scholarly journals Role of Combining Anticoagulant and Antiplatelet Agents in COVID-19 Treatment: A Rapid Review

Author(s):  
Kamal Matli ◽  
Raymond Farah ◽  
Mario Maalouf ◽  
Christy Costanian ◽  
Nibal Chamoun ◽  
...  

ABSTRACTAlthough primarily affecting the respiratory system, COVID-19 causes multiple organ damage. One of its grave consequences is a prothrombotic state that manifests as thrombotic, microthrombotic, and thromboembolic events.Therefore, understanding the effect of antiplatelet and anticoagulation therapy in the context of COVID-19 treatment is important. The aim of this rapid review is to highlight the role of thrombosis in COVID-19 and provide new insights on the use of antithrombotic therapy in its management. A rapid systematic review was performed using preferred reporting items for systematic reviews. Papers published in English on antithrombotic agent use and COVID-19 complications were eligible. Results showed that the use of anticoagulants increased survival and reduced thromboembolic events in patients. However, despite the use of anticoagulants, patients still suffered thrombotic events likely due to heparin resistance. Data on antiplatelet use in combination with anticoagulants in the setting of COVID-19 is quite scarce. Current side effects of anticoagulation therapy emphasize the need to update treatment guidelines. In this rapid review, we address a possible modulatory role of antiplatelet and anticoagulant combination against COVID□19 pathogenesis. This combination may be an effective form of adjuvant therapy against COVID□19 infection. However, further studies are needed to elucidate potential risks and benefits associated with this combination.It was not appropriate or possible to involve patients or the public in the design, or conduct, or reporting, or dissemination plans of our research

Open Heart ◽  
2021 ◽  
Vol 8 (1) ◽  
pp. e001628
Author(s):  
Kamal Matli ◽  
Raymond Farah ◽  
Mario Maalouf ◽  
Nibal Chamoun ◽  
Christy Costanian ◽  
...  

Although primarily affecting the respiratory system, COVID-19 causes multiple organ damage. One of its grave consequences is a prothrombotic state that manifests as thrombotic, microthrombotic and thromboembolic events. Therefore, understanding the effect of antiplatelet and anticoagulation therapy in the context of COVID-19 treatment is important. The aim of this rapid review was to highlight the role of thrombosis in COVID-19 and to provide new insights on the use of antithrombotic therapy in its management. A rapid systematic review was performed using preferred reporting items for systematic reviews. Papers published in English on antithrombotic agent use and COVID-19 complications were eligible. Results showed that the use of anticoagulants increased survival and reduced thromboembolic events in patients. However, despite the use of anticoagulants, patients still suffered thrombotic events likely due to heparin resistance. Data on antiplatelet use in combination with anticoagulants in the setting of COVID-19 are quite scarce. Current side effects of anticoagulation therapy emphasise the need to update treatment guidelines. In this rapid review, we address a possible modulatory role of antiplatelet and anticoagulant combination against COVID-19 pathogenesis. This combination may be an effective form of adjuvant therapy against COVID-19 infection. However, further studies are needed to elucidate potential risks and benefits associated with this combination.


2021 ◽  
Vol 17 (6) ◽  
pp. 67-70
Author(s):  
I.I. Gorelkin ◽  
V.N. Kapusta ◽  
I.A. Buinyi ◽  
E.V. Bachtina ◽  
S.A. Zhmychova

Coronavirus disease is severe in the elderly and in people with chronic diseases such as diabetes mellitus, heart disease, chronic obstructive pulmonary disease, and cancers. It is generally accepted that in children, COVID-19 is much milder, and often is even asymptomatic. But there are some children who, against the background of the coronavirus infection, developed multisystem inflammatory syndrome (MIS-C). Its pathophysiology is not fully understood. There are several hypotheses about the mechanisms of MIS-C development. It is assumed that the syndrome develops due to an excessive immune response to the virus. Having some similar mechanisms with Kawasaki disease, macrophage activation syndrome, the development of MIS-C still has significant diffe-rences. Multiple organ damage occurs due to systemic inflammation, hypoxia, tissue ischemia. As a result, multiple organ dysfunction syndrome develops. Clinical manifestations are specific and reflect changes in all body systems. Laboratory studies revealed an increase in inflammatory markers, transaminases, creatinine, urea, coagulation disturbances. Treatment of multisystem inflammatory syndrome includes immunomodulatory and glucocorticoid therapies. Antibiotics, anticoagulants, antiplatelet agents are also administered, and in case of renal failure symptoms — dialysis replacement therapy. The article describes cases of successful treatment of children with multisystem inflammatory syndrome associated with COVID-19, which show that MIS-C can mask a large number of diseases. Attention should be paid to the need for hospitalization of such patients into a unit with the possibility of hemodialysis, to the different approaches to treatment, the importance of renal replacement therapy. If the above requirements are met, it is possible to achieve a complete recovery of patients.


2021 ◽  
Vol 22 (12) ◽  
pp. 6249
Author(s):  
Jaewoong Jang ◽  
Jaewon Song ◽  
Inae Sim ◽  
Young V. Kwon ◽  
Yoosik Yoon

Sepsis is characterized by multiple-organ dysfunction caused by the dysregulated host response to infection. Until now, however, the role of the Wnt signaling has not been fully characterized in multiple organs during sepsis. This study assessed the suppressive effect of a Wnt signaling inhibitor, Wnt-C59, in the kidney, lung, and liver of lipopolysaccharide-induced endotoxemic mice, serving as an animal model of sepsis. We found that Wnt-C59 elevated the survival rate of these mice and decreased their plasma levels of proinflammatory cytokines and organ-damage biomarkers, such as BUN, ALT, and AST. The Wnt/β-catenin and NF-κB pathways were stimulated and proinflammatory cytokines were upregulated in the kidney, lung, and liver of endotoxemic mice. Wnt-C59, as a Wnt signaling inhibitor, inhibited the Wnt/β-catenin pathway, and its interaction with the NF-κB pathway, which resulted in the inhibition of NF-κB activity and proinflammatory cytokine expression. In multiple organs of endotoxemic mice, Wnt-C59 significantly reduced the β-catenin level and interaction with NF-κB. Our findings suggest that the anti-endotoxemic effect of Wnt-C59 is mediated via reducing the interaction between β-catenin and NF-κB, consequently suppressing the associated cytokine upregulation in multiple organs. Thus, Wnt-C59 may be useful for the suppression of the multiple-organ dysfunction during sepsis.


2008 ◽  
Vol 13 (1) ◽  
pp. 7-13 ◽  
Author(s):  
Cesare Cuspidi ◽  
Cristiana Valerio ◽  
Carla Sala ◽  
Arturo Esposito ◽  
Meilikè Masaidi ◽  
...  

2005 ◽  
Vol 126 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Sevgin Özlem İşeri ◽  
Göksel Şener ◽  
Beyhan Saǧlam ◽  
Nursal Gedik ◽  
Feriha Ercan ◽  
...  
Keyword(s):  

2018 ◽  
Vol 44 (02) ◽  
pp. 102-113 ◽  
Author(s):  
Sophie Maiocchi ◽  
Imala Alwis ◽  
Mike Wu ◽  
Yuping Yuan ◽  
Shaun Jackson

AbstractIschemia–reperfusion (IR) injury is a common complication of a variety of cardiovascular diseases, including ischemic stroke and myocardial infarction (MI). While timely re-establishment of blood flow in a thrombosed artery is the primary goal of acute therapy in these diseases, paradoxically, reperfusion of ischemic tissue can cause widespread microvascular dysfunction that significantly exacerbates organ damage. Reperfusion injury is associated with activation of the humoral and cellular components of the hemostatic and innate immune systems and also with excessive reactive oxygen species production, endothelial dysfunction, thrombosis, and inflammation. Platelets are critical mediators of thromboinflammation during reperfusion injury and a hyperactive platelet phenotype may contribute to an exaggerated IR injury response. This is particularly relevant to diabetes which is characteristically associated with hyperactive platelets, significantly worse IR injury, increased organ damage, and increased risk of death. However, the mechanisms underlying vulnerability to IR injury in diabetic individuals is not well defined, nor the role of “diabetic platelets” in this process. This review summarizes recent progress in understanding the role of platelets in promoting microvascular dysfunction and inflammation in the context of IR injury. Furthermore, the authors discuss aspects of the thromboinflammatory function of platelets that are dysregulated in diabetes. They conclude that diabetes likely enhances the capacity of platelets to mediate microvascular thrombosis and inflammation during IR injury, which has potentially important implications for the future design of antiplatelet agents that can reduce microvascular dysfunction and inflammation.


2020 ◽  
Vol 7 (3) ◽  
pp. 5-19
Author(s):  
Nikhil Nair ◽  
Ronith Chakraborty ◽  
Zubin Mahajan ◽  
Aditya Sharma ◽  
Sidarth Sethi ◽  
...  

Tuberous sclerosis complex (TSC) is a genetic condition caused by a mutation in either the TSC1 or TSC2 gene. Disruption of either of these genes leads to impaired production of hamartin or tuberin proteins, leading to the manifestation of skin lesions, tumors and seizures. TSC can manifests in multiple organ systems with the cutaneous and renal systems being the most commonly affected. These manifestations can secondarily lead to the development of hypertension, chronic kidney disease, and neurocognitive declines. The renal pathologies most commonly seen in TSC are angiomyolipoma, renal cysts and less commonly, oncocytomas. In this review, we highlight the current understanding on the renal manifestations of TSC along with current diagnosis and treatment guidelines.


2021 ◽  
pp. 004947552098277
Author(s):  
Madhu Kharel ◽  
Alpha Pokharel ◽  
Krishna P Sapkota ◽  
Prasant V Shahi ◽  
Pratisha Shakya ◽  
...  

Evidence-based decision-making is less common in low- and middle-income countries where the research capacity remains low. Nepal, a lower-middle-income country in Asia, is not an exception. We conducted a rapid review to identify the trend of health research in Nepal and found more than seven-fold increase in the number of published health-related articles between 2000 and 2018. The proportion of articles with Nepalese researchers as the first authors has also risen over the years, though they are still only in two-thirds of the articles in 2018.


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