Systemic lupus erythematosus (SLE) is a potentially fatal multiorgan inflammatory disease that primarily affects females. Due to the heterogeneity of clinical manifestations and lack of laboratory tests that are both specific and sensitive for the disease, diagnosis of SLE can often be difficult. Although the precise etiology remains to be fully elucidated, it is probable that various environmental, genetic, and hormonal factors contribute to the development of the disease. Patients with SLE have an increased risk for premature thrombosis and/or atherosclerosis, with up to half experiencing a thrombotic event. Furthermore, antiphospholipid antibodies probably play a key role in the development of thrombosis by affecting various hemostatic protein interactions with phospholipids and cell surfaces as well as platelet function. Despite recent advances in knowledge related to the factors that contribute to the pathophysiology of SLE, numerous challenges related to earlier diagnosis as well as the prediction and prevention of thrombotic events remain to be fully addressed.
Antiphospholipid antibodies contribute to the development of thrombosis, although precise mechanisms remain to be elucidated. We determined the effects of affinity-purified anti-beta(2)-glycoprotein 1 (anti-β(2)GP1) and anti-prothrombin (anti-PT) antibodies on in vitro platelet aggregation. Adenosine diphosphate (ADP) and collagen-induced platelet aggregation were performed using platelet-rich plasma ([PRP] 250 × 10(9)/L). Antiphospholipid antibodies (1.25-10 μg/mL) were preincubated with PRP for 10 minutes at 37°C prior to the addition of agonist. Anti-β(2)GP1 antibodies significantly reduced platelet aggregation (percentage area under the curve; %AUC) in a concentration-dependent manner using both 5 μmol/L (P < .001) and 2.5 μmol/L (P = .038) ADP but did not significantly affect the rate of aggregation. Anti-PT antibodies significantly enhanced 5 µg/mL collagen-induced platelet aggregation (%AUC; P = .034) but did not affect ADP-induced platelet aggregation. These results suggest (1) interactions and effects of antiphospholipid antibodies on platelets are agonist and concentration dependent and (2) anti-β(2)GP1 antibodies may inhibit dense granule release and/or inhibition of the arachidonic acid pathway.
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