Anti-β2 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 anticardiolipin antibodies (aCL) reflects in vivo platelet activation. However the majority of autoimmune aPL are directed to beta(2) glycoprotein I (beta(2)GPI) or prothrombin (II). We investigated the relationship of these antibodies with 11-DH-TXB2 urinary excretion in 33 patients with aPL. The urinary 11-DH-TXB2 was measured by EIA after extraction on octadecyl columns and purification on silica gel columns, which was validated by thin-laver chromatography/EIA procedure. A significantly increased 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 excretion 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 moderate/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 correlation 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 data show that the observed platelet activation in aPL patients is related to the presence of antibodies reacting with beta(2)GPI.