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Related Experiment Video

Updated: Jul 6, 2026

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
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The antiphospholipid syndrome.

Jacob H Rand1

  • 1Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA. jacobrand@aol.com

Annual Review of Medicine
|November 5, 2002
PubMed
Summary

Antiphospholipid antibody syndrome involves blood clots and pregnancy loss. Research identifies key targets like beta2GPI, paving the way for better diagnostics and treatments for this autoimmune disorder.

Area of Science:

  • Immunology
  • Hematology
  • Autoimmune Diseases

Background:

  • Antiphospholipid (aPL) antibody syndrome is an autoimmune disorder characterized by thrombosis and/or pregnancy loss.
  • Key targets are antibodies binding to phospholipids, with phospholipid-binding cofactors like beta2GPI gaining recognition.
  • Pathogenic mechanisms involve disruption of anticoagulant pathways and induction of procoagulant factors on endothelial cells.

Purpose of the Study:

  • To review advances in understanding antiphospholipid antibody syndrome.
  • To highlight the role of phospholipid-binding cofactors as true immunologic targets.
  • To discuss current diagnostic and therapeutic strategies and future research directions.

Main Methods:

  • Review of recent scientific literature on antiphospholipid antibody syndrome.

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  • Analysis of evidence implicating phospholipid-binding cofactors (e.g., beta2GPI).
  • Evaluation of current diagnostic assays and anticoagulant therapies.

    • Main Results:

    • Beta2GPI is identified as a primary target for aPL antibodies.
    • aPL antibodies may impair anticoagulant mechanisms and promote procoagulant activity.
    • Current diagnosis relies on clinical criteria and empirical laboratory tests.

    Conclusions:

    • Understanding cofactor roles is crucial for aPL antibody syndrome.
    • Mechanistically based diagnostic tests are anticipated.
    • Improved therapies targeting disease mechanisms are expected.