Pediatric patients aged 10 to 19 diagnosed with COVID-19 have a higher risk of developing type 2 diabetes within six months compared to those diagnosed with other respiratory infections, according to researchers at Case Western Reserve University School of Medicine.
The research follows an analysis of metadata showing an increased risk of type 2 diabetes in adults. The meta-analysis found a 66% higher average risk of developing diabetes after SARS-CoV-2 infection in adults. In the current retrospective study, “SARS-CoV-2 infection and new-onset type 2 diabetes in pediatric patients, 2020 to 2022,” published in Open JAMA Networkthe researchers looked to see if a similar pattern existed in children.
The study analyzed a cohort of 613,602 pediatric patients aged 10 to 19 years. After propensity score matching, this cohort was divided equally into two groups: 306,801 patients diagnosed with COVID-19 and 306,801 patients diagnosed with other respiratory infections (ORI).
A subset of the cohort with obesity and COVID or ORI was also analyzed, with two groups of 16,469 patients.
The research compared the incidence of new diagnoses of type 2 diabetes one, three and six months after the initial respiratory infection. The relative risks (RR) of developing type 2 diabetes after COVID-19 were found to be significantly higher than for people with ORI.
Specifically, the RR was 1.55 (95% CI: 1.28 to 1.89) at one month, 1.48 (95% CI: 1.24 to 1.76) at three months and 1.58 (95% CI: 1.35 to 1.85) at six months after infection. .
Analyzes of smaller subgroups revealed even higher risks among children classified as overweight, with RRs of 2.07 at one month, 2.00 at three months, and 2.27 at six months. Hospitalized patients also showed increased risks, with RRs of 3.10 at one month, 2.74 at three months, and 2.62 at six months after COVID-19 diagnosis.
The study concluded that SARS-CoV-2 infection is associated with a higher incidence of type 2 diabetes diagnoses in children than in those with other respiratory infections. More research is needed to determine whether diabetes persists or is a recoverable disease that reverses itself later in life.
Although COVID-19 may seem like an unintuitive cause of type 2 diabetes, we do not currently understand what triggers this disease. It is often linked to being overweight, being less active, eating processed foods, or having a family history of type 2 diabetes, indicating both an environmental and possibly genetic basis.
Insulin resistance is the main effect of type 2 diabetes on the body. Insulin is a hormone made in the pancreas that is essential for removing glucose from the blood by binding it to receptor sites on cells, where the glucose is absorbed and used as energy to power the cell.
Insulin resistance, at the physiological level, generally means that the availability of binding sites in cells is downregulated. This resistance can occur if the cells have received too much insulin. Downregulation of binding sites leaves more unbound glucose in the bloodstream, which the brain interprets as needing the pancreas to produce more insulin. This negative feedback loop often causes the disease to progress.
The current retrospective analysis can only see past correlations between COVID-19 and the cohort studied and cannot identify causality. Future research will be needed to determine whether COVID-19 directly interferes with any of the systems related to glucose sensing and insulin regulation by the brain, insulin production in the pancreas, or cell binding capacity.
More information:
Margaret G. Miller et al, SARS-CoV-2 infection and new-onset type 2 diabetes in pediatric patients, 2020 to 2022, Open JAMA Network (2024). DOI: 10.1001/jamanetworkopen.2024.39444
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