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The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
Published on: November 1, 2015
Lupus, antiphospholipid syndrome, and stroke: An attempt to crossmatch
Georges El Hasbani1, Imad Uthman2
1Department of Internal Medicine, St Vincent's Medical Center, Bridgeport, CT, USA.
Insights
Systemic Lupus Erythematosus and Antiphospholipid Syndrome increase stroke risk, particularly with antiphospholipid antibodies. Management focuses on prevention and anticoagulation, though optimal strategies require further research.
Area of Science:
- Rheumatology
- Neurology
- Hematology
Background:
- Cerebrovascular accidents (CVAs), or strokes, are frequent thrombotic events in Systemic Lupus Erythematosus (SLE) and Antiphospholipid Syndrome (APS).
- Antiphospholipid antibodies (aPLs) significantly increase stroke incidence in SLE patients, often affecting large cerebral vessels.
- Mechanisms involve neuroinflammation and blood-brain barrier disruption, alongside traditional cardiovascular risk factors.
Purpose of the Study:
- To review the role of antiphospholipid antibodies in stroke pathogenesis within SLE and APS.
- To discuss current and potential therapeutic strategies for stroke prevention and management in these conditions.
- To highlight knowledge gaps regarding non-criteria aPLs and anticoagulation efficacy.
Main Methods:
- Literature review of studies on stroke in SLE and APS.
- Analysis of the impact of criteria and non-criteria antiphospholipid antibodies on cerebrovascular events.
- Evaluation of current management guidelines for primary and secondary stroke prevention.
Main Results:
- Presence of aPLs, including specific non-criteria antibodies, is an independent stroke risk factor.
- Warfarin is a secondary prevention tool, but optimal targets and combination therapies remain debated.
- Limited data exists on Direct Oral Anticoagulants (DOACs) for stroke in these patient populations.
Conclusions:
- Stroke in SLE/APS is multifactorial, with aPLs playing a key role.
- Primary prevention involves antiplatelet agents and SLE disease control.
- Further research is needed to clarify anticoagulation strategies, especially concerning novel agents and non-criteria aPLs.
Abstract:
Cerebrovascular accidents (CVAs) or strokes are part of the common thrombotic manifestations of Systemic Lupus Erythematosus (SLEs) and Antiphospholipid syndrome (APS). Such neurological thrombotic events tend to occur in patients with SLE at a higher frequency when Antiphospholipid antibodies (aPLs) are present, and tend to involve the large cerebral vessels. The mechanism of stroke in SLE can be driven by complement deposition and neuroinflammation involving the blood-brain barrier although the traditional cardiovascular risk factors remain major contributing factors. Primary prevention with antiplatelet therapy and disease activity controlling agent is the basis of the management. Anticoagulation via warfarin had been a tool for secondary prevention, especially in stroke recurrence, although the debate continues regarding the target international normalized ratio (INR). The presence of either of the three criteria antiphospholipid antibodies (aPLs) and certain non-criteria aPL can be an independent risk factor for stroke. The exact mechanism for the involvement of the large cerebral arteries, especially in lupus anticoagulant (LAC) positive cases, is still to be deciphered. The data on the role of non-criteria aPL remain very limited and heterogenous, but IgA antibodies against β2GPI and the D4/5 subunit as well as aPS/PT IgG might have a contribution. Anticoagulation with warfarin has been recommended although the optimal dosing or the utility of combination with antiplatelet agents is still unknown. Minimal data is available for direct oral anticoagulants (DOACs).
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