Abstract
Background Novel coronavirus disease 2019 (COVID-19), an acute respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), rapidly progressed to a global pandemic. Currently, there are limited effective medications approved for this deadly disease. Objective To investigate the potential predictors of COVID-19 mortality and risk factors for hyperinflammation in COVID-19. Methods Retrospective analysis was carried out in 1,149 patients diagnosed with COVID-19 in Tongji Hospital, Wuhan, China, from 1/13/2020 to 3/15/2020. Results We found significant differences in the rates of hyperuricemia (OR: 3.17, 95% CI: 2.13-4.70; p < 0.001) and hypoalbuminemia (OR: 5.68, 95% CI: 3.97-8.32; p < 0.001) between deceased and recovered patients. The percentages of hyperuricemia in deceased patients and recovered patients were 23.6% and 8.9%, respectively, which were higher than the reported age-standardized prevalence of 6.2% in Chinese population. Of note, the percentages of both IL-6 and uric acid levels in survived COVID-19 patients were above 90%, suggesting that they might be good specificity for indicators of mortality in COVID-19 patients. The serum level of uric acid (UA) was positively associated with ferritin, TNF-α, and IL-6 but not with anti-inflammatory cytokine IL-10. In addition, the levels of these proinflammatory cytokines in COVID-19 patients showed a trend of reduction after uric acid lowering therapy. Conclusions Our results suggest that uric acid, the end product of purine metabolism, was increased in deceased patients with COVID-19. In addition, the serum level of uric acid was positively associated with inflammatory markers. Uric acid lowering therapy in COVID-19 patients with hyperuricemia may be beneficial.
Highlights
Coronavirus disease 19 (COVID-19) caused by the ribonucleic acid (RNA) virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in Wuhan City, Hubei Province, China, has spread rapidly across the world
Patients who died from COVID-19 had higher hyperinflammation markers than patients who survived: lactate dehydrogenase (LDH, odds ratios (ORs): 25.14, 95% CI: 17.06-37.53; p < 0:0001), AST (OR: 5.08, 95% CI: 3.67-7.05;
The percentages of hyperuricemia in deceased patients and recovered patients were 23.6% and 8.9%, respectively, which are higher than the reported age-standardized prevalence of 6.2% in Chinese population [7]
Summary
Coronavirus disease 19 (COVID-19) caused by the ribonucleic acid (RNA) virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in Wuhan City, Hubei Province, China, has spread rapidly across the world. At the time of drafting this manuscript (Oct. 19, 2020), the worldwide death toll from the COVID-19 pneumonia eclipsed 1,000,000 [1], and the number of people infected continues to slowly climbed upward Predictors such as high-sensitivity C-reactive protein (hsCRP), aspartate aminotransferase (AST), and D-dimer for mortality of COVID-19 patients had been determined [2], more risk predictors and prognostic factors still desperately needed to been found to improve the treatment programs for infected patients, especially for patients with other underlying diseases (such as identified risk factors indicator cardiac troponin I to preexisting concurrent cardiovascular or cerebrovascular diseases [3]; BMI for COVID-19 severity in the population living with diabetes in hospital admission [4]). The levels of these proinflammatory cytokines in COVID-19 patients showed a trend of reduction after uric acid lowering therapy. Our results suggest that uric acid, the end product of purine metabolism, was increased in deceased patients with COVID-19. Uric acid lowering therapy in COVID-19 patients with hyperuricemia may be beneficial
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