A perturbation of antithrombin-III and protein C coupling associates with an increase of anti-β2-glycoprotein I antibody in non-antiphospholipid antibody syndrome cerebral ischemia

Anti-beta2-glycoprotein I antibody (abetaGPI) has been recognized in raising the risk of cerebral ischemia in patients with antiphospholipid antibody syndrome (APS), especially by protein C (PC) axis perturbation. Although a high potential is also seen in non-APS patients, the mechanism is substantially unknown. In the present study, we examined the effect of abetaGPI on PC and antithrombin-III (AT-III) activity in non-APS patients with non-cardiac cerebral ischemia (NCCI). A total of 111 NCCI patients and 30 healthy controls were enrolled. They were free of APS manifestation, and their anticardiolipin antibody and lupus anticoagulant tests were within normal range. There were 14.4% patients found to have an abnormal increase of blood OGPL The PC, AT-III, albumin, aminotransferases, creatinine, prothrombin time and activated partial thromboplastin time did not differ between our patients and controls, or patients with or without increased abetaGPI. However, a marked decrease of the PC/AT-III ratio was found in patients with increased abetaGPI. The correlation between PC and AT-III activity was highly significant in patients with an increase of abetaGPI (P = 0.001), only marginal in controls (P = 0.042), and was insignificant in patients with a normal abetaGPI (P = 0.277). The abetaGPI did not correlate to PC or AT-III activity in either patients or controls. These findings suggest that high PC/AT-III coupling may relate to NCCI in non-APS patients associated with an increase of abetaGPI. This coupling effect seems not to be caused by abetaGPI directly. (C) 2002 Lippincott Williams Wilkins.