Background Thrombocytopenia is a non-criteria manifestation of antiphospholipid syndrome (APS). Antiphospholipid antibodies (aPL) have been shown to activate platelet through multiple mechanisms. In patients with idiopathic/immune thrombocytopenia, aPL have been shown to increase the risk of thrombosis. Conversely, it remains unclear whether thrombocytopenia increases the risk of thrombosis in patients who have aPL.
Objectives To evaluate the relationship between thrombocytopenia and thrombosis in patients who have aPL.
Methods A single center retrospective study comprising 670 consecutive patients who underwent testing for aPL including lupus anticoagulant, anticardiolipin antibodies (IgG and M), anti-β2-glycoprotein I antibodies (IgG and M), and phosphatidylserine-dependent antiprothrombin antibodies (IgG and M) between January 2004 and December 2006. Excluded were patients who had been followed-up for ≤1 year.
Results Of 524 patients included in this study, 187 had systemic lupus erythematosus, 70 rheumatoid arthritis, and 33 primary APS. At least one of aPL was positive in 241 patients. The prevalence of thrombocytopenia was not different in aPL positive and negative patients (24% vs 18%, p=0.11). In aPL positive group, patients with thrombocytopenia experienced arterial thrombosis (46% vs. 17%, p<0.001), venous thrombosis (27% vs. 7%, p<0.001), and recurrent thrombosis (10% vs. 2%, p=0.006) more frequently than patients without thrombocytopenia. Lupus anticoagulant (56% vs. 35%, p=0.006) and phosphatidylserine-dependent antiprothrombin antibodies (57% vs 34%, p=0.001) were more prevalent in patients with thrombocytopenia than in those without. Higher aPL score (Otomo K, et al. Arthritis Rheum 2012), were detected higher (p=0.001) in patients with thrombocytopenia than in those without. In aPL negative group, conversely, patients with and without thrombocytopenia similarly experienced thrombosis (23% vs 16%, p=0.23).
Conclusions Our data indicate that thrombocytopenia is associated with the risk of thrombosis in aPL positive patients providing new insight into the pathophysiology of aPL mediated platelet activation.
Disclosure of Interest None declared