Antiphospholipid antibody syndrome |
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Authors: | Bradley S. Jacobs MD Steven R. Levine MD |
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Affiliation: | (1) Department of Neurology, University Health Center, Wayne State University School of Medicine, 8C, 4201 St. Antoine, 48201-2153 Detroit, MI, USA |
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Abstract: | Opinion statement When the diagnosis of antiphospholipid antibody syndrome (aPS) is being considered in persons who have experienced an ischemic stroke or a transient ischemic attack, it is important to gauge how well the history and laboratory data fit with this diagnosis as opposed to other causes of infarct. The fewer the number of typical vascular disease risk factors and the more confirmatory the laboratory findings (ie, high anticardiolipin antibody titers or presence of lupus anticoagulant), the stronger the suspicion of aPS. There are no good prospective randomized data on stroke prevention with any form of therapy following a first stroke or transient ischemic attack associated with antiphospholipid antibody (aPL). Short-term anticoagulation with an International Normalized Ratio (INR) of 2.0 to 3.0 may be considered in these cases, as could antiplatelet agents if no clear cardiac source is found. If anticoagulation is chosen, if there is no recurrence, and if the level of aPL appears to decline, a change to a stroke prevention medication that may carry less risk, such as an antiplatelet agent, may be appropriate. In patients with more typical vascular disease risk factors and less confirmatory laboratory evidence of aPS (ie, low to moderate titer of anticardiolipin antibodies and lack of other clinical or serologic evidence of aPS), a more conservative approach may be considered and antiplatelet therapy initiated. In either situation, close follow-up for recurrent thrombosis and aPL can help determine whether more or less aggressive (risky) therapies should be considered. Results of randomized controlled trials of different treatment options for aPS are awaited. |
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