Abstract
Type 1 diabetes mellitus is heterogeneous in many facets. The patients suffered from type 1 diabetes present several levels of islet function as well as variable number and type of islet-specific autoantibodies. This study was to investigate prevalence and heterogeneity of the islet autoantibodies and clinical phenotypes of type 1 diabetes mellitus; and also discussed the process of islet failure and its risk factors in Chinese type 1 diabetic patients. A total of 1,291 type 1 diabetic patients were enrolled in this study. Demographic information was collected. Laboratory tests including mixed-meal tolerance test, human leukocyte antigen alleles, hemoglobinA1c, lipids, thyroid function and islet autoantibodies were conducted. The frequency of islet-specific autoantibody in newly diagnosed T1DM patients (duration shorter than half year) was 73% in East China. According to binary logistic regressions, autoantibody positivity, longer duration and lower Body Mass Index were the risk factors of islet failure. As the disease developed, autoantibodies against glutamic acid decarboxylase declined as well as the other two autoantibodies against zinc transporter 8 and islet antigen 2. The decrease of autoantibodies was positively correlated with aggressive beta cell destruction. Autoantibodies can facilitate the identification of classic T1DM from other subtypes and predict the progression of islet failure. As there were obvious heterogeneity in autoantibodies and clinical manifestation in different phenotypes of the disease, we should take more factors into consideration when identifying type 1 diabetes mellitus.
Highlights
Type 1 diabetes mellitus (T1DM) is a T-cell-mediated autoimmune disease in which insulin-producing beta cells in pancreatic islets of Langerhans are selectively destroyed, leading to insulin deficiency and dysregulation of glucose metabolism (Atkinson and Maclaren, 1994; Eisenbarth, 1986; Gillespie, 2006; Zhang et al, 2008)
It is estimated that 30%–50% of the genetic risk for type 1 diabetes can be attributed to the human leukocyte antigen alleles (HLA) region (Noble et al, 1996)
Islet function and islet-specific autoantibody positivity declined faster in classic T1DM compared with latent autoimmune diabetes of adult (LADA) patients
Summary
Type 1 diabetes mellitus (T1DM) is a T-cell-mediated autoimmune disease in which insulin-producing beta cells in pancreatic islets of Langerhans are selectively destroyed, leading to insulin deficiency and dysregulation of glucose metabolism (Atkinson and Maclaren, 1994; Eisenbarth, 1986; Gillespie, 2006; Zhang et al, 2008). The strongest genetic association for type 1 diabetes is HLA class II genes, while HLA class I alleles influence susceptibility to T1DM and humoral autoimmunity. The identification and study of these autoantibodies associated with T1DM (Baekkeskov et al, 1990; Bonifacio et al, 1995; Bottazzo et al, 1974; Palmer et al, 1983; Wenzlau et al, 2007) have emphasized their roles as biomarkers in diagnosis (Wasserfall and Atkinson, 2006), prognosis, patient treatment stratification (Christie et al, 2002; Hagopian et al, 2011), tolerating therapies as well as providing insights into pathophysiology of the disease (Ludvigsson et al, 2008). With highly sensitive laboratory assays, the autoantibodies positivity among European T1DM patients at diagnosis was nearly 98% (Wenzlau et al, 2007). It might due to the unsensitive or unspecific assays, or testing far from diagnosis as antibody titers diminish, yet-to-beidentified auto-antigens, or foremost heterogeneity of islet autoantibodies in Chinese population (Lu et al, 2012; Wang et al, 2007; Zhou et al, 2013)
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