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
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.