help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2008-1209
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nakanishi, K.
Right arrow Articles by Watanabe, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakanishi, K.
Right arrow Articles by Watanabe, C.
Related Collections
Right arrow Autoimmunity
Right arrow Diabetes and Insulin
The Journal of Clinical Endocrinology & Metabolism Vol. 93, No. 12 4759-4766
Copyright © 2008 by The Endocrine Society

Rate of β-Cell Destruction in Type 1 Diabetes Influences the Development of Diabetic Retinopathy: Protective Effect of Residual β-Cell Function for More Than 10 Years

Koji Nakanishi and Chizuru Watanabe

Department of General Internal Medicine and Metabolism, Toranomon Hospital, Kawasaki 213-8587, Japan; and the Okinaka Memorial Institute for Medical Research, Tokyo 105-8470, Japan

Address all correspondence and requests for reprints to: Koji Nakanishi, Department of General Internal Medicine and Metabolism, Toranomon Hospital, 1-3-1 Kajigaya, Takatsu-ku, Kawasaki, Kanagawa 213-8587, Japan. E-mail: koji01{at}toranomon.gr.jp.

Context: 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.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2008 by The Endocrine Society