.
Authors: E M Lipner; Y Tomer; J A Noble; M C Monti; J T Lonsdale; B Corso; W C L Stewart; D A Greenberg Journal: Hum Immunol Date: 2013-01-29 Impact factor: 2.850