Clinical, metabolic, immunologic and genotypic characteristics in non-pediatric patients with type 1A diabetes mellitus.: Onset and short-term prognosis

BACKGROUND AND OBJECTIVE: Around 50% of new cases of type 1 diabetes mellitus (DM1) are seen in subjects aged above 15 years. It is of particular interest the characterization of such a population. The aims of our study were: a) to characterize a group of non-pediatric subjects with DM1 at the onset of the disease; b) to evaluate the prognosis of the disease under conventional intensive insulin therapy, and c) to investigate the presence of mutations in the HNF-1alpha gene in those subjects who did not display pancreatic autoimmune markers. SUBJECTS AND METHOD: All subjects with an age 15 and : 35 years recently diagnosed DM1 (19982001) were included in the study. Pancreatic cell function was assessed by glucagon test (at onset and at 12 months). The presence of pancreatic autoantibodies, GAD, IA2 and IAA was evaluated. HLA class II genes and the 10 exons of HNF-1alpha gene were analyzed from genomic DNA. RESULTS: We studied 86 subjects (32 women, 23.9 [5.3] year-old). Eighty percent of subjects were positive for any of the studied autoantibodies. Alone or in combination, GAD was positive in 68.6% of subjects, IA2 in 45.3% and IAA in 27.9% of them. Most frequent haplotype was DRB1*0301-DQA1*0501-DQB*0201. There were no differences with regard to clinical, metabolic or genetic characteristics among those subjects with or without presence of pancreatic autoantibodies (at onset and at 12 months). We did not find mutations in the HNF-1a gene in any of the subjects included in our study. After 12 months of follow-up, P cell function remained unaltered in comparison with that observed at the onset of the disease. CONCLUSIONS: Clinical, immunological and HLA characteristics of a non-pediatric DM1 population are in agreement with expected results. The absence of pancreatic autoimmune markers neither rules out the existence of type 1A diabetes mellitus nor is associated with mutations in the MODY-3 gene. A therapeutic programme using conventional intensified insulin treatment prevents the impairment of insulin secretory capacity for a short-term follow-up.