Reply to Rheumatologists’ perspective on coronavirus disease 19: is heparin the dark horse for COVID-19?

Ahmed, Sakir; Anirvan, Prajna

doi:10.1007/s10067-020-05145-w

Cited by 10 publications

(9 citation statements)

References 11 publications

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“…A larger retrospective study with the data of 17 Spanish hospitals has also confirmed the mortality benefit of heparin after adjusting for age and gender [ 123 ]. Beyond the benefit of anticoagulation, heparin also has antiarrhythmic properties [ 124 ] and can even oppose classical RAAS activation [ 125 ].…”

Section: Targeting Thrombosis In Severe Covid-19mentioning

confidence: 99%

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

2020

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The pathogenesis of Coronavirus disease 2019 (COVID-19) is gradually being comprehended. A high number of thrombotic episodes are reported, along with the mortality benefits of heparin. COVID-19 can be viewed as a prothrombotic disease. We overviewed the available evidence to explore this possibility. We identified various histopathology reports and clinical case series reporting thromboses in COVID-19. Also, multiple coagulation markers support this. COVID-19 can be regarded as a risk factor for thrombosis. Applying the principles of Virchow's triad, we described abnormalities in the vascular endothelium, altered blood flow, and platelet function abnormalities that lead to venous and arterial thromboses in COVID-19. Endothelial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) with the release of procoagulant plasminogen activator inhibitor (PAI-1), and hyperimmune response with activated platelets seem to be significant contributors to thrombogenesis in COVID-19. Stratifying risk of COVID-19 thromboses should be based on age, presence of comorbidities, D-dimer, CT scoring, and various blood cell ratios. Isolated heparin therapy may not be sufficient to combat thrombosis in this disease. There is an urgent need to explore newer avenues like activated protein C, PAI-1 antagonists, and tissue plasminogen activators (tPA). These should be augmented with therapies targeting RAAS, antiplatelet drugs, repurposed antiinflammatory, and antirheumatic drugs.

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Section: Targeting Thrombosis In Severe Covid-19mentioning

confidence: 99%

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

2020

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“…Thrombosis is an integral part of COVID-19. Conversely, the mortality benefit of heparin in COVID-19 seems to extend beyond the conventional anti-coagulation properties [ 45 ]. The various roles of endothelial cells, turbulent blood flow, and platelet dysfunction included in Virchow’s triad are discussed in detail elsewhere [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

COVID-19 and the clinical course of rheumatic manifestations

2021

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The manifestations of COVID-19 have been evolving over time. Various post-COVID-19 syndromes are being recognised. Various viruses have been implicated in the pathogenesis of autoimmune diseases, and we expect a similar outcome with the severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2). The SARS-CoV-2 virus penetrates various tissues and organs and has a predisposition to lead to endotheliitis that may cause vascular manifestations including thrombosis. SARS-CoV-2 has been shown to activate Toll-like receptors and the complement system. It perpetuates NETosis and leads to autoantibody formation. These predispose to systemic autoimmunity. Both reactive arthritis and connective tissue disorders such as lupus and inflammatory myositis have been reported after COVID-19. Other reported autoimmune disorders include haemolytic anaemia, immune thrombocytopenia, cutaneous vasculitis, and Guillain Barré-like acute demyelinating disorders. The multisystem inflammatory syndrome in children and its adult counterpart are another post-COVID-19 entity that presents as an admixture of Kawasaki disease and staphylococcal toxic shock syndrome. Patients with preexisting rheumatic diseases may flare during the SARS-CoV-2 infection. They may develop novel autoimmune features also. The immune-suppressants used during the acute COVID-19 illness may confound the outcomes whereas comorbidities present in patients with rheumatic diseases may mask them. There is an urgent need to follow-up patients recovering from COVID and monitor autoantibody production in the context of rheumatic manifestations. Key Points • COVID-19 is associated with both innate and acquired immune reactions and production of various autoantibodies. • Various immune-mediated manifestations such as arthritis, myositis, haemolytic anaemia, thrombocytopenia, and acute demyelination may develop after COVID-19. • Longitudinal cohort data are warranted to describe, predict, and test prevent various rheumatic manifestations in post-COVID-19 subjects.

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“…11,12 ACE2 normally degrades angiotensin II, and SARS-CoV-2-mediated downregulation of ACE2 may lead to accumulation of angiotensin II, which may contribute to a procoagulant state. 13 Injury to the endothelium initiated by SARS-CoV-2 entry into these cells is thought to play a key role, and likely explains the pathologic evidence of diffuse endotheliitis in multiple organs, including lungs, kidneys, heart and intestines. 5 The endotheliopathy may lead to an inflammatory host response characterized by excessive immune activation and cytokine storm, which promotes hypercoagulability and thrombosis.…”

Section: How Does Sars-cov-2 Lead To Disordered Coagulation?mentioning

confidence: 99%

Anticipating and managing coagulopathy and thrombotic manifestations of severe COVID-19

Godoy

Goligher

Lawler

et al. 2020

CMAJ

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(COVID-19), the disease resulting from infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibits a broad spectrum of manifestations and severity. Although most patients do not require admission to hospital, about 10%-15% of symptomatic patients are admitted, of whom about 20% receive intensive care. 1 Thrombosis is a prominent clinical feature of COVID-19, and between 5% and 30% of in-hospital patients develop a clinically apparent thrombotic event. 2-4 Emerging evidence suggests that endothelial injury resulting from SARS-CoV-2 cellular invasion and a subsequent dysregulated host response involving inflammatory and coagulation pathways plays a critical role in the progression of severe COVID-19. 5 Macrovascular and microvascular thrombosis may contribute to organ failure, multisystem injury and death. 6,7 However, the optimal prevention and treatment of thrombosis in COVID-19 remains uncertain. 8 We review emerging evidence regarding COVID-19 coagulopathy (Box 1) and discuss current therapeutic directions and unanswered questions.

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Reply to Rheumatologists’ perspective on coronavirus disease 19: is heparin the dark horse for COVID-19?

Cited by 10 publications

References 11 publications

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

COVID-19 and the clinical course of rheumatic manifestations

Anticipating and managing coagulopathy and thrombotic manifestations of severe COVID-19

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