Acceleration of type 1 diabetes onset during the COVID-19 pandemic.

Authors

Andrew Kanouse, Michael McDonagh, Joanna S Fishbein, Parissa Salemi

Published in

Frontiers in endocrinology. Volume 17. Pages 1841034. Epub Jul 31, 2026.

Abstract

Studies since the beginning of the COVID-19 pandemic suggest an increase in new cases of type 1 diabetes (T1D) but the etiology of this increase remains unclear.
To examine whether there was a change in yearly proportions of newly diagnosed T1D by a single-center tertiary pediatric endocrinology practice in the post-pandemic era in comparison to pre-pandemic, T1D presenting characteristics, and the relationship of T1D antibodies both in those diagnosed before the pandemic versus those diagnosed after and those with COVID-19 versus other or no known respiratory viral illnesses.
The study consisted of a retrospective chart review of children diagnosed with T1D between January 2018 and May 2022, stratifying them into cohorts based on respiratory infection status: known COVID-19 respiratory infection (COVID), other upper respiratory infection (URI), and no known viral respiratory infection (NONE). There was comparison of autoantibody positivity (type, number, and titer) between cohorts using non-parametric tests and descriptive statistics.
A total of 351 patients were included (mean age 9.8 ± 4.2 years; 59.4% male; 48.4% White, 18.2% African American, 8.3% Asian, 15.4% Hispanic/Latino, 24.8% other). At diagnosis, mean hemoglobin A1c (HbA1c) was 11.5 ± 2.3%. Overall T1D rates did not differ significantly between pre-pandemic (n=162, 46%) and post-pandemic (n=189, 54%) eras but new cases fluctuated significantly by year (p = 0.001). New annual cases peaked in 2020 (2.4%), representing a statistically significant increase from 2019 (1.4%, p = 0.0005) and a subsequent significant decline by 2022 (1.1%, p = 0.0006). Patients were stratified by infection history within 2 months of diagnosis: COVID (n=23, 6.6%), URI (n=53, 15.1%), and NONE (n=275, 78.4%). No significant differences were observed between these groups regarding body mass index, HbA1c, or diabetic ketoacidosis (DKA) severity. Among those with antibody data (n=236), positivity rates were 72.5% for zinc transporter antibody, 80.0% for glutamic acid decarboxylase, 51.5% for islet cell antibody, and 47.3% for islet antigen 2 antibody. There were no statistically significant differences in antibody titers or the number of positive antibodies between the disease cohorts or pre- and post-pandemic cohorts.
These findings suggest that the COVID-19 pandemic may have accelerated disease progression in predisposed individuals rather than inducing T1D through COVID-19-mediated autoimmunity.

PMID:
42601853
Bibliographic data and abstract were imported from PubMed on 15 Aug 2026.

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