Anti-cardiolipin antibodies (ACA) belong to the group of anti-phospholipid antibodies (aPL). Their occurrence was first demonstrated in sera of syphilis patients, but later they have also been described frequently in SLE (systemic lupus erythematosus) patients (prevalence 30-40%) and in patients with other rheumatic diseases. The antiphospholipid syndrome (APS), also known as “Hughes syndrome”, is characterized by typical clinical features such as arterial/venous thrombosis or recurrent miscarriages together with persistently positive tests for aPL. In contrast to “secondary APS” which occurs in association with SLE or other rheumatic disorders, there is no evidence for another relevant underlying disease in primary APS. New criteria for classification of the antiphospholipid syndrome have been defined recently.
Anti-cardiolipin antibodies in infectious diseases and in APS can be distinguished with respect to their dependence on cofactors: whereas ACA from patients with infectious diseases recognize the pure phospholipid as antigen, binding of ACA from patients with APS requires β2-glycoprotein I as a cofactor. For this reason, ACA ELISAs need β2- glycoprotein I to be incorporated into the assay.
The so-called ‘lupus anticoagulant' (LA) describes a phenomenon that is related to the presence of antiphospholipid antibodies. It is defined by the measurement of antibody dependent coagulation inhibition in vitro. ACA/LA are considered to be of significant diagnostic relevance, as a correlation has been found between these antibodies and a tendency towards thromboses. This results in an increased incidence of venous/arterial thromboses, thrombocytopenia, livido reticularis, habitual abortion and neurological manifestations in ACA/LA-positive patients. Elevated levels of ACA/LA may also be found in patients with cerebrovascular insufficiency or myocardial infarction. aPL are thought to play a direct role in the pathogenesis of APS.
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