Viral infections and their relationship with catastrophic antiphospholipid syndrome: a possible pathogenic mechanism of severe COVID‐19 thrombotic complications

Mendoza‐Pinto, Claudia; Escárcega, Ricardo O.; Garcı́a-Carrasco, Mario; Bailey, David J.; Gálvez-Romero, José Luis; Cervera, Ricard

doi:10.1111/joim.13123

Cited by 19 publications

(24 citation statements)

References 8 publications

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“…For these patients, severe cases cause acute and lethal pneumonia, developing the severe acute respiratory syndrome (SARS). This later is not confined to the respiratory tract, as demonstrated by clinical evidence of the involvement of multiple organs [2] . Based on experimental research, in vitro studies, laboratory analyses from patient’s samples, comparative analyses between the SARS and the Middle East respiratory syndrome (MERS) infection, and computational modeling studies, the course of the disease is still being understood and there are gaps regarding the understanding concerning the evolution, pathogenesis and, mainly, therapeutic strategies [3] .…”

Section: Introductionmentioning

confidence: 93%

COVID-19: Can the symptomatic SARS-CoV-2 infection affect the homeostasis of the gut-brain-microbiota axis?

2020

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COVID-19 is associated with acute and lethal pneumonia, causing the severe acute respiratory syndrome (SARS), which is not confined to the respiratory tract, as demonstrated by clinical evidence of the involvement of multiple organs, including the central nervous system (CNS). In this context, we hypothesized that both oligosymptomatic and symptomatic patients present an imbalance in the microbiota-gut (immune system) and nervous system axis, worsening the clinical picture. The brain constantly receives a direct and indirect influence from the intestine, more specifically from the immune system and intestinal microbiota. The presence of SARS-CoV-2 in the intestine and CNS, can contribute to both neurological disorders and gut immune system imbalance, events potentialized by an intestinal microbiota dysbiosis, aggravating the patient’s condition and causing more prolonged harmful effects.

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Section: Introductionmentioning

confidence: 93%

COVID-19: Can the symptomatic SARS-CoV-2 infection affect the homeostasis of the gut-brain-microbiota axis?

2020

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“…Another possible factor contributing to the thrombotic complications observed in respiratory viral infections, such as those caused by influenza A/H1N1 and SARS-CoV-2, is antiphospholipid syndrome (APS) [51]. In this regard, antiphospholipid antibodies have been identified in COVID-19 patients [52].…”

Section: Sars-cov-2 Infection and Antiphospholipid Syndromementioning

confidence: 99%

SARS-CoV-2 infection and thrombotic complications: a narrative review

Moschonas

Tselepis

2021

J Thromb Thrombolysis

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The current, global situation regarding the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) pandemic and its potentially devastating clinical manifestations, i.e. coronavirus disease 2019 (COVID-19), took the world by storm, as millions of people have been infected worldwide and more than 1,600,000 patients have succumbed. Infection induced by various respiratory viruses may lead to thrombotic complications. Infection-elicited thrombosis may involve a repertoire of distinct, yet interconnected pathophysiological mechanisms, implicating a hyperinflammatory response, platelet activation and triggering of the coagulation cascade. In the present review, we present current knowledge on the pathophysiological mechanisms that may underlie thrombotic complications in SARS-CoV-2 infection. Furthermore, we provide clinical data regarding the incidence rate of thrombotic events in several viral respiratory infections that cause acute respiratory distress syndrome, including SARS-CoV-2 infection and finally we summarize current recommendations concerning thromboprophylaxis and antithrombotic therapy in patients with thrombotic complications related to SARS-CoV-2 infection.

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“…Interestingly, the interconnected complement and coagulation cascades, which are being increasingly documented in COVID-19, has been long recognized in antiphospholipid syndrome (APS) [ 107 ] . Given that several publications report antiphospholipid antibodies in patients with COVID-19 [ [108] , [109] , [110] ], despite them not fulfilling the Sydney criteria for APS [ 111 ], it is difficult to ignore how much the clinical and immunopathological picture of APS resembles that of the autopsy findings of an exaggerated inflammatory state and thrombosis in many COVID-19 patients [ 112 , 113 ].…”

Section: Innate Immune Response: Friend or Foe?mentioning

confidence: 99%

On the genetics and immunopathogenesis of COVID-19

Jacob

2020

Clinical Immunology

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Most severe cases with COVID-19, especially those with pulmonary failure, are not a consequence of viral burden and/or failure of the ‘adaptive’ immune response to subdue the pathogen by utilizing an adequate ‘adaptive’ immune defense. Rather it is a consequence of immunopathology, resulting from imbalanced innate immune response, which may not be linked to pathogen burden at all. In fact, it might be described as an autoinflammatory disease. The Kawasaki-like disease seen in children with SARS-CoV-2 exposure might be another example of similar mechanism.

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Viral infections and their relationship with catastrophic antiphospholipid syndrome: a possible pathogenic mechanism of severe COVID‐19 thrombotic complications

Cited by 19 publications

References 8 publications

COVID-19: Can the symptomatic SARS-CoV-2 infection affect the homeostasis of the gut-brain-microbiota axis?

COVID-19: Can the symptomatic SARS-CoV-2 infection affect the homeostasis of the gut-brain-microbiota axis?

SARS-CoV-2 infection and thrombotic complications: a narrative review

On the genetics and immunopathogenesis of COVID-19

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