Version 2 2022-06-21, 15:49Version 2 2022-06-21, 15:49
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posted on 2022-06-21, 15:49authored byMassimo Pietropaolo, Peter Hotez, Nick Giannoukakis
Pancreatic Angiotensin
Converting Enzyme 2 receptor (ACE2) expression, together with increased
prevalence of insulin-requiring hyperglycemia in COVID-19 patients, suggested
that SARS CoV-2 pancreatic infection might trigger a beta cell-selective inflammation
precipitating autoimmune type 1 diabetes (T1D). We examined T1D incidence in
COVID-19 patients inside a large, global population using a "big data"
approach. The incidence in 0-30 year-old confirmed COVID-19 patients over an
approximately 15 month period from the beginning of the COVID-19 pandemic was
compared to an age-matched non-COVID-19 population inside the TriNetX COVID-19
Research Network (>80 million de-identified patient electronic medical
records globally). The cohorts were used to generate outcomes of T1D
post-index. In ages up to 18, the incidence of insulin-requiring diabetes that
could represent T1D in patients with already-diagnosed, confirmed COVID-19 was statistically-indistinguishable
from the non-COVID-19 control population. In contrast, in ages 19-30, the
incidence was statistically-greater. These data suggest
that the incidence of T1D among COVID-19 patients <30 years of age, at least
up to this time since the beginning of the pandemic, is not greater when
compared to a non-COVID-19 age, sex, and BMI-matched population. Nevertheless, we
caution that COVID-19 patients could be asymptomatic of a diabetic/pre-diabetic
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 beta cell autoimmunity, eventually
progressing to dysglycemia and clinical T1D at higher rates.
Funding
We are greatly thankful to the McNair Medical Institute at The Robert and Janice McNair Foundation for supporting our research on Type 1 diabetes (to Massimo Pietropaolo).