Incidence and risk factors of venous thromboembolism in ANCA-associated vasculitis: a metaanalysis and metaregression

Hansrivijit, Panupong; Trongtorsak, Angkawipa; Gadhiya, Kinjal P; Lnu, Kriti; Dimech, Christina T.; Cheungpasitporn, Wisit; Lecker, Stewart H.

doi:10.1007/s10067-021-05589-8

Cited by 17 publications

(5 citation statements)

References 52 publications

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“…Increased baseline disease activity measured by the Birmingham Vasculitis Activity Score (BVAS) and renal involvement portended greater risk of VTE. A longer duration of follow-up also associated with increased VTE [15]. Venous thromboses might be presenting features of AAV [16,17].…”

Section: The Association Of Anti-neutrophil Cytoplasmic Antibody (Anca) and Anca-associated Vasculitis With Thrombosismentioning

confidence: 99%

Mechanisms of thrombosis in ANCA-associated vasculitis

et al. 2021

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Patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) have a two- to threefold greater risk of developing venous as well as arterial thrombotic events. Although such thrombotic events are more commonly seen during phases of active AAV, they are also recognized to occur during AAV in remission. Endothelial injury is a key pathogenic event in AAV. Endothelial injury can be caused by neutrophil activation and release of thrombogenic tissue factor into the circulation. Neutrophil activation further results in the formation of neutrophil extracellular traps (NETs). NETs contribute to thrombosis by expressing tissue factor. NETs have also been detected in cutaneous thrombi from patients with AAV induced by hydralazine. Activated neutrophils in AAV patients release thrombogenic microparticles loaded with tissue factor which further enhances clotting of blood. Antiphospholipid antibodies (APLs) have been detected in up to a third of AAV and might also be induced by drugs such as cocaine adulterated with levamisole and propylthiouracil, which are known to trigger AAV. Such APLs further drive the thrombosis in AAV. Once thrombogenesis occurs, the homeostatic mechanisms resulting in clot dissolution are further impaired in AAV due to anti-plasminogen antibodies. The ongoing pandemic of coronavirus disease 2019 (COVID-19) is associated with endothelial injury and NETosis, mechanisms which are in common with AAV. Reports of new-onset AAV following COVID-19 have been described in the literature, and there could be shared mechanisms driving these processes that require further evaluation.

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Section: The Association Of Anti-neutrophil Cytoplasmic Antibody (Anca) and Anca-associated Vasculitis With Thrombosismentioning

confidence: 99%

Mechanisms of thrombosis in ANCA-associated vasculitis

et al. 2021

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“…In der ANCA-assoziierten Gruppe konnte eine starke Assoziation mit einem erhöhten VTE-Risiko nachgewiesen werden. Eine Metaanalyse ergab eine gepoolte Inzidenz von 12,4% VTE bei Patienten mit ANCA-assoziierter Vaskulitis, davon 63,4% TVT und 26,3% PE [72]. Darüber hinaus erwies sich das Vorhandensein von Myeloperoxidase-ANCA als der stärkste Faktor, der mit einer ersten Episode oder einem Wiederauftreten einer VTE assoziiert war.…”

Section: Autoimmunerkrankungen Und Das Risiko Einer Vteunclassified

Risiko venöser Thromboembolien bei Autoimmunerkrankungen: Eine umfassende Übersicht

Menichelli,

Cormaci,

Marucci

et al. 2024

Kompass Autoimmun

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Autoimmunerkrankungen haben spezifische pathophysiologische Mechanismen, die zu einem erhöhten Risiko für arterielle und venöse Thrombosen führen. Das Risiko einer venösen Thromboembolie (VTE) variiert je nach Art und Stadium der Erkrankung sowie der begleitenden Therapie. In dieser Übersichtsarbeit werden die häufigsten Autoimmunerkrankungen wie Anti-Phospholipid-Syndrom, entzündliche Myositis, Polymyositis und Dermatomyositis, rheumatoide Arthritis, Sarkoidose, Sjögren-Syndrom, autoimmunhämolytische Anämie, systemischer Lupus erythematodes, systemische Sklerose, Vaskulitis und chronisch-entzündliche Darmerkrankungen behandelt. Darüber hinaus geben wir einen Überblick über die Pathophysiologie, die für das VTE-Risiko bei jeder Autoimmunerkrankung verantwortlich ist, und berichten über die aktuellen Indikationen für eine gerinnungshemmende Therapie zur Primär- und Sekundärprävention von VTE.

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“…Для пациентов с АНЦА-СВ характерны гиперкоагуляция и риск тромбозов [22][23][24]; присоединение COVID-19 становится дополнительным фактором, повышающим риск тромбоэмболических осложнений [25-27], в связи с чем в представленном случае использовали интенсивную антикоагулянтную терапию. В патогенезе коагулопатии при обоих заболеваниях предполагается общий механизм, получивший название «тромбовоспаление», обусловленный гиперпродукцией провоспалительных цитокинов, индуцирующих дисфункцию эндотелиальных клеток, образованием нейтрофильных внеклеточных ловушек, патологической активацией системы комплемента, другими реакциями [24][25][26].…”

Section: рис 4 кт легких на 24-й день болезни: обратное развитие пато...unclassified

COVID-19 in a patient with granulomatosis with polyangiitis: Management tactics

Iskhakova

Sukhorukova

Badeeva

et al. 2023

Naučno-praktičeskaâ revmatologiâ

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Patients with ANCA-associated vasculitis (AAV) cause extreme alertness during the coronavirus disease 2019 (COVID-19) pandemic, associated with many factors: the initial damage to the respiratory system (upper respiratory tract, lungs) and kidneys, immunosuppressive treatments, difficult prognosis of COVID-19 with the risk of AAV exacerbation. We present a clinical case of а moderate COVID-19 in a patient with granulomatosis with polyangiitis, who received anti-B cell therapy with rituximab (RTX) for a long time. Coronavirus pneumonia developed one year after RTX, while B-lymphocyte depletion persisted. In order to achieve an adequate antiviral immune response and prevent hyperinflammation, treatment was carried out with antiviral drugs, anticoagulants, convalescent plasma, human normal immunoglobulin, and interleukin-6 antagonist tocilizumab. Possible predictors of severe COVID-19 in patients with AAV are discussed.

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Incidence and risk factors of venous thromboembolism in ANCA-associated vasculitis: a metaanalysis and metaregression

Cited by 17 publications

References 52 publications

Mechanisms of thrombosis in ANCA-associated vasculitis

Mechanisms of thrombosis in ANCA-associated vasculitis

Risiko venöser Thromboembolien bei Autoimmunerkrankungen: Eine umfassende Übersicht

COVID-19 in a patient with granulomatosis with polyangiitis: Management tactics

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