Anticardiolipin IgG Autoantibody Level Is an Independent Risk Factor for COVID‐19 Severity

Bertin, Daniel; Brodovitch, Alexandre; Beziane, Abdou; Hug, Sylvia; Bouamri, Afaf; Mège, Jean Louis; Heim, Xavier; Bardin, Nathalie

doi:10.1002/art.41409

Cited by 70 publications

(77 citation statements)

References 6 publications

(1 reference statement)

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“…Furthermore, a prospective cohort study of 24 patients with COVID-19 who had venous thromboembolism revealed weakly positive anticardiolipin IgM and antiβ2glycoprotein I IgM in only 2 patients [120]. Another retrospective cohort study of 56 COVID-19 patients pointed to an independent association of anticardiolipin IgG with low oxygen saturation and other severe disease manifestations [121]. Only 1 patient with anticardiolipin IgG had a stroke in that study.…”

Section: Antiphospholipid Antibodiesmentioning

confidence: 88%

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: Antiphospholipid Antibodiesmentioning

confidence: 88%

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

2020

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“…3 From a respiratory infection, COVID-19 can rapidly evolve into a systemic disease, as evidenced by the extrapulmonary manifestations ( Figure 2). Systemic manifestations are associated with an inflammatory syndrome (elevated serum levels of interleukin-6 , alarmins and inflammatory chemokines), a profound lymphopenia, coagulopathy in multiple vascular territories, either related to a systemic immunopathology (as exemplified by the presence of anticardiolipin IgA, anti-β2 -glycoprotein IgA and IgG antibodies and cold agglutinin [20][21][22][23][24][25][26] ), a direct infection of endothelial cells of lung capillaries expressing the SARS-CoV-2 angiotensin converting enzyme 2 receptor 27,28 or a hyperactivated innate immune response 29 (Figure 2). Finally, the incidence and severity of COVID-19 correlate with risk factors and comorbidities, such as older age, cancer, obesity, cardiovascular diseases and diabetes linked to immuno-senescence, immunosuppression or immunopathologies.…”

Section: Introductionmentioning

confidence: 99%

Immune responses during COVID-19 infection

et al. 2020

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Over the past 16 years, three coronaviruses (CoVs), severe acute respiratory syndrome CoV (SARS-CoV) in 2002, Middle East respiratory syndrome CoV (MERS-CoV) in 2012 and 2015, and SARS-CoV-2 in 2020, have been causing severe and fatal human epidemics. The unpredictability of coronavirus disease-19 (COVID-19) poses a major burden on health care and economic systems across the world. This is caused by the paucity of in-depth knowledge of the risk factors for severe COVID-19, insufficient diagnostic tools for the detection of SARS-CoV-2, as well as the absence of specific and effective drug treatments. While protective humoral and cellular immune responses are usually mounted against these betacoronaviruses, immune responses to SARS-CoV2 sometimes derail towards inflammatory tissue damage, leading to rapid admissions to intensive care units. The lack of knowledge on mechanisms that tilt the balance between these two opposite outcomes poses major threats to many ongoing clinical trials dealing with immunostimulatory or immunoregulatory therapeutics. This review will discuss innate and cognate immune responses underlying protective or deleterious immune reactions against these pathogenic coronaviruses.

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“…plasma B cells), aPL target platelet membrane phospholipids leading to abnormal clots formation in veins and/or arteries (thrombosis) that can occur also with inflammation (phlebitis). Thus, it was observed in SARS-CoV-2 positive subjects that anticardiolipin antibodies (aCL IgG) profile (>15 U/mL) was associated to disease severity (i.e.respiratory distress) while those patients have not a previous record history of thrombosis [ 12 ]. Authors concluded that aCL IgG may be a risk marker in COVID-19 patients.…”

mentioning

confidence: 99%

Cholesterol, inflammation, and phospholipids: COVID-19 share traits with cardiovascular disease

Pimentel

Rodriguez‐Alcalá

2021

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Anticardiolipin IgG Autoantibody Level Is an Independent Risk Factor for COVID‐19 Severity

Cited by 70 publications

References 6 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

Immune responses during COVID-19 infection

Cholesterol, inflammation, and phospholipids: COVID-19 share traits with cardiovascular disease

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