Abstract

Acquired thrombophilia is commonly associated with detection of autoantibodies against phospholipid-protein complexes that include lupus anticoagulant, anticardiolipin antibodies, anti-prothrombin and anti-beta-2 glycoprotein I antibodies. The anti-phospholipid syndrome is present when these autoantibodies are found in association with clinical manifestations that include venous or arterial thromboembolism or pregnancy morbidity, such as recurrent spontaneous miscarriages, fetal deaths, second or early third trimester fetal deaths or fetal growth retardation. Because the diagnosis of antiphospholipid syndrome is based on laboratory data, optimal performance and interpretation of the tests is essential. However, heterogeneity of the autoantibodies and absence of gold standard assays makes analysis of laboratory results a challenge for pathologists and clinicians alike. As a further complication to rational use and interpretation of the tests, the causal relationship of aPLs and thrombosis is difficult to establish as they are present in normal, asymptomatic individuals, with thrombotic events occurring only in approximately 30% of patients with antiphospholipid antibodies. Obstetric complications are also difficult to correlate meaningfully with test results because of heterogeneity in study populations, and changes in anti-coagulant management and the threshold for its use in everyday practice over time. Characterisation of the molecular basis of the pathogenic mechanisms involved in the syndrome will hopefully provide a more rational basis for definition of the syndrome, the use of diagnostic tests and management in the future.

Full Text
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