Can we withdraw anticoagulation in patients with antiphospholipid syndrome after seroconvertion?
Introduction
High morbidity and mortality due to recurrence of thrombotic events is the main concern in patients with antiphospholipid syndrome (APS) [1]. Current evidence-based guidelines recommend long-term oral anticoagulation (OAC) as prophylaxis of new thrombotic manifestations of APS. The decision on the duration and intensity of this treatment should be based on the clinical features and immunological profile. According to the guidelines, patients with definite APS and a first venous thrombotic event should receive long-term OAC to an international normalized ratio (INR) target of 2.0–3.0 (the so called conventional-intensity anticoagulation). On the other side, patients with definite APS and an arterial thrombotic event should receive high-intensity anticoagulation therapy to an INR target between 3.0 and 4.0. However, long-term OAC has also been associated to a wide broad of hemorrhagic complications [2].
Especial attention has recently been payed to a small subset of patients who fulfill APS criteria but in whom aPL become persistently negative [3].
We systematically reviewed the available evidence investigating the clinical outcome of APS patients with aPL seroconversion (negativization) in whom anticoagulation was stopped when compared to those in whom therapy was continued regardless the aPL profile. Moreover, we aim to discuss the molecular basis for the aPL pathogenicity and the available evidence of non-criteria aPL and their association with thrombosis.
Section snippets
Systematic review of the available evidence on aPL seroconversion
The aim of this systematic review is to identify the available evidence on the clinical experience of thrombotic APS patients with persistent negative aPL. We also focused on those cases where anticoagulation was stopped after patients showed persistent negativity to conventional aPL tests.
Molecular basis for the antiphospholipid antibody pathogenicity
The underlying mechanisms by which aPL can induce a thrombophilic phenotype and clinical manifestations are still under investigation. In this section, we will review the available evidence on molecular basis for aPL pathogenicity based mainly on the studies carried out by a group of the authors of the present manuscript (SS, RM, BML, LPC, CMJ). The aim to review these mechanisms is to show the profound changes that aPL induces at different levels of coagulation and inflammatory pathways.
Non-classification criteria antiphospholipid antibodies and thrombosis
Data gathered in recent years explored the relationship between three groups of antiphospholipid antibodies, not currently included in the classification criteria and the development of thrombotic events. In this section, we will summarize available data on Prothrombin/phosphatidylserine complex, antibodies directed to the Domain I of β2GPI and IgA aPL, and their association with thrombotic risk.
Conclusions
aPL seroconversion and its definition is a rising topic of interest in the field of APS. Although there are reports in the literature supporting the discontinuation of antithrombotic treatment in some patients with primary APS in whom aPL became persistently negative, we still do not have enough data to make sound recommendation whether or not and when stopping oral anticoagulation therapy in APS patients with seroconversion.
In particular, there is concern about the changes induced by aPL in
Acknowledgments
None.
Disclosure of conflicts of interest
None declared.
Funding
None declared.
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Cited by (0)
- 1
Sciascia S, Coloma-Bazán E contributed equally to this work.
- 2
Cervera R, Cuadrado MJ contributed equally to this work.