Abstract

BackgroundBasic studies suggest that statins as add-on therapy may benefit patients with COVID-19; however, real-world evidence of such a beneficial association is lacking.ObjectiveWe investigated differences in SARS-CoV-2 test positivity and clinical outcomes of COVID-19 (composite endpoint: admission to intensive care unit, invasive ventilation, or death) between statin users and nonusers.MethodsTwo independent population-based cohorts were analyzed, and we investigated the differences in SARS-CoV-2 test positivity and severe clinical outcomes of COVID-19, such as admission to the intensive care unit, invasive ventilation, or death, between statin users and nonusers. One group comprised an unmatched cohort of 214,207 patients who underwent SARS-CoV-2 testing from the Global Research Collaboration Project (GRCP)-COVID cohort, and the other group comprised an unmatched cohort of 74,866 patients who underwent SARS-CoV-2 testing from the National Health Insurance Service (NHIS)-COVID cohort.ResultsThe GRCP-COVID cohort with propensity score matching had 29,701 statin users and 29,701 matched nonusers. The SARS-CoV-2 test positivity rate was not associated with statin use (statin users, 2.82% [837/29,701]; nonusers, 2.65% [787/29,701]; adjusted relative risk [aRR] 0.97; 95% CI 0.88-1.07). Among patients with confirmed COVID-19 in the GRCP-COVID cohort, 804 were statin users and 1573 were matched nonusers. Statin users were associated with a decreased likelihood of severe clinical outcomes (statin users, 3.98% [32/804]; nonusers, 5.40% [85/1573]; aRR 0.62; 95% CI 0.41-0.91) and length of hospital stay (statin users, 23.8 days; nonusers, 26.3 days; adjusted mean difference –2.87; 95% CI –5.68 to –0.93) than nonusers. The results of the NHIS-COVID cohort were similar to the primary results of the GRCP-COVID cohort.ConclusionsOur findings indicate that prior statin use is related to a decreased risk of worsening clinical outcomes of COVID-19 and length of hospital stay but not to that of SARS-CoV-2 infection.

Highlights

  • COVID-19 is caused by SARS-CoV-2, and started in Wuhan, China

  • After propensity score matching among patients who underwent SARS-CoV-2 testing, we found there were no major imbalances in the baseline covariates between the 2 groups assessed by standardized mean differences (SMDs) (Table 2; SMD all

  • After propensity score matching among patients who tested positive for SARS-CoV-2, we found there were no major imbalances in the baseline covariates between the 2 groups assessed by SMD (Table 3; SMD all

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Summary

Introduction

COVID-19 is caused by SARS-CoV-2, and started in Wuhan, China. The World Health Organization (WHO) declared COVID-19 a pandemic on March 12, 2020 [1,2]. During the period from January 1, 2020, to May 31, 2020, the number of daily confirmed COVID-19 cases was less than 2000 and the cumulative number of COVID-19 cases was 11,468 with 270 deaths [3,4] During this pandemic phase, efficient strategies for triage and therapeutics are crucial due to the high number of patients with SARS-CoV-2 infection, and the relatively limited facilities and medical resources [1,2]. Previous studies have suggested potential therapeutic candidates, including antimalarial drugs [5], antivirals such as lopinavir and ritonavir in combination [6], remdesivir [7], previous bacillus Calmette–Guérin (BCG) vaccination [8], famotidine [9], and immunoglobulin-containing sera from convalescent patients with COVID-19 [10]. Basic studies suggest that statins as add-on therapy may benefit patients with COVID-19; real-world evidence of such a beneficial association is lacking

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