Prevalence rates of antiphospholipid antibodies in ischemic stroke patients.

In cerebrovascular disorders with an underlying immune abnormality, antiphospholipid antibodies, of which there are numerous types, are the leading cause of thrombosis in the absence of acquired risk factors (1). To define and characterise these antibodies, we studied their prevalence rates in patients who had experienced cerebral infarction, and investigated the relationships among the antibodies. This study involved 250 patients, 155 males and 95 females (average age 72 years), with cerebral infarction who visited our hospitals. Of these patients, one male and four females (average age 39 years) had systemic lupus erythematosus (SLE) as an underlying disease. Levels of antiphospholipid antibodies, including β2-glycoprotein I-dependent anticardiolipin antibody (β2-GPI aCL), IgG anticardiolipin antibody (IgG aCL), lupus anticoagulant (LA), phosphatidylserine-dependent antiprothrombin antibody (PS/PT), antiphosphatidylserine antibody (PS), and antiphosphatidylinositol antibody (PI), were determined in the 250 patients. The level of antinuclear antibody was also measured in patients positive for PI or PS. Assessment of the presence of various antibodies was carried out in patients in the chronic stage, at least 1 month after the onset of all type of cerebral infarction. Fig. 1 shows the prevalence rates of the antibodies in the 250 patients with cerebral infarction. They were 2.8% (7/ 250) for β2-GPI aCL, 12.0% (30/250) for IgG aCL, 9.2% (23/250) for LA, 7.2% (18/250) for PS/PT, 9.6% (24/250) for PS, and 8.8% (22/250) for PI. Among the 23 patients positive for LA, 18 (78.2%) were also positive for PS/PT. Patients aged 50 years or under accounted for 5.2% of the 250 patients (13/250), and of these, 5 had underlying SLE (1 male and 4 females, average age 39). Of these 5 patients, 80% (4/5) were positive for both β2-GPI aCL and LA, and 40% were positive for PI or PS as well asβ2-GPI aCL or LA. One was negative for β2-GPI aCL and LA, and positive for PI, PS, and PS/PT. Among the 250 patients, 13.6% (34/250) were positive for either PI or PS, and 6.8% (17/250) were positive for both. Of the 34 patients positive for either PI or PS, 8.8% (3/34) were positive for LA and 8.8% (3/34) were positive for β2-GPI aCL, with 70.6% (24/34) positive for antinuclear antibody. One patient was positive for all of PI, PS, β2-GPI aCL, LA, and antinuclear antibody. Previous reports have suggested that the presence of antiphospholipid antibody is a risk factor for cerebral infarction in those aged under 45 or 50 years (2). The Antiphospholipid Antibodies in Stroke Study (APASS) (3) reported that in patients with antiphospholipid antibody, the risk of cerebral infarction was 2.31 times higher than in those negative for the antibody, and Brey et al (4) reported a 1.5 times higher risk over an observation period of 20 years. In our study of 250 patients with cerebral infarction, the prevalence rates of the antiphospholipid antibodies β2-GPI aCL, LA, PI, PS, and PS/PI were higher in patients aged 50 or under with underlying SLE than in those without SLE, suggesting that the presence of antiphospholipid antibody may be a risk factor for cerebral infarction in young adult in SLE patients. Antiphospholipid antibodies include anticardiolipin antibody, LA, and antibodies specific to anionic phospholipids, including PS and PI (5). As mentioned above, PI and PS were detected in 9.6% and 8.8%, respectively, of the 250 patients with cerebral infarction, and 79.2% of these patients tested positive for antinuclear antibody. Of the 250 patients, there