The mechanism of thrombosis with inflammation was complex, for example, tumor necrosis factor-alpha (TNF-α) and CRP could induce white blood cells to express tissue factors and activate endogenous coagulation, TNF-α and interleukin 1 beta inhibited the anticoagulation system of protein C and antithrombin III, CRP suppressed fibrinolytic activity, and thus promoted thrombosis.[15,16] The antiphospholipid antibodies including lupus anticoagulant, anticardiolipin (aCL) antibodies, and antiphosphatidic acid antibody had positive effect on thrombosis. Here, CRP is linked to systemic lupus erythematosus.