Antibodies to Glutamic Acid Decarboxylase Reveal Latent Autoimmune Diabetes Mellitus in Adults With a Non—Insulin-Dependent Onset of Disease

Author:

Tuomi Tiinamaija1,Groop Leif C1,Zimmet Paul Z1,Rowley Merrill J1,Knowles William1,Mackay Ian R1

Affiliation:

1. Centre for Molecular Biology and Medicine, Monash University Clayton, Victoria, Australia Department of Medicine, Helsinki University Central Hospital Helsinki, Finland International Diabetes Institute Caulfield, Victoria, Australia Miles Research Laboratories West Haven, Connecticut

Abstract

The classification of adults with diabetes mellitus can be invalidated by patients who initially present as NIDDM but who later become frankly insulin dependent. In some of these, the pathogenesis could be similar to that in IDDM, namely autoimmune destruction of the pancreatic β-cells. We studied 102 patients >35 yr of age at diabetes onset who had initially been nonketotic and non-insulin-dependent for ≥6 mo. They were classified according to glucagonstimulated C-peptide levels into an insulin-deficient group (n = 33) and a non-insulin-deficient group (n = 69). We measured antibodies to GAD, islet cell cytoplasm, thyroid antigens, and gastric parietal cells in both groups. Anti-GAD was significantly higher in the insulin deficient group, 76% (25 of 33), than in the non-insulin deficient group, 12% (8 of 69), and this difference was substantially greater than that shown for ICAs. Thus, in a proportion of adults who present with NIDDM, a slowly evolving autoimmune insulitis can be revealed by testing for anti-GAD. This could have important connotations not only for early intervention, but also for the correct classification of diabetes.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

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