CORRELATION OF ANTIPHOSPHOLIPID ANTIBODIES AND PROTEIN-S DEFICIENCY WITH THROMBOSIS IN HIV-INFECTED MEN

Citation
Kl. Hassell et al., CORRELATION OF ANTIPHOSPHOLIPID ANTIBODIES AND PROTEIN-S DEFICIENCY WITH THROMBOSIS IN HIV-INFECTED MEN, Blood coagulation & fibrinolysis, 5(4), 1994, pp. 455-462
Citations number
31
Categorie Soggetti
Hematology
ISSN journal
09575235
Volume
5
Issue
4
Year of publication
1994
Pages
455 - 462
Database
ISI
SICI code
0957-5235(1994)5:4<455:COAAAP>2.0.ZU;2-I
Abstract
Antiphospholipid antibodies (aPL) and free protein S (PSF) deficiency have been associated with clinical thrombosis. Previous reports descri bed a high prevalence of these abnormalities in HIV-infected individua ls, but suggested there was little associated clinical thrombosis. A c ohort of 74 HIV-infected men were studied for aPL, PSF deficiency and the development of thrombosis. aPL, predominantly anticardiolipin anti bodies (aCL), were detected in 86% and PSF deficiency in 33%. While 42 % of men with aPL also had low PSF levels, there was no correlation be tween aCL titres or most measures of aPL and PSF levels. However, a st rong correlation was noted between a subset of aPL that reacted to pho sphatidyfethanolamine by hexagonal array assay and low PSF levels. The re was no significant correlation between aPL, PSF deficiency and clin ical features (medication use, opportunistic infection, CD4 cell count ) of HIV in 60 patients for whom clinical information was available. T he overall incidence of thrombosis in this group was 18%, and thrombos is developed in 6.6% of those followed prospectively over a median fol low-up of 12 months. Development of thrombosis was not significantly c orrelated with aPL or PSF deficiency, but the high prevalence of these abnormalities may necessitate larger study groups to determine the ri sk associated with these coagulation changes. Study of a larger group with careful analysis of subsets of aPL, especially those associated w ith low PSF levels, and longer clinical follow-up could identify the H IV-infected individuals at risk for thrombosis.