Glutamic acid decarboxylase antibodies (GADA) is the most important factor for prediction of insulin therapy within 3 years in young adult diabetic patients not classified as Type 1 diabetes on clinical grounds.
BACKGROUND
Differentiation between Type 1 and Type 2 diabetes in adults is difficult at diagnosis. In this study we tested the hypothesis that autoantibodies at diagnosis are predictive for insulin treatment within 3 years in patients initially not classified as Type 1 diabetes.


METHODS
In a nationwide population-based study, blood samples were obtained from 764 patients, all diagnosed with diabetes during a 2-year period. At diagnosis, 583 (76%) were classified as Type 1, 110 (14%) as Type 2 and 71 (9.3%) could not be classified.


RESULTS
Among patients not classified as Type 1 diabetes, 52 (47%) of Type 2 and 42 (59%) of unclassified patients were positive for islet cell antibodies (ICA), glutamic acid decarboxylase antibodies (GADA) or tyrosine phosphatase antibodies (IA-2A). These patients (n=94) had lower body mass index (BMI) (p<0.001) and lower C-peptide (p<0.001) compared to the autoantibody negative patients (n=87). Compared to clinically classified Type 1 diabetes patients positive for autoantibodies (n=477), they have higher BMI (p<0.001), higher C-peptide (p<0.001) and the same levels of ICA, GADA and IA-2A. After 3 years, 93% of autoantibody positive patients initially not classified as Type 1 were on insulin. When ICA, GADA, IA-2A, BMI and C-peptide were tested in a multiple logistic regression, only GADA was significant for insulin treatment within 3 years (OR=18.8; 95% CI 1.8-191) in patients treated with diet or oral drugs at diagnosis.


CONCLUSIONS
A correct classification is difficult in adult diabetic patients. The presence of pancreatic autoantibodies, especially GADA, at diagnosis of diabetes are highly predictive for insulin therapy within 3 years from diagnosis.
Törn
C
C
Department of Medicine, University Hospital, Lund, Sweden. Carina.Torn@med.lu.se
Landin-Olsson
M
M
Ostman
J
J
Scherstén
B
B
Arnqvist
H
H
Blohmé
G
G
Björk
E
E
Bolinder
J
J
Eriksson
J
J
Littorin
B
B
Nyström
L
L
Sundkvist
G
G
Lernmark
A
A
D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000145:classification* / Q000188:drug therapy*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000145:classification* / Q000188:drug therapy*; D003937:Diagnosis, Differential; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D007515:Islets of Langerhans / Q000276:immunology; D007527:Isoenzymes / Q000276:immunology*; D011237:Predictive Value of Tests; D013548:Sweden
D001323:Autoantibodies; D002096:C-Peptide; D007004:Hypoglycemic Agents; C096322:ICA512 autoantibody; D007328:Insulin; D007527:Isoenzymes; C024211:islet cell antibody; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2