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      Red Blood Cell Distribution Is a Significant Predictor of Severe Illness in Coronavirus Disease 2019

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          Abstract

          Introduction

          As red blood cell distribution width (RDW) significantly predicts clinical outcomes in patients with respiratory tract infections and in those with critical illnesses, we performed a critical analysis of the literature to explore the potential prognostic role of this laboratory parameter in coronavirus disease 2019 (COVID-19).

          Methods

          An electronic search was conducted in Medline, Scopus and Web of Science, using the keywords “coronavirus disease 2019” OR “COVID-19” AND “red blood cell distribution width” OR “RDW” in all fields, up to the present time, with no language restriction. Studies reporting the value of RDW-CV in CO­VID-19 patients with or without severe illness were included in a pooled analysis.

          Results

          The pooled analysis included 3 studies, totaling 11,445 COVID-19 patients' samples (2,654 with severe disease; 23.2%). In all investigations RDW-CV was higher in COVID-19 patients with severe illness than in those with mild disease, with differences between 0.30 and 0.70%. The pooled analysis, despite consistent heterogeneity ( I 2: 88%), revealed that the absolute RDW-CV value was 0.69% higher (95% CI 0.40–0.98%; p < 0.001) in COVID-19 patients with severe illness compared to those with mild disease.

          Conclusion

          These results, along with data published in other studies, support the use of RDW for assessing the risk of unfavorable COVID-19 progression.

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          Most cited references 23

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          Red blood cell distribution width and mortality risk in a community-based prospective cohort.

          Red blood cell distribution width (RDW), an automated measure of red blood cell size heterogeneity (eg, anisocytosis) that is largely overlooked, is a newly recognized risk marker in patients with established cardiovascular disease (CVD). It is unknown whether RDW is associated with mortality in the general population or whether this association is specific to CVD. We examined the association of RDW with all-cause mortality and with CVD, cancer, and chronic lower respiratory tract disease mortality in 15 852 adult participants in the Third National Health and Nutrition Examination Survey (1988-1994), a nationally representative sample of the US population. Mortality status was obtained by matching to the National Death Index, with follow-up through December 31, 2000. Estimated mortality rates increased 5-fold from the lowest to the highest quintile of RDW after accounting for age and 2-fold after multivariable adjustment (P(trend) < .001 for each). A 1-SD increment in RDW (0.98%) was associated with a 23% greater risk of all-cause mortality (hazard ratio [HR], 1.23; 95% confidence interval [CI], 1.18-1.28) after multivariable adjustment. The RDW was also associated with risk of death due to CVD (HR, 1.22; 95% CI, 1.14-1.31), cancer (1.28; 1.21-1.36), and chronic lower respiratory tract disease (1.32; 1.17-1.49). Higher RDW is associated with increased mortality risk in this large, community-based sample, an association not specific to CVD. Study of anisocytosis may, therefore, yield novel pathophysiologic insights, and measurement of RDW may contribute to risk assessment.
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            Red cell distribution width and all-cause mortality in critically ill patients.

            Red cell distribution width is a predictor of mortality in the general population. The prevalence of increased red cell distribution width and its significance in the intensive care unit are unknown. The objective of this study was to investigate the association between red cell distribution width at the initiation of critical care and all cause mortality. Multicenter observational study. Two tertiary academic hospitals in Boston, MA. A total of 51,413 patients, aged ≥ 18 yrs, who received critical care between 1997 and 2007. None. The exposure of interest was red cell distribution width as a predictor of mortality in the general population. The prevalence of increased red cell distribution width and its significance in the intensive care unit are unknown and categorized a priori in quintiles as ≤ 13.3%, 13.3% to 14.0%, 14.0% to 14.7%, 14.7% to 15.8%, and >15.8%. Logistic regression examined death by days 30, 90, and 365 postcritical care initiation, inhospital mortality, and bloodstream infection. Adjusted odds ratios were estimated by multivariable logistic regression models. Adjustment included age, sex, race, Deyo-Charlson index, coronary artery bypass grafting, myocardial infarction, congestive heart failure, hematocrit, white blood cell count, mean corpuscular volume, blood urea nitrogen, red blood cell transfusion, sepsis, and creatinine. Red cell distribution width was a particularly strong predictor of all-cause mortality 30 days after critical care initiation with a significant risk gradient across red cell distribution width quintiles after multivariable adjustment: red cell distribution width 13.3% to 14.0% (odds ratio [OR], 1.19; 95% confidence interval [CI], 1.08-1.30; p 15.8% (OR, 2.61; 95% CI, 2.37-2.86; p 15.8% quintiles, respectively, compared with those with red cell distribution width ≤ 13.3%. Estimating the receiver operating characteristic area under the curve shows that red cell distribution width has moderate discriminative power for 30-day mortality (area under the curve = 0.67). Red cell distribution width is a robust predictor of the risk of all-cause patient mortality and bloodstream infection in the critically ill. Red cell distribution width is commonly measured, inexpensive, and widely available and may reflect overall inflammation, oxidative stress, or arterial underfilling in the critically ill.
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              Hematological findings in SARS patients and possible mechanisms (review).

              Severe acute respiratory syndrome (SARS) is a new human infectious disease. The causative agent of SARS is a novel coronavirus (SARS-CoV). This report summarizes the hematological findings in SARS patients and proposes the possible mechanisms of SARS-CoV related abnormal hematopoiesis. Hematological changes in patients with SARS are common and include lymphopenia, thrombocytopenia and occasionally leukopenia. A significant decrease was also observed in peripheral CD4+ and CD8+ T lymphocyte subsets and it was related to onset of SARS. A number of potential mechanisms may be involved. The development of auto-immune antibodies or immune complexes triggered by viral infection may play a major role in inducing lymphopenia and thrombocytopenia. Moreover, SARS-CoV may also directly infect hematopoietic stem/progenitor cells via CD13 or CD66a inducing their growth inhibition and apoptosis. The receptor for group I and III CoV is aminopeptidase N (CD13). CD13 has been identified in human bone marrow CD34+ cells, platelets, megakaryocytes, myeloid cells, and erythroid cells, but not in lymphocytes. The common receptor for group II CoV is CEACAM1a (CD66a). CD66a is an adhesion molecule expressed on bone marrow CD34+ cells, platelets, granulocytes and activated lymphocytes. In addition, glucocorticoids could induce lymphopenia and the use of steroids may account for the decrease of lymphocytes in some SARS patients. The increased consumption of platelets and/or the decreased production of platelets in the damaged lungs are a potential alternative but often overlooked mechanism that can contribute to thrombocytopenia in severe critical pulmonary conditions.
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                Author and article information

                Journal
                Acta Haematol
                Acta Haematol
                AHA
                Acta Haematologica
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.com )
                0001-5792
                1421-9662
                25 August 2020
                : 1-5
                Affiliations
                aSection of Clinical Biochemistry, University of Verona, Verona, Italy
                bCardiac Intensive Care Unit, The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
                cDepartment of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, Valencia, Spain
                Author notes
                *Giuseppe Lippi, Section of Clinical Biochemistry, University Hospital of Verona, Piazzale Ludovico Antonio Scuro, 10, IT–37134 Verona (Italy), giuseppe.lippi@ 123456univr.it

                Brandon M. Henry and Fabian Sanchis-Gomar share equal senior authorship of this work.

                Article
                aha-0001
                10.1159/000510914
                7490490
                Copyright © 2020 by S. Karger AG, Basel

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

                Page count
                Figures: 1, Tables: 1, References: 31, Pages: 5
                Categories
                Systematic Review

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