Fasting glucose levels and glycemic fluctuations have been found to be independently associated with poor prognosis in adults hospitalized for COVID-19—regardless of diabetes status, shows a study published in Diabetes Care.
Approximately 7-20% of all COVID-19 patients also have diabetes, but even more patients have hyperglycemia likely due to undiagnosed diabetes, a history of poor glucose control, glucocorticoid therapy, and stress hyperglycemia.
In this study, which was a case series of 548 patients treated for COVID-19 at the Central Hospital of Wuhan in China between January 2 and March 23, 2020, researchers suggest that glucose control is “critical for inpatients with and without diabetes to reduce the risk of in-hospital adverse events.”
“To the best of our knowledge, we report for the first time the association between glucose variability and adverse COVID-19 outcomes, which might add to the knowledge of glycemic control strategies for COVID-19 and provide insights for further research,” wrote researchers who were led by Liegang Liu, PhD, and Li Yu of the Huazhong University of Science and Technology in Wuhan.
A previous study reported that hyperglycemia can increase cytokine levels. And, Codo et al. writing in Cell Metabolism last year reported that elevated glucose levels and glycolysis promote SARS-CoV-2 replication and proinflammatory cytokines.
This study included patients between 39-68 years (mean age 57 years). Of all 548 patients, 54% were women, 36% had hypertension, 18% had diabetes, 10% had cardiovascular disease, 7% had cerebrovascular disease, 7% had chronic pulmonary disease, and 6% had chronic kidney disease. By March, 11% of the 548 died.
Stratified by glucose, those with high (>10 mmol/L) blood glucose were older (P <.001), with more comorbidities (all P £.04, except chronic pulmonary disease), and had poorer outcomes including acute respiratory disease syndrome and death (all P <.001) compared with patients who had low (£6.1 mmol/L) blood glucose.
Patients with preexisting diabetes were at increased mortality risk (adjusted hazard ratio [aHR], 1.83; 95% CI, 1.04-3.21; P =.03), as were those with high peak blood glucose (aHR, 1.85; 95% CI, 1.37-2.49) and high average blood glucose (aHR, 1.83; 95% CI, 1.19-2.82).
Positive associations between average blood glucose levels and mortality were observed among men (HR, 3.22; 95% CI, 2.36-4.39), individuals aged ³60 years (HR, 2.99; 95% CI, 2.23-4.02), those treated with glucocorticoids (HR, 3.10; 95% CI, 2.25-4.26), patients with diabetes (HR, 3.03; 95% CI, 1.49-6.18), and without hypertension (HR, 3.84; 95% CI, 2.46-6.01).
Fluctuations of blood glucose were positively associated with mortality among women (HR, 3.42; 95% CI, 1.44-8.11), individuals aged ³60 years (HR, 2.24; 95% CI, 1.37-3.66), those not treated with glucocorticoids (HR, 2.67; 95% CI, 1.38-5.17), and patients without diabetes (HR, 2.18; 95% CI, 1.40-3.41) or hypertension (HR, 1.96; 95% CI, 1.13-3.40).
The authors reported several limitations to the study, including the lack of real-time continuous glucose monitoring and HbA1c was not routinely monitored. Plus, the study was conducted at a single hospital.
Still, the evidence suggests that “maintaining glucose homeostasis has direct and immediate benefits for inpatients with hyperglycemia or diabetes, it is important to evaluate the potential clinical benefits of early effective glucose control for patients infected with SARS-CoV-2. Measurements of admission HbA1c, in-hospital random blood glucose, or postprandial blood glucose may assist blood glucose management and the hypoglycemia strategy. Optimizing medication regimens to attenuate glucose swings is equally important,” the authors wrote.
- Chen L, Sun W, Liu, Y, et al. Association of Early-Phase In-Hospital Glycemic Fluctuation With Mortality in Adult Patients With Coronavirus Disease 2019. Diabetes Care. 2021;dc200780. doi:10.2337/dc20-0780.
- Codo A, Davanzo GG, Monteiro L, et al. “Elevated glucose levels favor SARS-CoV-2 infection and monocyte response through a HIF-1a/glycolysisdependent axis.” Cell Metabolism. 2020;32:437–446. e5