ANTI-BETA(2) GLYCOPROTEIN-I ANTIBODIES AND PLATELET ACTIVATION IN PATIENTS WITH ANTIPHOSPHOLIPID ANTIBODIES - ASSOCIATION WITH INCREASED EXCRETION OF PLATELET-DERIVED THROMBOXANE URINARY METABOLITES

Platelet activation may contribute to the increased risk of thrombotic complications in patients with antiphospholipid antibodies (aPL). The increased urinary excretion of 11-dehydro-thromboxane B-2 (11-DH-TXB2 ) reported in patients with lupus anticoagulant (LA) and/or anticardio lipin antibodies (aCL) reflects in vivo platelet activation. However t he majority of autoimmune aPL are directed to beta(2) glycoprotein I ( beta(2)GPI) or prothrombin (II). We investigated the relationship of t hese antibodies with 11-DH-TXB2 urinary excretion in 33 patients with aPL. The urinary 11-DH-TXB2 was measured by EIA after extraction on oc tadecyl columns and purification on silica gel columns, which was vali dated by thin-laver chromatography/EIA procedure. A significantly incr eased excretion of 11-DH-TXB, was found in aPL patients as compared to 18 normal controls (p < 0.01). But no differences were seen in the ex cretion of 11-DH-TXB2 between patients with or without LA, or aCL. The number of patients with anti-II antibodies was too small to draw any conclusion. In contrast, patients with anti-P,GPI antibodies IgG at mo derate/high titre (group A, n = 14) had higher levels of urinary 11-DH -TXB2 than those at low titre or negative (group B, n = 20) (p = 0.01) . The group A of patients presented an increase in 11-DH-TXB, compared to controls (p < 0.001), but no statistically significant difference was found between patients from the group B and normal controls. A cor relation between levels of urinary 11-DH-TXB, and titre of antibodies was only found for anti-beta(2)GPI-IgG (r(5) = 0.51, p < 0.005). Our d ata show that the observed platelet activation in aPL patients is rela ted to the presence of antibodies reacting with beta(2)GPI.