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Antiphospholipid antibodies and antiphospholipid syndrome
1Lupus Research Unit, Rayne Institute, St. Thomas' Hospital, London, UK.
Current Opinion in Rheumatology
|September 1, 1995
Summary
Antiphospholipid syndrome (APS) involves thrombosis, often linked to beta 2-glycoprotein I. Long-term anticoagulation is crucial for preventing recurrent thrombosis in APS patients.
Area of Science:
- Immunology
- Hematology
- Pathology
Background:
- Antiphospholipid syndrome (APS) is a significant autoimmune disorder characterized by recurrent thrombosis.
- Thrombosis in APS affects various vessel sizes and presents histopathologically as bland thrombi without inflammation.
- Over a decade since its detailed description, research continues to elucidate APS pathogenesis and clinical manifestations.
Purpose of the Study:
- To review current understanding of antiphospholipid syndrome (APS) pathophysiology and clinical aspects.
- To highlight new findings on the role of beta 2-glycoprotein I (β2GPI) in APS.
- To provide updated treatment recommendations for APS-associated thrombosis.
Main Methods:
- Review of recent clinical and experimental data on APS.
- Analysis of new biological insights into beta 2-glycoprotein I (β2GPI) function.
- Evaluation of histopathologic findings in APS-related thrombotic events.
Main Results:
- Animal models are yielding critical data on APS clinical and pathogenic features.
- Emerging evidence underscores the significance of beta 2-glycoprotein I (β2GPI) in APS pathogenesis.
- The presentation of phospholipid antigens is crucial, with β2GPI playing a key role.
Conclusions:
- Long-term anticoagulation therapy is essential for managing antiphospholipid syndrome (APS).
- Maintaining a high international normalized ratio (INR) is necessary to prevent recurrent thrombosis in APS.
- Further research into beta 2-glycoprotein I (β2GPI) is vital for understanding and treating APS.