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  •   COVID-19
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  •   COVID-19
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COVID-19 and ethnicity: A novel pathophysiological role for inflammation

 
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Fecha
2020-10
Autor
Vepa, Abhinav et al.
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Resumen
Introduction There have been recent mounting concerns regarding multiple reports stating a significantly elevated relative-risk of COVID-19 mortality amongst the Black and Minority Ethnic (BAME) population. An urgent national enquiry investigating the possible reasons for this phenomenon has been issued in the UK. Inflammation is at the forefront of COVID-19 research as disease severity appears to correlate with pro-inflammatory cytokine dysregulation. This narrative review aims to shed light on the novel, pathophysiological role of inflammation in contributing towards the increased COVID-19 mortality risk amongst the BAME population. Methods Searches in PubMed, Medline, Scopus, medRxiv and Google Scholar were performed to identify articles published in English from inception to 18th June 2020. These databases were searched using keywords including: ‘COVID-19’ or ‘Black and Minority Ethnic’ or ‘Inflammation’. A narrative review was synthesized using these included articles. Results We suggest a novel pathophysiological mechanism by which acute inflammation from COVID-19 may augment existing chronic inflammation, in order to potentiate a ‘cytokine storm’ and thus the more severe disease phenotype observed in the BAME population. Obesity, insulin resistance, cardiovascular disease, psychological stress, chronic infections and genetic predispositions are all relevant factors which may be contributing to elevated chronic systemic inflammation amongst the BAME population. Conclusion Overall, this review provides early insights and directions for ongoing research regarding the pathophysiological mechanisms that may explain the severe COVID-19 disease phenotype observed amongst the BAME population. We suggest ‘personalization’ of chronic disease management, which can be used with other interventions, in order to tackle this.
URI
https://doi.org/10.1016/j.dsx.2020.06.056
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  • Technical documents and research evidence on COVID-19

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