Affiliation:
1. The Department of Immunobiology, National Public Health Institute, Helsinki
2. Department of Medicine, University of Helsinki, Finland
Abstract
SummaryAntiphospholipid antibodies in patients with “antiphospholipid syndrome” may be directed at least in part against plasma phospholipid-binding proteins, such as Β2-glycoprotein I or prothrombin, which are involved in the control of thrombosis and haemostasis. IgG-class antibodies against prothrombin and Β2-glycoprotein I were measured by enzyme-linked immunoassay in initially healthy middle-aged dyslipid-aemic men (non-high-density lipoprotein >5.2 mml/1). Serum samples had been drawn at entry to a 5-year coronary primary-prevention trial with gemfibrozil from 106 subjects who experienced either a non-fatal myocardial infarction or cardiac death during the follow-up and from 106 subjects without coronary episodes, matched for treatment group (gemfibrozil/placebo) and geographical area.The antiprothrombin antibody level, as expressed in optical density units, was significantly higher in patients than in controls (0.26 ±0.17 versus 0.22 ±0.09; p<0.02). A high level of antiprothrombin antibodies (highest tertile of distribution) predicted a 2.5-fold increase in the risk (95% confidence interval 1.2-5.3) of myocardial infarction or cardiac death. The distribution of IgG-class antibodies against (Β2-glycoprotein I did not differ significantly between cases and controls. The joint effect of antiprothrombin antibodies and other factors associated with hypercoagulative state: triglyceride level, lipoprotein(a) and smoking, was multiplicative for the risk. Antiprothrombin antibodies are a new immunological predictor of myocardial infarction and the effect of these antibodies may be mediated by hypercoagulative mechanisms.
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