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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2000-6-27
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pubmed:abstractText |
We examined the role of autoantibodies to beta2-GPI and prothrombin (PT) in the inhibition of annexin V binding to cardiolipin (CL) and the association with clinical manifestations of the anti-phospholipid syndrome (APS). Plasma samples from 59 patients with anti-phospholipid (aPL) antibodies were studied. Affinity purification of total IgG and IgG anti-ss2-GPI antibodies was performed using staphylococcal protein A and phospholipid liposomes. Annexin V binding to CL was significantly inhibited by 31/59 (53%) aPL+ plasma samples. There was a significant association between annexin V inhibition and elevated levels of IgG anti-cardiolipin (aCL) (r = -0.62; P < 0.001), IgG anti-ss2-GPI (r = -0.67; P < 0. 001) and a weaker association with lupus anti-coagulant (r = -0.27; P = 0.05). There was no association with other isotypes of aCL and anti-ss2-GPI or with anti-PT of any isotype. In patients with clinical manifestations of the APS there were higher levels of IgG aCL (median (range) Z score): 10.0 (0-17.6) versus 5.0 (0-16.1); P = 0.03), IgG anti-ss2-GPI (4.5 (0-11.3) versus 0.9 (0-9.7); P = 0.02) and greater inhibition of annexin V binding to CL (-3.4 (-11.4-0.6) versus -1.1 (-10.8-1.2); P = 0.22). Odds ratios for the laboratory assays and the presence of clinical manifestations of the APS varied between 0.38 and 4.16, with the highest values for IgG aCL (4.16), IgG anti-ss2-GPI (3.28) and annexin V inhibition (2.85). Additional experiments with affinity-purified IgG antibodies indicated that inhibition of annexin V binding was dependent upon the concentration of ss2-GPI and anti-ss2-GPI antibodies. These results indicate that inhibition of annexin V binding to procoagulant phospholipid surfaces is dependent upon anti-ss2-GPI antibodies and suggest a role for annexin V in the pathogenesis of the APS.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10844535-10211887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10844535-10225244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10844535-10403256,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/10844535-9716593
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
120
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
537-43
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10844535-Annexin A5,
pubmed-meshheading:10844535-Antibodies, Antiphospholipid,
pubmed-meshheading:10844535-Antiphospholipid Syndrome,
pubmed-meshheading:10844535-Cardiolipins,
pubmed-meshheading:10844535-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:10844535-Glycoproteins,
pubmed-meshheading:10844535-Humans,
pubmed-meshheading:10844535-Immunoglobulin G,
pubmed-meshheading:10844535-Membrane Glycoproteins,
pubmed-meshheading:10844535-Prothrombin,
pubmed-meshheading:10844535-beta 2-Glycoprotein I
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pubmed:year |
2000
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pubmed:articleTitle |
Anti-beta2-glycoprotein I (GPI) autoantibodies, annexin V binding and the anti-phospholipid syndrome.
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pubmed:affiliation |
Division of Rheumatology, Department of Medicine, Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia, Canada. jhanly@is.dal.ca
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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