Treatment of thrombosis associated with immunological risk factors

The clinical management of the antiphospholipid syndrome is aimed at assess ing the thrombotic risk of an individual in order to undertake primary prev ention for the asymptomatic subject positive for antiphospholipid antibodie s or prophylaxis of major ischaemic events for the patient who has already experienced thrombosis. Lack of immunological parameters with a clear predi ctive value and the current concept that thrombosis is a multifactorial dis ease suggest that all the known acquired and genetic thrombotic risk factor s should be taken into account in antiphospholipid syndrome. Low-dose aspir in and hydroxychloroquine have been proven useful in primary prevention. Wh ile convincing evidence has been provided that aspirin and hydroxychloroqui ne do not prevent secondary thrombosis, much debate has recently developed on the level of oral anticoagulation needed to guarantee this prevention. M ain concerns are also related to duration of anticoagulation therapy, risk of bleeding, and the increased risk of thrombosis as a result of withdrawal of the anticoagulant. Low-molecular-weight heparin has recently emerged as a valid and safe alternative for those conditions that require transient i nterruption or withdrawal of anticoagulation. Although treatment of the cat astrophic antiphospholipid syndrome is largely empirical, the therapeutic a pproach based on plasmapheresis associated with immunosupression or intrave nous immunoglobulin seems to be the most promising. Most attention has rece ntly been paid to the role of oxidative stress in the pathogenesis of antip hospholipid syndrome, as a correlation between lipid peroxidation and antip hospholipid antibodies has been demonstrated. Our studies showed that lipid peroxidation may contribute to the activation of the dotting system observ ed in antiphospholipid syndrome and that markers of both procoagulant state and increased lipid peroxidation can be modified by experimental antioxida nt treatment.