By Pooja Toshniwal PahariaOct 14 2022Reviewed by Aimee Molineux In a recent review published in Thrombosis Research, researchers reported the mechanisms involved in coronavirus disease 2019 coagulopathy and the significance of severe acute respiratory syndrome coronavirus 2 infections for cancer patients concerning outcomes, thromboembolic complication risks and consequences of management strategies.
Mechanisms of COVID-19 coagulopathy Severe COVID-19 has caused significant morbidity, including multiple organ dysfunction and respiratory insufficiency, and deaths. Age, obesity, and comorbidities such as hypertension, pulmonary disorders, and diabetes are established risk factors for COVID-19 severity.
NETs promote the formation of thrombus by activating the intrinsic clotting pathway and provide a platform for erythrocytes, platelets, and procoagulants like vWF . Therefore, NETosis markers such as citrullinated histone H3 and myeloperoxidase -deoxyribonucleic acid complex are elevated in severe SARS-CoV-2 infections.
It has been documented that mild and severe COVID-19 patients have six-fold and three-fold higher risks of developing pulmonary embolism and venous thrombosis, respectively, the most prominent risk factor for which was the presence of active neoplasms. Venous thromboembolism has been reported to be higher among patients who received anti-neoplastic therapy in recent times compared to those who did not .
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Frontiers | Myocarditis in SARS-CoV-2 infection vs. COVID-19 vaccination: A systematic review and meta-analysisBackground: To compare the incidence of myocarditis in COVID-19 vaccines and SARS-CoV-2 infection groups. Methods: Electronic databases (MEDLINE, Scopus, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews and the World Health Organization Global Literature on Coronavirus Disease) and trial registries were searched to April 2022, for randomized controlled trials and observational cohort studies reporting the risk of myocarditis associated with the COVID-19 vaccines and the risk associated with SARS-CoV-2 infection. We estimated the effect of COVID-19 infection and vaccines on rates of myocarditis by random-effects meta-analyses using the generic inverse variance method. Meta-regression analyses were conducted to assess the effect sex and age on the incidence of myocarditis. Results: We identified 22 eligible studies consisting of 55.5 million vaccinated cohort and 2.5 million in the infection cohort. Median age was 49 years (interquartile range (IQR): 38-56), and 49% (IQR: 43% to 52%) were male. Of patients diagnosed with myocarditis, 3.48 (%) were hospitalized and 0.05 (%) died. The relative risk (RR) for myocarditis was 7 times in the infection group than vaccination group (RR: 15 (95% CI: 11.09 - 19.81, infection group) and RR: 2.0 (95% CI: 1.44-2.65, vaccine group). Of patients who developed myocarditis after receiving the vaccine or having the infection, 61 (IQR: 39% -87%) were male. Meta- regression analysis indicated that male sex and young age were associated with myocarditis. A slow decline in the rates of myocarditis was observed as a function of time from vaccination. Risk of bias assessment was moderate. Conclusions: In this systematic review and meta-analysis, we found that the risk of incident myocarditis is about 7 times higher in persons who were infected with SARS-CoV-2 virus than those who received the vaccine. These findings support continued use of mRNA COVID-19 vaccines among all eligible persons aged ≥5 years penn_state “They found the risk of myocarditis was 15 times higher in COVID-19 patients, regardless of vaccination status” penn_state title a bit misleading:) physorg_com penn_state All the reports and statistics I've read say differently.
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JCI - Improved control of SARS-CoV-2 by treatment with nucleocapsid-specific monoclonal antibody
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