The antiphospholipid syndrome and SLE: is there a clue in the link between complement and coagulation?

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Abstract
The heterogenous immunoglobulins known as antiphospholipid antibodies (APLA) or . lupus 'anticoagulants' (LA) are prevalent in lupus patients and have been implicated in life-threatening thromboembolic events1-3. Unfortunately, observing the presence of these antibodies in an individual does not predict the likelihood of an event nor does it predict when it may occur4-6. A pathogenic role for these antibodies is supported by the observ ation that high titers and IgG isotype confer an increased risk of thromboembolism7. Addi tionally, numerous reports indicate that isolated patient antibodies interfere with various elements of the coagulation cascade8-15. Nevertheless, attempts to correlate specific anti body characteristics with the future likelihood of a hypercoagulable event in an individual patient16 have been unsuccessful to date. Given such uncertainty combined with the poten tial complications of anticoagulant medications, patients are generally not treated until sig nificant morbidity has occurred. Finally, because of the apparent high rate of reoccurrence 17 most patients must remain on anticoagulant therapy indefinitely, regardless of need.