Abstract

IntroductionAdult-onset autoimmune diabetes (AID) has two different phenotypes: classic type 1 diabetes mellitus (T1DM), with insulin requirement just after diagnosis, and latent autoimmune diabetes in adults (LADA). The purpose of this study is to characterize patients with AID followed on a tertiary centre, comparing classic T1DM and LADA.MethodsWe collected data from patients with diabetes and positive islet autoantibodies, aged 30 years old and over at diagnosis. Patients who started insulin in the first 6 months were classified as T1DM and patients with no insulin requirements in the first 6 months were classified as LADA. Data regarding clinical presentation, autoantibodies, A1C and C-peptide at diagnosis, pharmacologic treatment and complications were analysed.ResultsWe included 92 patients, 46 with classic T1DM and 46 with LADA. The percentage of females was 50% in T1DM group and 52.1% in LADA group. The median age at diagnosis was 38 years (IQR–15) for T1DM and 42 years (IQR–15) for LADA (p = 0.057). The median time between diagnosis of diabetes and diagnosis of autoimmune aetiology was 0 months in T1DM group and 60 months in LADA group (p < 0.001). The mean BMI at diagnosis was 24.1 kg/m2 in T1DM group and 26.1 kg/m2 in LADA group (p = 0.042). In T1DM group, 67.4% of the patients had more than one positive autoantibody, comparing to 41.3% of LADA patients (p = 0.012). There was no statistical difference in what concerns to title of GAD autoantibodies, A1C and C-peptide at diagnosis of autoimmune aetiology. The presence of symptoms at diagnosis was associated with T1DM group (p < 0.001). The median daily insulin dose was 40 IU for T1DM (0.58 IU/kg) and 33.5 IU for LADA (0.57 IU/kg), with no statistical difference. LADA patients were more often under non-insulin antidiabetic drugs (p = 0.001). At 10 years follow up, 21.1% of T1DM patients and 63.3% of LADA patients had microvascular complications (p = 0.004). Diabetic nephropathy was present in 23.5% of T1DM patients and 53.3% of LADA patients (p = 0.047). At the last evaluation, 55.6% of T1DM and 82.6% of LADA patients had metabolic syndrome and this difference was independent of diabetes duration.ConclusionPatients with classic T1DM presented more often with symptoms, lower BMI and higher number of autoantibodies, which may be related to a more aggressive autoimmune process. Patients with LADA developed more frequently microvascular complications for the same disease duration, namely diabetic nephropathy, and had more often metabolic syndrome.

Highlights

  • Adult-onset autoimmune diabetes (AID) has two different phenotypes: classic type 1 diabetes mellitus (T1DM), with insulin requirement just after diagnosis, and latent autoimmune diabetes in adults (LADA)

  • LADA and T1DM share common genetic and immune characteristics, LADA patients seem to match some features of type 2 diabetes (T2DM), like being often overweight/obese, physically inactive and having other criteria for the metabolic syndrome, which leads to insulin resistance [1, 3, 5]

  • We conducted a retrospective cohort study at our tertiary care centre, including patients with diabetes mellitus (DM) and one or more positive diabetes-related autoantibodies—glutamic acid decarboxylase antibodies (GADA), islet cell antibodies (ICA), tyrosine phosphatase-like insulinoma antigen 2 antibodies (IA2) and endogenous insulin antibodies (IAA)—in blood samples analysed between the 1st January 2007 and the 30th June 2017 at our laboratory

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Summary

Introduction

Adult-onset autoimmune diabetes (AID) has two different phenotypes: classic type 1 diabetes mellitus (T1DM), with insulin requirement just after diagnosis, and latent autoimmune diabetes in adults (LADA). LADA and T1DM share common genetic and immune characteristics, LADA patients seem to match some features of type 2 diabetes (T2DM), like being often overweight/obese, physically inactive and having other criteria for the metabolic syndrome, which leads to insulin resistance [1, 3, 5]. Both autoimmunity and insulin resistance play important roles in the pathogenesis of LADA and, depending on the predominant factor, the phenotype will be more T1DM-like or T2DM-like [1, 6]

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