ABSTRACT
BACKGROUND: COVID-19 rapidly progresses to acute respiratory failure and mortality. A pandemic needs an urgent requirement for low-cost and easy-access tools that assess the infection evolution. The neutrophil-lymphocyte ratio (NLR) is an inflammatory biomarker used in several diseases. AIM: To estimate the association between NLR > 3 with mortality in hospitalized patients with COVID 19. METHODS: NLR was analyzed in patients with COVID-19 seen at Hospital Fernandez between March and August 2020. Patients were grouped in those with NLR < 3 and those with NLR > 3. Clinical characteristics and mortality were analyzed and compared between groups. A multivariable regression model was used to estimate the association between NLR > 3 and mortality. RESULTS: We included 711 patients with COVID-19. In a multivariable regression model, NLR > 3 associated with mortality (OR 3.8; 95% CI 1.05 to 13.7; p 0.04) adjusting by age, days of hospitalization, intensive care requirement, severe pneumonia, C-reactive protein levels, arterial hypertension, and comorbidities. CONCLUSION: NLR was associated with mortality, and it is an accessible and easy tool to use in the first evaluation of hospitalized patients with COVID-19.
Subject(s)
COVID-19 , Argentina/epidemiology , Humans , Lymphocyte Count , Lymphocytes , Neutrophils , Retrospective StudiesABSTRACT
Severe coronavirus disease 2019 (COVID-19) is associated with an overactive inflammatory response mediated by macrophages. Here, we analyzed the phenotype and function of neutrophils in patients with COVID-19. We found that neutrophils from patients with severe COVID-19 express high levels of CD11b and CD66b, spontaneously produce CXCL8 and CCL2, and show a strong association with platelets. Production of CXCL8 correlated with plasma concentrations of lactate dehydrogenase and D-dimer. Whole blood assays revealed that neutrophils from patients with severe COVID-19 show a clear association with immunoglobulin G (IgG) immune complexes. Moreover, we found that sera from patients with severe disease contain high levels of immune complexes and activate neutrophils through a mechanism partially dependent on FcγRII (CD32). Interestingly, when integrated in immune complexes, anti-severe acute respiratory syndrome coronavirus 2 IgG antibodies from patients with severe COVID-19 displayed a higher proinflammatory profile compared with antibodies from patients with mild disease. Our study suggests that IgG immune complexes might promote the acquisition of an inflammatory signature by neutrophils, worsening the course of COVID-19.