Latent Autoimmune Diabetes Mellitus in Adults (LADA): the Role of Antibodies to Glutamic Acid Decarboxylase in Diagnosis and Prediction of Insulin Dependency

Diabetic Medicine - Tập 11 Số 3 - Trang 299-303 - 1994
Paul Zimmet1, Jaakko Tuomilehto2, Ian R. Mackay2, Merrill J. Rowley2, W. Knowles3, Matthew L. Cohen1, D. Lang1
1International Diabetes Institute, Monash University Melbourne, Australia
2Centre for Molecular Biology and Medicine, Monash University, Melbourne, Australia
3Miles Research Laboratories, West Haven, USA.

Tóm tắt

Type 1 diabetes mellitus in adults may present in a manner similar to that of Type 2 diabetes but with a late development of insulin dependency. We studied 65 patients who presented with ‘adult‐onset’ diabetes after the age of 30 years. Of these patients, 19 required insulin therapy. The insulin‐treated patients were significantly younger, their onset of diabetes was at an earlier age, and their postprandial serum C‐peptide levels were lower than those of the non‐insulin‐treated group. Moreover, the insulin‐treated subjects had a higher mean concentration of antibodies to glutamic acid decarboxylase (GAD) (66.8 ± 10.2 units) than the patients who did not require insulin (9.9 ± 1.9 units) (p < 0.001) and their frequency of anti‐GAD positivity was 73.7% versus 4.3% (p < 0.001). Thus, among patients attending a diabetes clinic, the majority (73.7%) of subjects who presented with diabetes after 30 years of age and who subsequently required therapy with insulin, actually have the islet cell lesion of Type 1 diabetes which progresses at a slower tempo than in children. We conclude that testing for anti‐GAD in adult‐onset non‐obese diabetic patients should be a routine procedure in order to detect latent insulin‐dependency at the earliest possible stage, since this assay can assist in the correct classification of diabetes, and more appropriate therapy.

Từ khóa


Tài liệu tham khảo

10.2337/diab.28.12.1039

World Health Organization Expert Committee on Diabetes Mellitus.Second Report.Technical Report Series 646. Geneva: WHO 1980.

Harris MI, 1992, The International Textbook of Diabetes Mellitus, 3

10.2337/diacare.15.2.232

10.1016/S0140-6736(89)91306-8

10.1007/BF00265547

10.1016/1056-8727(93)90016-R

10.2337/diacare.9.2.129

10.1111/j.1464-5491.1991.tb01629.x

10.1007/BF00869258

10.2337/diacare.16.5.841

Groop L., 1986, Islet cell antibodies identify latent type I diabetes in patients aged 35–75 at diagnosis, Diabetes, 35, 237, 10.2337/diab.35.2.237

Groop L., 1988, Organ‐specific autoimmunity and HLA‐DR antigens as markers for beta‐cell destruction in patients with type II diabetes, Diabetes, 37, 99, 10.2337/diab.37.1.99

Rowley MJ, 1992, Antibodies to glutamic acid decarboxylase discriminate major types of diabetes mellitus, Diabetes, 41, 548, 10.2337/diab.41.4.548

10.2337/diab.42.2.359

10.1172/JCI116195

10.1007/BF00404145

10.2337/diabetes.40.8.943

Scott R., 1993, Antibodies to glutamic acid decarboxylase (GAD) predict insulin‐deficiency in adult onset diabetes mellitus, Diabetes, 42, 220A

10.1172/JCI112903

10.1056/NEJM198605223142106

10.1203/00006450-199312000-00018

10.1111/j.1464-5491.1989.tb01266.x

10.1007/BF00282516

Skyler JS, 1993, Immune intervention in type 1 diabetes mellitus, Diabetes Rev, 1, 15

Thông tin
Thông tin xuất bản

Diabetic Medicine

Tập 11 Số 3

299-303

Thông tin tác giả