Abstract

Background: Emerging studies have described and analyzed epidemiological, clinical, laboratory, and radiological features of COVID-19 patients. Yet, scarce information is available regarding the association of lipid profile features and disease severity and mortality.Methods: We conducted a prospective observational cohort study to investigate lipid profile features in patients with COVID-19. From 9 February to 4 April 2020, a total of 99 patients (31 critically ill and 20 severely ill) with confirmed COVID-19 were included in the study. Dynamic alterations in lipid profiles were recorded and tracked. Outcomes were followed up until 4 April 2020.Results: We found that high-density lipoprotein-cholesterol (HDL-C) and apolipoprotein A-1 (apoA-1) levels were significantly lower in the severe disease group, with mortality cases showing the lowest levels (p < 0.0001). Furthermore, HDL-C and apoA-1 levels were independently associated with disease severity (apoA-1: odds ratio (OR): 0.651, 95% confidence interval (CI): 0.456–0.929, p = 0.018; HDL-C: OR: 0.643, 95% CI: 0.456–0.906, p = 0.012). For predicting disease severity, the areas under the receiver operating characteristic curves (AUCs) of HDL-C and apoA-1 levels at admission were 0.78 (95% CI, 0.70–0.85) and 0.85 (95% CI, 0.76–0.91), respectively. For in-hospital deaths, HDL-C and apoA-1 levels demonstrated similar discrimination ability, with AUCs of 0.75 (95% CI, 0.61–0.88) and 0.74 (95% CI, 0.61–0.88), respectively. Moreover, patients with lower serum concentrations of apoA-1 (<0.95 g/L) or HDL-C (<0.84 mmol/l) had higher mortality rates during hospitalization (log-rank p < 0.001). Notably, levels of apoA-1 and HDL-C were inversely proportional to disease severity. The survivors of severe cases showed significant recovery of apoA-1 levels at the end of hospitalization (vs. midterm apoA-1 levels, p = 0.02), whereas the mortality cases demonstrated continuously lower apoA-1 levels throughout hospitalization. Correlation analysis revealed that apoA-1 and HDL-C levels were negatively correlated with both admission levels and highest concentrations of C-reactive protein and interleukin-6.Conclusions: Severely ill COVID-19 patients featured low HDL-C and apoA-1 levels, which were strongly correlated with inflammatory states. Thus, low apoA-1 and HDL-C levels may be promising predictors for severe disease and in-hospital mortality in patients suffering from COVID-19.

Highlights

  • As Coronavirus Disease 2019 (COVID-19) continues to spread worldwide, millions of people across hundreds of countries have been impacted

  • Based on multivariate analysis, we found that apolipoprotein A-1 (apoA-1) (OR: 0.651 95% CI: 0.456– 0.929, p = 0.018) and high-density lipoprotein-cholesterol (HDL-C) (OR: 0.643 95% CI: 0.456–0.906, p = 0.012) were still independently associated with severity after adjusting for well-recognized risk factors: i.e., age and albumin, D-dimer, C-reactive protein (CRP), and interleukin6 (IL-6) levels (Table 2)

  • Levels of apoA-1 and HDL-C were inversely proportional to disease severity, with mortality cases showing continuously lower levels across hospitalization (Figures 4E,F)

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Summary

Introduction

As Coronavirus Disease 2019 (COVID-19) continues to spread worldwide, millions of people across hundreds of countries have been impacted. Epidemiological data show that most cases are mild, severely ill patients rapidly progress to acute respiratory disease, multi-organ failure, and septic shock, with a remarkably increased mortality rate. Mounting evidence suggests that an impaired immune function and hyper-inflammatory response are characteristics of COVID-19 severity and mortality [1,2,3]. Systemic inflammation and sepsis are prevalent metabolic disorders accompanying severe COVID-19 [4]. Proteome analysis suggests that patients with severe COVID-19 display dysregulated lipid metabolism [5]. The characteristics and dynamic changes in lipid profiles in COVID19 patients, as well as their predictive value in disease severity and mortality, remain largely unknown. Scarce information is available regarding the association of lipid profile features and disease severity and mortality

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