Antiplatelet and anticoagulant agents for primary prevention of thrombosis in individuals with antiphospholipid antibodies

Bała, Małgorzata M; Paszek, Elżbieta; Leśniak, Wiktoria; Wloch-Kopec, Dorota; Jasińska, Katarzyna; Undas, Anetta

doi:10.1002/14651858.cd012534.pub2

Cited by 27 publications

(14 citation statements)

References 91 publications

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“…For this study, we enrolled women of reproductive age and the main criterion of the patient's selection was aPL positivity, which can be viewed as a limitation of the study. Similar subject selection strategy has been implemented by several researchers over the last few years, which in our view represents an important opportunity to raise awareness of potential adverse outcomes for aPL-positive pregnancies [5,[51][52][53][54][55]. Potential risk of aPL-positivity underestimation was reinforced by a recent study, which reported that aPL-positive women who did not fulfil the APS criteria had comparable pregnancy outcomes, gestational period, arterial and/or venous thrombosis, compared those with confirmed APS [56].…”

Section: Discussionmentioning

confidence: 88%

17β-Estradiol Promotes Proinflammatory and Procoagulatory Phenotype of Innate Immune Cells in the Presence of Antiphospholipid Antibodies

et al. 2020

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Antiphospholipid syndrome (APS) is the most common cause of acquired thrombophilia and recurrent spontaneous miscarriages associated with extended persistence of antiphospholipid antibodies (aPL). How circulating aPL and high-17β-estradiol (E2) environment contribute to the pregnancy complications in APS is poorly defined. Therefore, we aimed to analyse whether E2 could be responsible for the immune cell hyperactivation in aPL- positive (lupus anticoagulant, anti-cardiolipin, anti-β2-glycoprotein) in women. For this, peripheral blood mononuclear cells (PBMCs) from 14 aPL- positive and 13 aPL- negative women were cultured in the presence or absence of E2, LPS or E2+LPS and cell immunophenotype and cytokine release were analysed. In the aPL+ group, E2 presence markedly increased the percentage of NK cells positive for CD69 (p < 0.05), monocytes positive for tissue factor (TF, CD142) (p < 0.05), and B cells expressing PD-L1 (p < 0.05), as well as the elevated production of IL-1β comparing to aPL- women (p < 0.01). Regardless of aPL positivity, E2 augmented the procoagulatory response elicited by LPS in monocytes. Our findings show the ability of E2 to promote proinflammatory and procoagulatory phenotype of innate immune cells in individuals with aPL positivity. Our data highlights the significant impact of female hormones on the activation of immune cells in the presence of aPL.

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Section: Discussionmentioning

confidence: 88%

17β-Estradiol Promotes Proinflammatory and Procoagulatory Phenotype of Innate Immune Cells in the Presence of Antiphospholipid Antibodies

et al. 2020

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“…If higher INR levels (3.0-4.0) are needed, the risk of bleeding, but predominantly mild, increases significantly, approximately 2 to 2.5 times [77,78]. As for antiplatelet agents, the rate of bleeding during their prophylactic or therapeutic use appears to be low, and major bleeding is rare [78,79]. The risk of bleeding increases after invasive procedures, likely due to the use of bridging therapy, the early reintroduction of antithrombotics, and aggressive antithrombotic policies [80,81].…”

Section: Bleeding Associated With Antithrombotic Agentsmentioning

confidence: 99%

Bleeding in Patients with Antiphospholipid Antibodies

Kubisz¹,

Holly²,

Staško³

2022

Antiphospholipid Syndrome - Recent Advances in Clinical and Basic Aspects

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The antiphospholipid antibodies (aPL) are commonly associated with thrombotic events and obstetric complications. However, apart from the bleeding complications of antithrombotic therapy, the acquired coagulopathy caused by the aPL, particularly by lupus anticoagulant and anticardiolipin antibodies, might be occasionally manifested as a hemorrhagic syndrome with various clinical severity. Bleeding symptoms vary from mild (mucocutaneous) up to life-threatening (gastrointestinal, intracranial). The bleeding may be the first manifestation of aPL or appear concomitantly with thrombosis. The underlying hemostatic changes include thrombocytopenia, platelet function disorders, and coagulation factor inhibitors or deficiencies, namely prothrombin, FVII, FVIII, FX, and FXI. Thrombocytopenia is the most common finding, seen in up to 53% of patients with aPL, although it is usually mild to moderate and associated with significant bleeding only in a minority of cases. Of interest, patients with severe thrombocytopenia appear to be less likely to suffer from thrombotic events. The involved pathophysiological mechanisms are heterogeneous. Non-neutralizing antibodies against coagulation factors resulting in increased clearance, specific antibodies against platelet membrane glycoproteins, increasing platelet activation and aggregation with subsequent consumption, and immune-mediated platelet clearance are among those identified. Immunosuppression, preferably with corticosteroids, represents the first-choice therapeutic approach. Plasmapheresis is efficient in the case of catastrophic antiphospholipid syndrome. Antithrombotic therapy can be challenging, but its administration should continue as much as possible.

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“…These results were also confirmed by a recent Cochrane Review, showing that LDA treatment is associated with a similar thrombosis risk when compared to VKA treatment with or without LDA. However, the risk of minor bleedings (nasal bleedings, menorrhagia) was reported to be higher in subjects receiving VKA plus LDA [ 64 ].…”

Section: Prevention Strategies In Apl Carriersmentioning

confidence: 99%

Risk Assessment and Antithrombotic Strategies in Antiphospholipid Antibody Carriers

et al. 2021

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Antiphospholipid antibodies (aPL) are a cluster of autoantibodies directed against plasma proteins with affinity for membrane phospholipids. The most frequently tested aPL are lupus anticoagulant (LA), anti-cardiolipin antibodies (aCL), and anti-β2-glycoprotein I antibodies (anti-β2GPI). aPL play a key pathogenic role in the development of the antiphospholipid syndrome (APS), a systemic autoimmune disease characterized by recurrent thrombotic and/or pregnancy complications in patients with persistent aPL. However, aPL positivity is occasionally documented in patients with no previous history of thrombotic or pregnancy morbidity. LA activity, multiple aPL positivity, high-titer aPL, and a concomitant systemic autoimmune disease are recognized risk factors for future thrombotic events in asymptomatic carriers. Moreover, an accelerated atherosclerosis with increased cardiovascular (CV) risk has also been associated with aPL positivity, thus exposing aPL carriers to fatal complications and chronic disability requiring cardiac rehabilitation. Overall, an accurate risk stratification is recommended for aPL-positive subjects in order to prevent both venous and arterial thrombotic complications. In this review, we provide an overview of the main antithrombotic and risk assessment strategies in aPL carriers.

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Antiplatelet and anticoagulant agents for primary prevention of thrombosis in individuals with antiphospholipid antibodies

Cited by 27 publications

References 91 publications

17β-Estradiol Promotes Proinflammatory and Procoagulatory Phenotype of Innate Immune Cells in the Presence of Antiphospholipid Antibodies

17β-Estradiol Promotes Proinflammatory and Procoagulatory Phenotype of Innate Immune Cells in the Presence of Antiphospholipid Antibodies

Bleeding in Patients with Antiphospholipid Antibodies

Risk Assessment and Antithrombotic Strategies in Antiphospholipid Antibody Carriers

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