HEPARIN COFACTOR-II DEFICIENCY IN PATIENTS INFECTED WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS

Citation
P. Toulon et al., HEPARIN COFACTOR-II DEFICIENCY IN PATIENTS INFECTED WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS, Thrombosis and haemostasis, 70(5), 1993, pp. 730-735
Citations number
54
Categorie Soggetti
Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
03406245
Volume
70
Issue
5
Year of publication
1993
Pages
730 - 735
Database
ISI
SICI code
0340-6245(1993)70:5<730:HCDIPI>2.0.ZU;2-O
Abstract
In human plasma, heparin cofactor II (HCII) is a thrombin inhibitor, w hose deficiency has been reported to be associated with recurrent thro mbosis. The finding of two cases of low plasma HCII activity in two pa tients infected with the human immunodeficiency virus (HIV) led us to investigate this coagulation inhibitor in the plasma of a larger popul ation of HIV-infected patients. The mean plasma HCII activity was sign ificantly lower in 96 HIV-infected patients than in 96 age- and sex-ma tched healthy individuals (0.75 +/- 0.24 vs 0.99 +/- 0.17 U/ml, p < 0. 0001). HCII antigen concentration was decreased to the same extent as the activity. The proportion of subjects with HCII deficiency was sign ificantly higher in the HIV-infected group than in healthy individuals (38.5% vs 2.1%). In addition, HCII was significantly lower in AIDS pa tients than in other HIV-infected patients, classified according to th e Centers for Disease Control (CDC) on the basis of an absolute number of circulating CD4+ lymphocytes below 200 x 10(6)/l. The link between HCII and immunodeficiency is further suggested by significant correla tions between HCII activity and both the absolute number of CD4+ lymph ocytes and the CD4+ to CD8+ lymphocyte ratio. Nevertheless, the mean H CII level was not different in the various groups of patients classifi ed according to clinical criteria, except in CDC IVD patients in whom HCII levels were significantly lower. In addition, no correlation coul d be demonstrated between HCII and protein S activities, another coagu lation inhibitor whose plasma level was also found to be decreased in HIV-infected patients. A similar prevalence of HCII deficiency was als o found in a small series of 7 HIV-infected patients who developed thr ombotic episodes, an unusual complication of the infection. This sugge sts that, in HIV-infected patients, HCII deficiency is not in itself t he causative factor for the development of thrombosis.