This study shows a higher spontaneous clinical remission rate than expected during the 1st yr after diagnosis. Preserved beta-cell function at entry predicts a greater chance of entering a remission, and a more rapid loss of beta-cell function was seen in patients without HLA-DR3 and -DR4.

Summary.In a cross-sectional study, sera of 81 adult diabetic in-patients were tested for the presence of pancreatic islet cell antibodies (ICA), both IgG and complement-fixing. All patients had been well controlled initially with oral hypoglycaemic agents and therefore had been classified as having Type 2 (non-insulin-dependent) diabetes. However, 14 were subsequently classified as Type 1 (insulin-dependent) because they became insulin-dependent within 2 months of diagnosis. Ten of these patients (71%) were ICA-positive. Sixty-seven patients had been non-insulin-dependent for at least 1 year after diagnosis. Circulating ICA were present in 18 patients and 16 of these (89%) required insulin therapy. Secondary oral hypoglycaemic agent failure developed within a mean period of 3.7 years after diagnosis. In contrast, in the ICA-negative subgroup (n = 49) insulin treatment became necessary in 29 patients. Secondary oral hypoglycaemic agent failure of these patients had developed after a mean period of 8.4years, which was significantly longer than in the ICA-positive patients (p < 0.01). Complement-fixing-ICA were detected only in sera with an ICA-IgG titre of at least 8, and its prevalence was similar in the sub-groups tested, i.e., the Type I diabetic patients and the patients with secondary oral hypoglycaemic agent failure. With HLA-DR typing, a significant excess of the DR3 antigen and heterozygous DR3/DR4 phenotypes was found in ICA-positive patients with secondary oral hypoglycaemic agent failure and in the Type 1 diabetic patients, which was comparable with the frequencies reported in juvenileonset Type 1 diabetes. The heterozygous DR3/W6 phenotype was significantly increased in the ICA-positive patients when compared with 13 ICA-negative patients. Thus, the presence of ICA and an excess of certain HLA-DR phenotypes identify a sub-group within the adult diabetic population with secondary oral hypoglycaemic agent failure which can be regarded as a retarded form of Type I diabetes.Key words: Islet cell antibody, complement-fixing islet cell antibody, HLA-DR phenotypes.Cytoplasmic antibodies to pancreatic islet cells (ICA) have been described in adult diabetic patients treated with oral hypoglycaemic agents and are associated with a high probability of becoming insulin-dependent within the near future. Considering the heterogeneity of diabetes, ICA-positive, apparently non-insulin-dependent diabetes may represent a retarded pathogenesis of Type I (insulin-dependent) diabetes [1,2]. This is supported by the observation that ICA-positive patients, even though initially controlled with oral hypoglycaemic agents, expressed a significant prevalence of HLA-DR3 and heterozygous DR3/DR4 phenotypes comparable with the frequencies found in juvenile onset Type 1 diabetes [3][4][5]. Subjects and methods SubjectsEighty-one patients (aged 30-75 years, mean_+ SEM age 50_+ 1 years) were initially well controlled with diet or additional oral hypoglycaemic agents and, therefore, had been classified as having Type 2 (noninsulin-dep...

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