Lupus anticoagulant and thromboembolism: Evaluation of fibrinogen, natural inhibitors and molecular markers of thrombosis

It has been speculated that an impairment in anticoagulant pathways (protein C (PC), protein S (PS), resistance to activated protein C (APC)), may contribute to the thrombotic tendency in lupus anticoagulant (LA) patients. Increased plasma levels of fibrinogen are predictive for arterial thrombosis and increased molecular markers of thrombosis are indicative for activation of the clotting cascade. We investigated 25 patients (20 women) with Lk All patients were stratified according to their thromboembolic history and women according to their history of fetal loss. Eighteen patients had a history of venous or arterial thrombosis, or both Seven of 16 women with at least one pregnancy had a history of fetal loss. The interrelation among the levels of fibrinogen, PC and PS, and resistance to APC, thrombin-antithrombin III complexes (TAT), prothrombin fragment F1 + 2, D-dimer and the history of thrombotic events and obstetric complications in patients with LA were evaluated LA patients with a history of venous or arterial thrombosis had a significantly higher fibrinogen level than LA patients without (mean 366 versus 304 mg/dl; P=0.018). Among 16 women a slightly lower mean TAT level in women with fetal loss was found (24 versus 43 ng/ml; P=0.02). No other statistically significant difference in the remaining parameters was yielded in both analyzed subgroups. The results of the study suggest an association between increased fibrinogen levels and the history of venous or arteria thrombosis, or both, in patients with Lk In the other investigated parameters, no relationship to the thrombotic or obstetric history was found.