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Clin Exp Immunol. 2010 Sep;161(3):444-52. doi: 10.1111/j.1365-2249.2010.04193.x.

Association of adiponectin, interleukin (IL)-1ra, inducible protein 10, IL-6 and number of islet autoantibodies with progression patterns of type 1 diabetes the first year after diagnosis.

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Department of Paediatrics, Glostrup University Hospital, Glostrup, Denmark.


The progression of type 1 diabetes after diagnosis is poorly understood. Our aim was to assess the relation of disease progression of juvenile-onset type 1 diabetes, determined by preserved beta cell function the first year after diagnosis, with systemic cytokine concentrations and number of autoantibodies. Juvenile patients (n = 227) had a meal-stimulated C-peptide test 1 and 6 months after diagnosis. On the basis of the C-peptide course for the duration of 1-6 months, four progression groups were defined: patients with persistently low beta cell function ('stable-low'), rapid progressers, slow progressers and remitters. Serum concentrations of adiponectin, interleukin (IL)-1ra, inducible protein 10 (IP-10), IL-6 and glutamic acid decarboxylase (GAD), IA-2A and islet-cell antibodies (ICA) were measured at 1, 6 and 12 months. We found that adiponectin concentrations at 1 month predicted disease progression at 6 months (P = 0·04). Patients with low adiponectin had a higher probability of becoming remitters than rapid progressers, odds ratio 3·1 (1·3-7·6). At 6 and 12 months, adiponectin differed significantly between the groups, with highest concentrations among stable-low and rapid progressers patients (P = 0·03 and P = 0·006). IL-1ra, IP-10 and IL-6 did not differ between the groups at any time-point. The number of autoantibodies differed significantly between the groups at 1 month (P = 0·04), where rapid progressers had the largest number. There was no difference between the groups in human leucocyte antigen-associated risk. We define progression patterns distinguishing patients diagnosed with low beta cell function from those with rapid decline, slow decline or actual increase in beta cell function, pointing to different mechanisms of disease progression. We find that adiponectin concentration at 1 month predicts, and at 6 and 12 months associates with, distinct progression patterns.

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