Unbound MEDLINE

Antibodies to beta2-glycoprotein I: a potential marker for clinical features of antiphospholipid antibody syndrome in patients with systemic lupus erythematosus. The Journal of rheumatology. [J Rheumatol] Journal article

 
TitleAntibodies to beta2-glycoprotein I: a potential marker for clinical features of antiphospholipid antibody syndrome in patients with systemic lupus erythematosus.
Author(s)Sanfilippo SS, Khamashta MA, Atsumi T, Amengual O, Bertolaccini ML, D'Cruz D, Amft N, Swana GT, Hughes GR 
InstitutionThe Rayne Institute and Department of Immunology, St. Thomas' Hospital, London, UK.
SourceJ Rheumatol 1998 Nov; 25(11):2131-4.
MeSHAdult
Aged
Antibodies
Antibodies, Anticardiolipin
Antibodies, Antinuclear
Antiphospholipid Syndrome
Biological Markers
DNA
Enzyme-Linked Immunosorbent Assay
Female
Glycoproteins
Humans
Immunoglobulin G
Lupus Erythematosus, Systemic
Male
Middle Aged
Research Support, Non-U.S. Gov't
Risk Factors
AbstractOBJECTIVE: To clarify risk factors for the development of clinical features of antiphospholipid syndrome (APS) in patients with anticardiolipin antibodies (aCL) in systemic lupus erythematosus (SLE).
METHODS: We studied 65 SLE patients, all with positive IgG and/or IgM aCL. Patients were divided into 2 groups; I: 29 SLE patients with features of APS (SLE/APS) and II: 36 aCL positive SLE patients without any feature of APS (SLE/aCL). Serum samples were collected from our serum bank. Anti-beta2-glycoprotein I (anti-beta2-GPI) were tested by ELISA using irradiated plates in the absence of cardiolipin. Anti-dsDNA antibodies were tested by standard Farr assay.
RESULTS: There were no major differences between SLE clinical manifestations in both groups. However, the frequency of IgG anti-beta2-GPI was markedly increased in SLE/APS (18/29, 62%) than in SLE/aCL (4/36, 11%) (chi-squared 18.6, p=0.0001). The levels of anti-dsDNA antibodies in the same samples were slightly lower in SLE/APS.
CONCLUSION: Our data suggest that increased levels of IgG anti-beta2-GPI may be a specific feature of SLE/APS patients rather than reflecting a polyclonal B cell activation.
Languageeng
Pub Type(s)Journal Article
PubMed ID9818654
  
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