Associations of body weight and COVID-19 with autoimmunity in pediatric new-onset type 1 diabetes: results from the prospective DPV registry

儿童新发1型糖尿病患者体重和COVID-19与自身免疫的关联:来自前瞻性DPV注册研究的结果

阅读:2

Abstract

INTRODUCTION: This study analyzed the effects of the COVID-19 pandemic and body weight on islet and endocrine autoimmunity in children with type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS: Data from 11 973 children and adolescents aged 0.5 to <18 years with new-onset T1D (2015-2023) from the Diabetes Prospective Follow-up Registry were evaluated. Rates of autoantibodies against beta cells (islet antigen 2 (IA2), zinc transporter 8 (ZnT8), glutamic acid decarboxylase (GAD), insulin), thyroid, transglutaminase (TGA), and adrenals were assessed. Logistic regression models adjusted for age and sex examined associations with COVID-19 and body mass index (BMI). RESULTS: 6136 (51%) children were diagnosed with T1D before, and 5837 (49%) after the beginning of the COVID-19 pandemic. Beta-cell autoantibodies were present in 94.3%, thyroid autoantibodies in 7.7%, TGA autoantibodies in 8.3%, and adrenal autoantibodies in 5.6%. During versus before COVID-19, IA2 and GAD autoantibody positivity significantly increased (63.3% vs 60.5%, p=0.002, and 65.9% vs 64.0%, p=0.04, respectively), ZnT8 autoantibodies declined (68.0% vs 71.9%, p=0.002), while insulin autoantibodies remained unchanged (p=0.06). Prevalence of IA2, ZnT8, and insulin, but not GAD autoantibodies, showed positive associations with BMI. Thyroid and TGA autoantibodies were not related, while adrenal autoantibodies were negatively related to the pandemic. CONCLUSIONS: The COVID-19 pandemic and body weight influenced autoimmunity in children with T1D. The rise in IA2 autoantibody positivity may suggest a faster progression from pre-existing autoimmunity to clinical disease. The pandemic did not appear to trigger associated endocrine autoimmunity.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。