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Aim To study the frequency of islet antibodies in a large cohort of clinic- and community-based patients with Type 2 diabetes in northern India. Methods We measured glutamic acid decarboxylase ( GAD) antibodies in 618 adults with Type 2 diabetes (378 patients with diabetes attending a hospital clinic, 240 patients diagnosed in a community survey) and in 192 healthy subjects residing in north India. Islet antigen 2 ( IA2) antibodies were also studied in a proportion of the patients with diabetes ( n = 492) and in a control population ( n = 191). GAD and IA2 antibodies were measured by immunoprecipitation of the respective 35S-labelled recombinant antigen. Results We found that GAD antibodies were present in nine (1.5%) patients with diabetes (clinic population: 0.8%, community study: 2.5%), a prevalence similar to that among the subjects without diabetes ( n = 2; 1%). IA2 antibodies were detected in seven patients with Type 2 diabetes (1.4%) and in two healthy control subjects (1.0%). The frequency of either GAD or IA2 antibodies was similar in people with and without diabetes (3.2 vs 2.1%). No subject was found to have both antibodies. Insulin requirement was higher among antibody-positive than among antibody-negative patients ( GAD antibody: 33 vs 6.3%; P = 0.001; GAD or IA2 antibody: 23.1 vs 6.4%; P = 0.02); however, other clinical features were similar in the two groups. Conclusions In the present north-Indian population with Type 2 diabetes, the overall prevalence of GAD antibodies and the prevalence of either GAD or IA2 antibodies were considerably lower than those reported in white European populations. [ABSTRACT FROM AUTHOR]

Objectives: To study the prevalence and clinical characteristics of islet antibody-negative (idiopathic) type 1 diabetes mellitus (T1DM) among Indian children and adolescents at the time of diagnosis of illness., Methods: In a hospital-based cross-sectional study, we studied 110 patients with T1DM aged ≤18 years. This included 61 patients with duration of diabetes ≤2 weeks (mean ± SD age of onset 9.9 ± 4.4 years) and 49 patients with duration 2 to 12 weeks. Antibodies against GAD65 (GADA), IA-2 (IA-2A) and zinc transporter 8 (ZnT8A), detected by radio-binding assay, were measured in all patients. Insulin autoantibody (IAA) was measured only in subjects with duration ≤2 weeks, using a competitive radio-binding assay., Results: The prevalence of GADA, IA-2A, and ZnT8A was 53%, 34%, and 29% respectively, while IAA (measured in 61 patients) was detected in 31%. All four antibodies were absent in 17 of 61 (28%) patients. The prevalence of islet antibody-negative patients was similar among both sexes and in children with onset younger and older than 10 years. ZnT8A was the only antibody detected in four patients, and its measurement resulted in 6% reduction in islet antibody-negative patients. Patients with idiopathic T1DM did not differ in their clinical features or fasting plasma C-peptide at the onset and after follow-up of 1 year. Compared with idiopathic T1DM, antibody-positive patients had an increased allele frequency of HLA DRB1*0301 (46% vs 14%, OR = 5.10 [confidence interval = 1.61-16.16], P = .003)., Conclusion: Nearly 30% of Indian patients were negative for all islet antibodies at the onset of T1DM. Patients with idiopathic T1DM had similar clinical features to antibody-positive subjects., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Aims: To determine the role of islet autoimmunity in the aetiology of different clinical subtypes of diabetes mellitus in young north Indian patients by measuring islet autoantibodies., Methods: In a cross-sectional study, 145 young patients with diabetes (onset < 30 years) were subdivided into the following categories: Type 1 diabetes (n = 83), malnutrition-modulated diabetes mellitus (MMDM, n = 31) and fibro-calculous pancreatic diabetes (FCPD, n = 31). MMDM subjects presented with emaciation and severe insulin-requiring but ketosis-resistant diabetes, while FCPD was associated with idiopathic chronic calcific pancreatitis. Antibodies to glutamic acid decarboxylase (GADA) and IA-2 (IA-2 A) were detected by immunoprecipitation of 35S-labelled recombinant antigens and cytoplasmic islet cell antibody (ICA) by indirect immunofluorescence., Results: GADA were present in a significant proportion (23%) of patients with MMDM. In contrast, IA-2 A was increased only among patients with Type 1 diabetes (22%), but not MMDM (3%, P < 0.05). Among patients with a duration of diabetes < 2 years, GADA and/or IA-2 A were found in 61% of Type 1 diabetic and 37% of MMDM patients (P < 0.01). MMDM patients who were positive for GADA had a shorter duration of diabetes, but did not differ in their age at onset of diabetes, body mass index, fasting plasma C-peptide, or frequency of thyroid microsomal and parietal cell antibodies. FCPD subjects had the lowest prevalence of autoantibodies: IA-2 and ICA were absent, while GADA were present in 7% (P < 0.05 vs. Type 1 diabetes)., Conclusions: GADA, though not IA-2 A, were present in a substantial proportion of patients with the MMDM variant of diabetes, suggesting that islet autoimmunity may play a role in its pathogenesis. In contrast, none of the islet antibodies was increased in subjects with FCPD, making it likely that it is a secondary type of diabetes.

The etiology of malnutrition-related diabetes mellitus (MRDM)--protein-deficient pancreatic diabetes (PDPD) and fibro-calculous pancreatic diabetes (FCPD)-is unclear. We studied the role of autoimmunity against pancreatic islet cells in the etiology of these two subtypes of MRDM by measuring islet-cell antibodies (ICA) in 23 patients with PDPD, 25 with FCPD and 62 with Type 1 diabetes. Three patients (13%) with PDPD had detectable ICA. Including a patient with a high titre of ICA (> 80 JDF units). The frequency of ICA in patients with PDPD was significantly lower than subjects with Type 1 diabetes (22/62, 35%; P < 0.05). Among patients studied at onset. ICA prevalence was lower in the PDPD patients (1/7, 14%) compared to subjects with Type 1 diabetes (8/20, 40%). No patient of FCPD had detectable ICA (P < 0.001 vs. Type 1 diabetes subjects). We conclude that autoimmunity may play a role in the etiology of some patients with the PDPD subtype of MRDM. However, FCPD is unlikely to have an autoimmune etiology.