THU0213 TRAASVIR STUDY: THROMBOTIC MANIFESTATIONS IN ANTIPHOSPHOLIPID ANTIBODY TRANSIENT POSITIVITY RELATED TO VIRAL INFECTIONS:

Background The mollecular pathogenesis of antiphospholipid syndrome is complex (environmental triggers, predisposed individuals). Previous studies suggested that infection may lead to the development of transiently elevated non-thrombogenic aPL antibodies. However, there are increasing case reports of patients with viral infections who develop antiphospholipid antibodies and thromboembolic events. Objectives To evaluate the role of acute viral infections in the development of thrombotic events related to aPL transitory (or permanent) positivity. Methods We include patients with a current viral infection that was diagnosed before elevated aPL antibodies were identified. One positive laboratory test either LA, aCL, or anti β2 GPI antibodies after a prior diagnosis of infection was required (< 3 months). Infection must be followed by thromboembolic manifestations (arterial or venous). A time frame of 3 months between infection diagnosis and recognition of aPL antibodies positivity was established. Normal PT and APTT test were observed in all previous patient’s blood tests. Results From January 2014 to date we have collected 40 cases with a demonstrated acute virosis and an aPL positive result with a thrombotic manifestation. 9 cases (22.5%) for Epstein-Barr virus, 17 cases (42.5%) were positive for CMV, 8 (20%) for Parvovirus B19, 3 cases were positive for Influenza A H1N1,3 for HIV, 1 for RSV, 1 for HCV and 1 case for Rotavirus. Lupus anticoagulant (L A) positivity was showed in 22 cases (55%), 15 cases (37.5%) tested positive for IgM anticardiolipin antibody and 13 cases (32.5%) also tested positive for IgM anti-β2GPI antibodies. Unfortunately, anti-prothrombin antibodies could not been analysed. The clinical manifestations were: leg deep venous thrombosis (17 cases) (42.5%), pulmonary embolism (5 cases) (12.5%), superior limbs (3 cases)(7.5%) livedoid vasculopathy (3 cases) (7.5%), splenic infarction (1 case), ovarian venous thrombosis (1 case). Only four arterial thromboses were observed: superior limbs (2 cases), digital ischemia (1case) and transverse myelitis (1 case). We have observed how the IgM virus related antibody became negative and the aPL became negative in parallel in 20/40 cases (50%). Conclusion We hypothesized that thrombotic manifestations of aPL-related acute viral infections are underdiagnosed, and probably in predisposed host, some viral infections may induce the transient apparition of aPL, mainly those with LA activity with potential pathogenic thrombotic properties. References [1] Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, Cervera R, et al. International consensus statement on an Update of classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006Feb;4(2):295-306. [2] Ascer E, Marques M, Gidlund M. M pneumoniae infection, pulmonary thromboembolism and antphospholipid antibodies. BMJ Case Rep. 2011Apr19;2011. [3] Abuaf N, Laperche S, Rajoely B, et al. Autoantibodies to phospholipids and to the coagulation proteins in AIDS. Thromb Haemost1997; 77: 856–861. Disclosure of Interests None declared