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Antiphospholipid antibody syndrome.

L R Sammaritano1, A E Gharavi

  • 1Division of Rheumatic Diseases, Hospital for Special Surgery, Cornell University Medical Center, New York, New York.

Clinics in Laboratory Medicine
|March 1, 1992
PubMed
Summary

Autoimmune antiphospholipid antibodies (aPL) cause thrombosis and pregnancy loss. Current treatments like anticoagulation and immunosuppressants lack proven efficacy, necessitating further research.

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The molecular basis of antiphospholipid syndrome.

Lupus·2003

Area of Science:

  • Rheumatology
  • Immunology
  • Hematology

Background:

  • Autoimmune antiphospholipid antibodies (aPL) are linked to thrombotic events, recurrent fetal loss, and other clinical manifestations.
  • Antiphospholipid antibody syndrome (APS) can occur independently or alongside systemic lupus erythematosus (SLE).
  • Diagnosis relies on detecting aPL via enzyme-linked immunoassay (anticardiolipin antibodies, aCL) or functional coagulation assays (lupus anticoagulant, LAC).

Purpose of the Study:

  • To summarize the clinical features, diagnostic criteria, potential mechanisms, and treatment strategies for autoimmune aPL and APS.
  • To differentiate autoimmune aPL from infection-induced aPL.
  • To highlight the current uncertainties in APS management.

Main Methods:

  • Review of existing literature on antiphospholipid antibodies and associated syndromes.
  • Analysis of diagnostic methods including aCL and LAC assays.
  • Discussion of proposed pathogenic mechanisms involving beta 2-glycoprotein I.
  • Examination of current therapeutic approaches and their limitations.

Main Results:

  • Autoimmune aPL are associated with vascular thrombosis, fetal loss, thrombocytopenia, livedo reticularis, and neurological abnormalities.
  • aPL recognition of phospholipids is influenced by antibody characteristics and phospholipid properties.
  • Beta 2-glycoprotein I is identified as a potential cofactor in aPL pathogenesis.
  • Autoimmune aPL exhibit distinct characteristics compared to infection-induced aPL.

Conclusions:

  • The precise mechanism of aPL action remains unclear, though beta 2-glycoprotein I inhibition is a leading theory.
  • Treatment for aPL syndrome is not standardized, with anticoagulation (heparin, coumadin, aspirin) being common.
  • The efficacy of corticosteroids, immunosuppressants, and plasmapheresis for severe cases requires further investigation.

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