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As previously demonstrated the risk of venous thromboembolic events appears higher in the first 6?months to 1?year after initiation of HRT and tends to decrease and even disappear overtime.1 Our patient, however, had taken this treatment for 10?years. Final diagnosis was that of a COP associated with secondary APS responsible of CVT, which is an unusual presentation. APS is a condition triggered by autoimmune and rheumatic diseases, infections, medications, neoplasms and other associations. APLa are directed against phospholipids or plasma proteins that are bound to phospholipids. They are responsible for the hypercoagulable state, the mechanism of which remains poorly understood. These antibodies include anticardiolipin and anti-�� 2-glycoprotein-I as well as lupus anticoagulant antibodies. Other autoantibodies exist and are directed against prothrombin, annexin V, phosphatidylserine, phosphatidylinositol and phosphatidylethanolamine. They must be positive in laboratory examination two times at least 12?weeks apart. Clinical expressions are related to arterial or venous thrombosis inducing deep vein thrombosis, cutaneous abnormalities, meprobamate thrombocytopenia as well as cerebrovascular disease as the most frequent neurological manifestation.2 Strokes and transient ischaemic attacks (TIAs) are the second most common clinical expression of primary antiphospholipid syndrome following venous thrombosis.3 On the other side, CVT is an extremely rare presentation of APS. This association has been poorly investigated because of the lack of reported cases and up to now, only a few were published. Meanwhile, Carhuapoma et al4 concluded that the presence of anticardiolipin antibody appears to predispose patients to develop CVT at a relatively younger age, to have more extensive cerebral venous system involvement and frequent thrombosis of the deep venous system. As a reminder, this case of CVT exhibited a right transverse and sigmoid sinus thrombus extended to proximal internal jugular vein. Moreover, Cesarman-Maus et al5 showed that antibodies against annexin A2, a binding site for ��2- glycoprotein- I that is highly expressed on cerebral endothelium, are significantly associated with autoimmune CVT. Possible therapies for APS consist in heparin, warfarin, antiplatelet agents and hydroxychloroquine. In our patient, subcutaneous UFH and LMWH were injected in the acute thrombotic phase. In addition, prednisone with co-amoxiclav was introduced for the pulmonary infiltrates. Unfortunately, the patient developed type II HIT responsible for the worsening of the thrombosis with a quasiocclusion of her cerebral sinus by local increase of the thrombus size without length extension. Type II HIT is an immune reaction against the association of heparin and platelet factor 4, a heparin neutralising protein contained in the �� granules of platelets.