Systematic Review of Antiphospholipid Antibodies in COVID-19 Patients: Culprits or Bystanders?

Foret, Thomas; Dufrost, Virginie; Mont, Lucie Salomon du; Costa, Patrícia; Lefèvre, Benjamin; Lacolley, Patrick; Régnault, V.; Zuily, Stéphane; Wahl, Denis

doi:10.1007/s11926-021-01029-3

Cited by 31 publications

(31 citation statements)

References 83 publications

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“…Numerous autoimmune manifestations associated with COVID-19 are described in the literature including the presence of several different autoantibodies ( 23 ). Anticardiolipin and other antiphospholipid antibodies were frequently reported in patients with COVID-19 ( 24 ) and were associated with a more severe disease course ( 25 ). It is likely that the presence of aCL in our patient reflects endothelial damage due to SARS-CoV-2 infection and could additionally contribute to the procoagulant state.…”

Section: Discussionmentioning

confidence: 99%

Case Report: Necrotizing Stomatitis as a Manifestation of COVID-19-Associated Vasculopathy

et al. 2021

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Necrotizing stomatitis is a rare, acute-onset disease that is usually associated with severely malnourished children or diminished systemic resistance. We describe a 1-year-old girl who developed necrotizing stomatitis, vasculitic rash, skin desquamation on the fingers and toes, and persistent hypertension after serologically confirmed SARS-CoV-2 infection. Her laboratory investigations revealed positive IgG anticardiolipin and IgG anti-β2 glycoprotein antibodies, and biopsy of the mucosa of the lower jaw showed necrosis and endothelial damage with mural thrombi. Swollen endothelial cells of small veins in the upper dermis were confirmed also by electron microscopy. As illustrated by our case, necrotizing stomatitis may develop as a rare complication associated with SARS-CoV-2 infection and can be considered as a part of the clinical spectrum of COVID-19 vasculopathy. The pathogenic mechanism could involve a consequence of inflammatory events with vasculopathy, hypercoagulability, and damage of endothelial cells as a response to SARS-CoV-2 infection.

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Section: Discussionmentioning

confidence: 99%

Case Report: Necrotizing Stomatitis as a Manifestation of COVID-19-Associated Vasculopathy

et al. 2021

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“…In this regard, it should be noted that endothelial damage is not unique to loPE, but is also present in eoPE [140] . 2) Anti-phospholipid antibodies (aPLA) have been shown to be elevated in a significant number of patients with COVID-19 [141] . In addition, aPLA represent an elevated risk factor for pregnant women with preeclampsia [139] .…”

Section: Covid-19 and Eopementioning

confidence: 99%

SARS- CoV-2 infection and oxidative stress in early-onset preeclampsia

Marı́n

Pujol

Rojas

et al. 2022

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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SARS-CoV-2 causes coronavirus disease 2019 (COVID-19) also in pregnant women. Infection in pregnancy leads to maternal and placental functional alterations. Pregnant women with vascular defects such as preeclampsia show high susceptibility to SARS-CoV-2 infection by undefined mechanisms. Pregnant women infected with SARS-CoV-2 show higher rates of preterm birth and caesarean delivery, and their placentas show signs of vasculopathy and inflammation. It is still unclear whether the foetus is affected by the maternal infection with this virus and whether maternal infection associates with postnatal affections. The SARS-CoV-2 infection causes oxidative stress and activation of the immune system leading to cytokine storm and next tissue damage as seen in the lung. The angiotensin-converting-enzyme 2 expression is determinant for these alterations in the lung. Since this enzyme is expressed in the human placenta, SARS-CoV-2 could infect the placenta tissue, although reported to be of low frequency compared with maternal lung tissue. Early-onset preeclampsia shows higher expression of ADAM17 (a disintegrin and metalloproteinase 17) causing an imbalanced renin-angiotensin system and endothelial dysfunction. A similar mechanism seems to potentially account for SARS-CoV-2 infection. This review highlights the potentially common characteristics of pregnant women with eoPE with those with COVID-19. A better understanding of the mechanisms of SARS-CoV-2 infection and its impact on the placenta function is determinant since eoPE/COVID-19 association may result in maternal metabolic alterations that might lead to a potential worsening of the foetal programming of diseases in the neonate, young, and adult.

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“…The obvious conclusion, which has been reached previously in studies of other autoimmune diseases, is that molecular mimicry may be necessary to induce auto‐reactive B and T cells but is clearly not sufficient to induce autoimmune disease . [ 22 , 83 , 84 , 85 , 86 ] This point is essential for understanding how many hospitalized COVID‐19 patients are found transiently to express anti‐phospholipid antibodies (aPL), anti‐PL4, b2GPI, and other blood cell antibodies [ 7 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 87 , 88 ] but only a fraction of these develop coagulopathies [ 25 , 30 , 87 , 88 ] and also why SARS‐CoV‐2 vaccines (to be discussed in “Implications of bacterial and viral coinfections for understanding vaccine‐induced coagulopathies”) often induce autoantibodies but rarely autoimmune disease. Mimicry may frequently induce autoantibody production but rarely leads to overt autoimmune disease or, alternatively, mimics may be perceived by the immune system as “self” antigens resulting in T cell tolerance.…”

Section: Discussionmentioning

confidence: 99%

COVID‐19 coagulopathies: Human blood proteins mimic SARS‐CoV‐2 virus, vaccine proteins and bacterial co‐infections inducing autoimmunity

Root‐Bernstein

2021

BioEssays

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Severe COVID‐19 is often accompanied by coagulopathies such as thrombocytopenia and abnormal clotting. Rarely, such complications follow SARS‐CoV‐2 vaccination. The cause of these coagulopathies is unknown. It is hypothesized that coagulopathies accompanying SARS‐CoV‐2 infections and vaccinations result from bacterial co‐infections that synergize with virus‐induced autoimmunity due to antigenic mimicry of blood proteins by both bacterial and viral antigens. Coagulopathies occur mainly in severe COVID‐19 characterized by bacterial co‐infections with Streptococci , Staphylococci , Klebsiella , Escherichia coli , and Acinetobacter baumannii . These bacteria express unusually large numbers of antigens mimicking human blood antigens, as do both SARS‐CoV‐2 and adenoviruses. Bacteria mimic cardiolipin, prothrombin, albumin, and platelet factor 4 (PF4). SARS‐CoV‐2 mimics complement factors, Rh antigens, platelet phosphodiesterases, Factors IX and X, von Willebrand Factor (VWF), and VWF protease ADAMTS13. Adenoviruses mimic prothrombin and platelet factor 4. Bacterial prophylaxis, avoidance of vaccinating bacterially infected individuals, and antigen deletion for vaccines may reduce coagulopathy risk. Also see the video abstract here: https://youtu.be/zWDOsghrPg8

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Systematic Review of Antiphospholipid Antibodies in COVID-19 Patients: Culprits or Bystanders?

Cited by 31 publications

References 83 publications

Case Report: Necrotizing Stomatitis as a Manifestation of COVID-19-Associated Vasculopathy

Case Report: Necrotizing Stomatitis as a Manifestation of COVID-19-Associated Vasculopathy

SARS- CoV-2 infection and oxidative stress in early-onset preeclampsia

COVID‐19 coagulopathies: Human blood proteins mimic SARS‐CoV‐2 virus, vaccine proteins and bacterial co‐infections inducing autoimmunity

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