Molecular mechanisms for thrombosis risk in Black people: a role in excess mortality from COVID‐19

Ramasamy, Roshan; Milne, Kate; Bell, Deanne; Stoneham, Sarah J.; Chevassut, Timothy

doi:10.1111/bjh.16869

Cited by 15 publications

(13 citation statements)

References 11 publications

(2 reference statements)

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“…It is noteworthy that some studies have looked for explanations for the higher mortality among blacks beyond the socioeconomic aspects, accounting for pathophysiological mechanisms. One relationship of interest is that among being black, COVID-19 and the risk of venous thrombosis [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

COVID-19 hospitalizations in Brazil’s Unified Health System (SUS)

et al. 2020

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Objective To study the profile of hospitalizations due to COVID-19 in the Unified Health System (SUS) in Brazil and to identify factors associated with in-hospital mortality related to the disease. Methods Cross-sectional study, based on secondary data on COVID-19 hospitalizations that occurred in the SUS between late February through June. Patients aged 18 years or older with primary or secondary diagnoses indicative of COVID-19 were included. Bivariate analyses were performed and generalized linear mixed models (GLMM) were estimated with random effects intercept. The modeling followed three steps, including: attributes of the patients; elements of the care process; and characteristics of the hospital and place of hospitalization. Results 89,405 hospitalizations were observed, of which 24.4% resulted in death. COVID-19 patients hospitalized in the SUS were predominantly male (56.5%) with a mean age of 58.9 years. The length of stay ranged from less than 24 hours to 114 days, with a mean of 6.9 (±6.5) days. Of the total number of hospitalizations, 22.6% reported ICU use. The odds on in-hospital death were 16.8% higher among men than among women and increased with age. Black individuals had a higher likelihood of death. The behavior of the Charlson and Elixhauser indices was consistent with the hypothesis of a higher risk of death among patients with comorbidities, and obesity had an independent effect on increasing this risk. Some states, such as Amazonas and Rio de Janeiro, had a higher risk of in-hospital death from COVID-19. The odds on in-hospital death were 72.1% higher in municipalities with at least 100,000 inhabitants, though being hospitalized in the municipality of residence was a protective factor. Conclusion There was broad variation in COVID-19 in-hospital mortality in the SUS, associated with demographic and clinical factors, social inequality, and differences in the structure of services and quality of health care.

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Section: Discussionmentioning

confidence: 99%

COVID-19 hospitalizations in Brazil’s Unified Health System (SUS)

et al. 2020

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“…It is noteworthy that African‐Americans are reported to have higher circulating levels of VWF, Factor VIII and fibrinogen [ 36 ]. The differences in endothelial function and molecular mechanisms of thrombosis risk due to genetic factors may lead to the ethnic disparities in COVID-19-associated thrombosis [ 37 ]. With respect to the comparison of endothelial dysfunction in Asians and other ethnicities, little data are available to make any conclusions.…”

Section: Mechanism Of Thrombus Formation In Covid-19mentioning

confidence: 99%

Ethnic differences in thromboprophylaxis for COVID-19 patients: should they be considered?

et al. 2021

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Thromboembolic events contribute to morbidity and mortality in coronavirus disease 2019 . As a result, thromboprophylaxis using low-molecular-weight heparin (LMWH) is universally recommended for hospitalized patients based on multiple guidelines. However, ethnic differences with respect to thrombogenicity have been reported and the incidence of thromboembolic events is considered to be lower in the Asian population. Despite the importance of thromboprophylaxis, bleeding is also a side effect that should be considered. We examine the data relating to potential ethnic differences in thrombosis and bleeding in COVID-19. Although sufficient data is not yet available, current evidence does not oppose routine anticoagulant use and thromboprophylaxis using a standard dose of LMWH for admitted patients regardless of ethnicity based on our review.

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“…hypertension, and cardiovascular disease [113] [114]. This suggests a role for additional 4 molecular factors that can contribute to a predisposition to thrombosis in the presence of 4…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, detailed demographic data, including breakdown by age, race, gender, and comorbidities, is incomplete; as of May 30, 2020, only 22% of reported cases have information on reported comorbidities and only 45% of reported cases nationwide were presented with demographic data sufficient to determine race [ 112 ]. In addition, there is increasing evidence that African-American populations are at higher risk of thrombotic events with COVID-19, even when adjusting for common risk factors such as BMI, diabetes, hypertension, and cardiovascular disease [ 113 ] [ 114 ]. This suggests a role for additional molecular factors that can contribute to a predisposition to thrombosis in the presence of COVID-19.…”

Section: Discussionmentioning

confidence: 99%

Potential impact on coagulopathy of gene variants of coagulation related proteins that interact with SARS-CoV-2

Holcomb

Alexaki

Hernandez

et al. 2020

Preprint

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Thrombosis has been one of the complications of the Coronavirus disease of 2019 (COVID-19), often associated with poor prognosis. There is a well-recognized link between coagulation and inflammation, however, the extent of thrombotic events associated with COVID-19 warrants further investigation. Poly(A) Binding Protein Cytoplasmic 4 (PABPC4), Serine/Cysteine Proteinase Inhibitor Clade G Member 1 (SERPING1) and Vitamin K epOxide Reductase Complex subunit 1 (VKORC1), which are all proteins linked to coagulation, have been shown to interact with SARS proteins. We computationally examined the interaction of these with SARS-CoV-2 proteins and, in the case of VKORC1, we describe its binding to ORF7a in detail. We examined the occurrence of variants of each of these proteins across populations and interrogated their potential contribution to COVID-19 severity. Potential mechanisms by which some of these variants may contribute to disease are proposed. Some of these variants are prevalent in minority groups that are disproportionally affected by severe COVID-19. Therefore, we are proposing that further investigation around these variants may lead to better understanding of disease pathogenesis in minority groups and more informed therapeutic approaches.Author summaryIncreased blood clotting, especially in the lungs, is a common complication of COVID-19. Infectious diseases cause inflammation which in turn can contribute to increased blood clotting. However, the extent of clot formation that is seen in the lungs of COVID-19 patients suggests that there may be a more direct link. We identified three human proteins that are involved indirectly in the blood clotting cascade and have been shown to interact with proteins of SARS virus, which is closely related to the novel coronavirus. We examined computationally the interaction of these human proteins with the viral proteins. We looked for genetic variants of these proteins and examined how these variants are distributed across populations. We investigated whether variants of these genes could impact severity of COVID-19. Further investigation around these variants may provide clues for the pathogenesis of COVID-19 particularly in minority groups.

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Molecular mechanisms for thrombosis risk in Black people: a role in excess mortality from COVID‐19

Cited by 15 publications

References 11 publications

COVID-19 hospitalizations in Brazil’s Unified Health System (SUS)

COVID-19 hospitalizations in Brazil’s Unified Health System (SUS)

Ethnic differences in thromboprophylaxis for COVID-19 patients: should they be considered?

Potential impact on coagulopathy of gene variants of coagulation related proteins that interact with SARS-CoV-2

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