Eosinopenia is associated with greater severity in patients with coronavirus disease 2019

Zhao, Lei; Zhang, Ye-Ping; Yang, Xinchun; Liu, Xin

doi:10.1111/all.14455

Cited by 43 publications

(53 citation statements)

References 10 publications

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“…Comparison of the dynamic profile of laboratory findings in severe patients revealed a sustained increase in leukocyte count, neutrophil count, biological markers, as well as continued decrease in platelet count, lymphopenia and eosinopenia in these patients. As previously reported, eosinopenia may be an indicator for SARS‐CoV‐2 infection, 14 and the degree of eosinopenia was associated with the severity of COVID‐19 34,35 . Persistent eosinopenia may be a predictor of disease severity and adverse clinical outcome during hospitalization, which is consistent with the results reported by Xie et al 34 The anti‐viral effect exhausts eosinophils and may be the cause of eosinopenia in COVID‐19 patients 36 .…”

Section: Discussionsupporting

confidence: 87%

Clinical, radiological, and laboratory characteristics and risk factors for severity and mortality of 289 hospitalized COVID‐19 patients

Zhang

Cao

Tan

et al. 2020

Allergy

186

136

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Background The coronavirus disease 2019 (COVID‐19) has become a global pandemic, with 10‐20% of severe cases and over 508,000 deaths worldwide. Objective This study aims to address the risk factors associated with the severity of COVID‐19 patients and the mortality of severe patients. Methods 289 hospitalized laboratory‐confirmed COVID‐19 patients were included in this study. Electronic medical records, including patient demographics, clinical manifestation, comorbidities, laboratory tests results, and radiological materials were collected and analyzed. According to the severity and outcomes of the patients, they were divided into three groups: non‐survived (n=49), survived severe (n=78), and non‐severe (n=162) groups. Clinical, laboratory and radiological data were compared among these groups. Principal component analysis (PCA) was applied to reduce the dimensionality and visualize the patients on a low‐dimensional space. Correlations between clinical, radiological and laboratory parameters were investigated. Univariate and multivariate logistic regression methods were used to determine the risk factors associated with mortality in severe patients. Longitudinal changes of laboratory findings of survived severe cases and non‐survived cases during hospital stay were also collected. Results Of the 289 patients, the median age was 57 years (range, 22 ‐ 88) and 155 (53.4%) patients were male. As of the final follow‐up date of this study, 240 (83.0%) patients were discharged from the hospital and 49 (17.0%) patients died. Elder age, underlying comorbidities, and increased laboratory variables, such as leucocyte count, neutrophil count, neutrophil‐to‐lymphocyte ratio (NLR), C‐reactive protein (CRP), procalcitonin (PCT), D‐dimer, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and blood urea nitrogen (BUN) on admission were found in survived severe cases compared to non‐severe cases. According to the multivariate logistic regression analysis, elder age, a higher number of affected lobes, elevated CRP levels on admission, increased prevalence of chest tightness/dyspnea and smoking history were independent risk factors for death of severe patients. A trajectory in PCA was observed from "non‐severe" towards "non‐survived" via "severe and survived" patients. Strong correlations between the age of patients, the affected lobe numbers and laboratory variables were identified. Dynamic changes of laboratory findings of survived severe cases and non‐survived cases during hospital stay showed that continuing increase of leucocytes and neutrophil count, sustained lymphopenia and eosinopenia, progressing decrease in platelet count, as well as high levels of NLR, CRP, PCT, AST, BUN, and serum creatinine were associated with in‐hospital death. Conclusions Survived severe and non‐survived COVID‐19 patients had distinct clinical and laboratory characteristics, which we...

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Section: Discussionsupporting

confidence: 87%

Clinical, radiological, and laboratory characteristics and risk factors for severity and mortality of 289 hospitalized COVID‐19 patients

Zhang

Cao

Tan

et al. 2020

Allergy

186

136

View full text Add to dashboard Cite

show abstract

“…Besides, it is thought that eosinophil exhaustion is associated with neutralization of virus by eosinophil-derived enzymes and that the intereleukin-33 (IL-33) pathway is affected by the virus. IL- 33 is responsible for eosinophil activation in the airways and bone marrow and ciliated epithelial cells, as the first target of coronavirus, are IL-33 positive epithelial cells (18).…”

Section: Discussionmentioning

confidence: 99%

The Impact of Peripheral Eosinophil Counts and Eosinophil to Lymphocyte Ratio (ELR) in the Clinical Course of COVID-19 Patients: A Retrospective Study

Georgakopoulou

Garmpis

Damaskos

et al. 2021

In Vivo

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“…In fatal cases of COVID-19, blood eosinophil counts were consistently reduced at hospital admittance 50 , whereas autopsies revealed an absence of eosinophils in lung specimens 51 . In addition, a low blood eosinophil count was identified as a risk factor (odds ratio = 10.2) for severe progression of COVID-19 52 , whereas the progressive increase of blood eosinophils was associated with disease recovery 24 . Recent studies have challenged the classic concept of eosinophil roles being restricted to helminthic parasitosis and allergic diseases 53 .…”

Section: Discussionmentioning

confidence: 98%

Pharmacological inhibition of the kinin-kallikrein system in severe COVID-19 – A proof-of-concept study

Mansour

Palma

Ulaf

et al. 2020

Preprint

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Coronavirus disease-19 (COVID-19) can develop into a severe respiratory syndrome that results in up to 40% mortality. Acute lung inflammatory edema is a major pathological finding in autopsies explaining O2 diffusion failure and hypoxemia. Only dexamethasone has been shown to reduce mortality in severe cases, further supporting a role for inflammation in disease severity. SARS-CoV-2 enters cells employing angiotensin converting enzyme 2 (ACE2) as a receptor, which is highly expressed in lung alveolar cells. ACE2 is one of the components of the cellular machinery that inactivates the potent inflammatory agent bradykinin, and SARS-CoV-2 infection could interfere with the catalytic activity of ACE2, leading to accumulation of bradykinin. In this open-label, randomized clinical trial, we tested two pharmacological inhibitors of the kinin-kallikrein system that are currently approved for the treatment of hereditary angioedema, icatibant and inhibitor of C1 esterase/kallikrein, in a group of 30 patients with severe COVID-19. Neither icatibant nor inhibitor of C1 esterase/kallikrein resulted in significant changes in disease mortality and time to clinical improvement. However, both compounds promoted significant improvement of lung computed tomography scores and increased blood eosinophils, which has been reported as an indicator of disease recovery. In this small cohort, we found evidence for a beneficial role of pharmacological inhibition of the kinin-kallikrein system in two markers that indicate improved disease recovery.

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Eosinopenia is associated with greater severity in patients with coronavirus disease 2019

Cited by 43 publications

References 10 publications

Clinical, radiological, and laboratory characteristics and risk factors for severity and mortality of 289 hospitalized COVID‐19 patients

Clinical, radiological, and laboratory characteristics and risk factors for severity and mortality of 289 hospitalized COVID‐19 patients

The Impact of Peripheral Eosinophil Counts and Eosinophil to Lymphocyte Ratio (ELR) in the Clinical Course of COVID-19 Patients: A Retrospective Study

Pharmacological inhibition of the kinin-kallikrein system in severe COVID-19 – A proof-of-concept study

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