AUTOANTIBODIES DIRECTED AGAINST PHOSPHOLIPIDS OR HUMAN BETA(2)-GLYCOPROTEIN-I IN HIV-SEROPOSITIVE PATIENTS - RELATIONSHIP WITH ENDOTHELIAL ACTIVATION AND ANTIMALONIC DIALDEHYDE ANTIBODIES

Citation
J. Constans et al., AUTOANTIBODIES DIRECTED AGAINST PHOSPHOLIPIDS OR HUMAN BETA(2)-GLYCOPROTEIN-I IN HIV-SEROPOSITIVE PATIENTS - RELATIONSHIP WITH ENDOTHELIAL ACTIVATION AND ANTIMALONIC DIALDEHYDE ANTIBODIES, European journal of clinical investigation, 28(2), 1998, pp. 115-122
Citations number
53
Categorie Soggetti
Medicine, Research & Experimental","Medicine, General & Internal
ISSN journal
00142972
Volume
28
Issue
2
Year of publication
1998
Pages
115 - 122
Database
ISI
SICI code
0014-2972(1998)28:2<115:ADAPOH>2.0.ZU;2-F
Abstract
Background We investigated the possible role of antiphospholipid (APA) and anti-human (2)-glycoprotein I (beta(2)-GPI) antibodies (Ab) in th rombosis and atherosclerosis in human immunodeficiency (HIV)-positive patients, in whom they seem to be more frequent. Methods We measured A PA and anti-beta(2)-GPI Ab in 58 HIV-positive patients together with m arkers of disease progression, circulating beta(2)-GPI, plasma lipids, biological markers of endothelial activation and integrity (plasma th rombomodulin, von Willebrand factor, vascular cell adhesion molecule 1 ) and with antimalonic dialdehyde antibodies (anti-MDA Ab). Results We found a 41% frequency of IgG APA in the HIV-positive patients. APA Ig Ms were rarely positive (7%), and anti-beta(2)-GPI IgGs were positive in 3.4% patients. There was no correlation between APA or anti-beta(2) -GPI Ab and the presence of opportunistic infections. Although plasma thrombomodulin, von Willebrand factor and vascular cell adhesion molec ule 1 were significantly increased in the HIV-positive patients, APA w as correlated only with vascular cell adhesion molecule 1, suggesting that APAs are correlated with endothelial activation but not with vasc ular endothelial lesions. A correlation between APA and anti-MDA IgG w as demonstrated using multivariate analysis (r = 0.542, P < 0.0001), s uggesting a relationship between the targets of these antibodies. Fina lly, IgG APAs are frequent in HIV infection but are not correlated wit h biological markers of endothelial injury. Conclusion Our results do not support a role for APA or anti-beta(2)-GPI in HIV-associated silen t vascular endothelial damage. However, the role of these autoantibodi es in clinically relevant thrombotic events should be investigated in HIV-positive patients.