Combination of activated protein C resistance and antibodies to phospholipids in the development of thrombosis.

An insufficient response to activated protein C (APC) resistance and antibodies against phospholipids (PLa) are frequent laboratory findings associated with thrombosis. Studies investigating the coexistance of these two factors in thrombophilic patients and in patients with autoimmune disorders are summarized. The investigation of thrombophilic patients has revealed PLa in 35%. About half of these patients had a combination of PLa and APC resistance proved by the Arg506-Gln mutation in factor V (FV). A combination of APC resistance with PLa in this group of patients did not increase the risk of thrombosis recurrence. In the PLa-positive patients with autoimmune disorders having thrombosis in 10% to 56%, the incidence of the Arg506-Gln mutation in FV was significantly lower and varied between 2% and 9%. A known ability of PLa to induce APC resistance experimentally was often a reason to avoid the determination of APC response in PLa-positive patients. We suggest that PLa may play a dual role in the development of thrombosis in the carriers of the Arg506-Gln mutation in FV. On the one hand, PLas favor thrombosis by maintaining the APC response at a constantly low level. On the other hand, preventing the interaction of coagulation proteins on the phospholipid surface PLa may protect them from hypercoagulation.