Published online Feb 26, 2023. doi: 10.12998/wjcc.v11.i6.1287
Peer-review started: October 30, 2022
First decision: November 27, 2022
Revised: December 17, 2022
Accepted: February 3, 2023
Article in press: February 3, 2023
Published online: February 26, 2023
Processing time: 117 Days and 3.4 Hours
New onset hyperglycemia is common in patients with severe coronavirus disease 2019 (COVID-19) infection. Cytokine storm and direct severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced pancreatic β-cell failure have been postulated to play a role in new-onset hyperglycemia.
Based on evidence regarding the "Immune-mediated inflammatory storm" during the COVID-19 illness. It has also been proposed that COVID-19 is likely associated with an increased risk of developing diabetes. This motivated us to study the underlying mechanisms contributing to new onset hyperglycemia in hospitalized COVID-19 cases.
To assess the validity of the cytokine-induced hyperglycemia hypothesis by evaluating the association between inflammatory markers and new onset hyperglycemia in non-diabetic patients with COIVD-19 infection.
A retrospective case-control study was conducted on adults without diabetes mellitus hospitalized for COVID-19 infection. The serum levels of glucose and inflammatory markers at presentation before initiation of corticosteroid were collected. Hyperglycemia was defined as glucose levels ≥ 140 mg/dL. Prespecified cutoffs were used for the inflammatory markers. Statistical methods of analysis were used to calculate the logistic regression for hyperglycemia.
Of the 520 patients screened, 248 met the inclusion criteria. Our study showed no association between C-reactive protein, ferritin, Lactate dehydrogenase, D-dimer levels, and new-onset hyperglycemia in non-diabetic patients with COVID-19 infection. We observed significantly higher mortality and length of stay in patients with hyperglycemia.
With new-onset hyperglycemia being closely associated with poor prognostic indices, it becomes pivotal to understand the underlying pathophysiological mechanisms behind the SARS-CoV-2 infection-induced hyperglycemia. This will help us better control the glycemic status and prevent new-onset hyperglycemia, thereby improving the clinical recovery of patients. Our study results indicate the low probability of the stress hyperglycemia hypothesis being the sole mechanism of SARS-CoV-2 infection-induced hyperglycemia but rather a multicausal pathogenesis leading to hyperglycemia that requires further research and understanding.
Basic science research that would help better understand the underlying pathophysiology and further clinical studies that assess the utility of different treatment strategies in managing hyperglycemia are required to improve the clinical outcomes of COVID-19.