Diabetes Research Center, Section of Endocrinology, Diabetes, and Metabolism, Baylor College of Medicine, Houston, TX.
Texas Children's Hospital Center for Vaccine Development, Departments of Pediatrics and Molecular Virology and Microbiology, National School of Tropical Medicine, Baylor College of Medicine, Houston, TX.
Diabetes. 2022 Dec 1;71(12):2656-2663. doi: 10.2337/db21-0831.
Pancreatic ACE2 receptor expression, together with increased prevalence of insulin-requiring hyperglycemia in patients with coronavirus disease 2019 (COVID-19), suggested that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pancreatic infection might trigger a β-cell-selective inflammation precipitating autoimmune type 1 diabetes (T1D). We examined T1D incidence in patients with COVID-19 inside a large, global population using a "big data" approach. The incidence in 0-30-year-old patients with confirmed COVID-19 over an ∼15-month period from the beginning of the COVID-19 pandemic was compared with an age-matched population without COVID-19 inside the TriNetX COVID-19 Research Network (>80 million deidentified patient electronic medical records globally). The cohorts were used to generate outcomes of T1D postindex. In those up to 18 years of age, the incidence of insulin-requiring diabetes that could represent T1D in patients with already diagnosed, confirmed COVID-19 was statistically indistinguishable from the control population without COVID-19. In contrast, in those aged 19-30 years, the incidence was statistically greater. These data suggest that the incidence of T1D among patients with COVID-19 <30 years of age, at least up to this time since the beginning of the pandemic, is not greater when compared with an age-, sex-, and BMI-matched population without COVID-19. Nevertheless, we caution that patients with COVID-19 could be asymptomatic of a diabetic/prediabetic state and therefore would not be expected to come to medical attention, remaining undiagnosed. Hence, it is still possible that asymptomatic virus-infected individuals could acquire β-cell autoimmunity, eventually progressing to dysglycemia and clinical T1D at higher rates.
胰腺 ACE2 受体的表达,以及 COVID-19 患者中胰岛素需求性高血糖的高发,表明严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)胰腺感染可能引发β细胞选择性炎症,促使自身免疫性 1 型糖尿病(T1D)发生。我们采用“大数据”方法,在一个大型全球人群中研究 COVID-19 患者的 T1D 发病率。将 COVID-19 确诊患者 0-30 岁人群在 COVID-19 大流行开始后约 15 个月内的确诊 COVID-19 患者与 TriNetX COVID-19 研究网络(全球 8000 多万份匿名患者电子病历)中年龄匹配无 COVID-19 的人群进行比较。这些队列用于生成索引后 T1D 的结局。在 18 岁以下人群中,已经确诊 COVID-19 的患者中需要胰岛素的糖尿病发病率(可能代表 T1D)与无 COVID-19 的对照组人群无统计学差异。相比之下,19-30 岁年龄组的发病率统计学上更高。这些数据表明,至少在 COVID-19 大流行开始至今的这段时间内,30 岁以下 COVID-19 患者的 T1D 发病率与无 COVID-19 的年龄、性别和 BMI 匹配人群相比并不更高。然而,我们提醒,COVID-19 患者可能无症状糖尿病/糖尿病前期状态,因此预计不会引起医疗关注,从而未被诊断。因此,无症状病毒感染个体仍有可能获得β细胞自身免疫,最终以更高的比例进展为血糖异常和临床 T1D。