Low-density lipoprotein cholesterol levels are associated with poor clinical outcomes in COVID-19

STRUCTURED ABSTRACTO_ST_ABSBackgroundC_ST_ABSSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the sole causative agent of coronavirus infectious disease-19 (COVID-19). MethodsWe performed a retrospective single-center study of consecutively admitted patients between March 1st and May 15th, 2020, with a definitive diagnosis of SARS-CoV-2 infection. The primary end-point was to evaluate the association of lipid markers with 30-days all-cause mortality in COVID-19. ResultsA total of 654 patients were enrolled, with an estimated 30-day mortality of 22.8% (149 patients). Non-survivors had lower total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-c) levels during the entire course of the disease with complete resolution among survivors. Both showed a significant inverse correlation with inflammatory markers and a positive correlation with lymphocyte count. In a multivariate analysis, LDL-c [≤] 69 mg/dl (hazard ratio [HR] 1.94; 95% confidence interval [CI] 1.14-3.31), C-reactive protein > 88 mg/dl (HR 2.44; 95% CI, 1.41-4.23) and lymphopenia < 1,000 (HR 2.68; 95% CI, 1.91-3.78) at admission were independently associated with 30-day mortality. This association was maintained 7 days after admission. ConclusionHypolipidemia in SARS-CoV-2 infection may be secondary to an immune-inflammatory response, with complete recovery in survivors. Low LDL-c serum levels are independently associated with higher 30-day mortality in COVID-19 patients.

Corticosteroid pulses for hospitalized patients with COVID-19. Effects on mortality and in-hospital stay.

Background: COVID-19 has high mortality in hospitalized patients, and we need effective treatments. Our objective was to assess corticosteroid pulses influence on 60-days mortality in hospitalized patients with severe COVID-19, intensive care admission, and hospital stay. Methods: We designed a multicenter retrospective cohort study in three teaching hospitals of Castilla y Leon, Spain (865.096 people). We selected patients with confirmed COVID-19 and lung involvement with a pO2/FiO2 < 300, excluding those exposed to immunosuppressors before or during hospitalization, patients terminally ill at admission, or died the first 24 hours. We performed a propensity score matching (PSM) adjusting covariates that modify the probability of being treated. Then we used a Cox regression model in the PSM group to consider factors affecting mortality. Findings: From 2933 patients, 257 fulfilled the inclusion and exclusion criteria. One hundred and twenty-four patients were on corticosteroid pulses, and 133 were not. 30{middle dot}3% (37/122) of patients died in the corticosteroid pulses group and 42{middle dot}9% (57/133) in the non-exposed cohort. These differences (12{middle dot}6% CI95% [8{middle dot}54-16{middle dot}65]) were statically significant (log-rank 4{middle dot}72, p=0{middle dot}03). We performed PSM using the exact method. Mortality differences remained in the PSM group (log-rank 5{middle dot}31, p=0{middle dot}021) and were still significant after a Cox regression model (HR for corticosteroid pulses 0{middle dot}561, p= 0{middle dot}039). There were no significant differences in intensive care admission rate (p=0{middle dot}173). The hospital stay was longer in the corticosteroid group (p<0,001). Interpretation: This study provides evidence about treatment with corticosteroid pulses in severe COVID-19 that might significantly reduce mortality. Strict inclusion and exclusion criteria with that selection process set a reliable frame to compare mortality in both exposed and non-exposed groups. Funding: There was no funding provided.