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

415

Citations

20

References

1994

Year

TLDR

Adult‑onset diabetes can resemble type 2 diabetes but often progresses to insulin dependence later in life. The authors examined 65 patients diagnosed with diabetes after age 30 to assess clinical and immunologic characteristics. Among these, 19 patients required insulin, were younger, had lower post‑prandial C‑peptide, and exhibited markedly higher GAD antibody levels (73.7 % positive versus 4.3 % in non‑insulin users), indicating that routine anti‑GAD testing can identify latent autoimmune diabetes early.

Abstract

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.

References

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