ASSESSMENT OF SOME PROTHROMBOTIC ACUTE PHASE REACTANTS IN HIV INFECTED NIGERIANS
Abstract
Background
HIV infection is known to increase the risk of venous thromboembolism by
2 to 10 folds. Studies have included the traditional risk factors such as
prolonged ill health, hospitalization, infection and the use of protease
inhibitors as possible causes. HIV infection being a chronic inflammatory
disease induces a derangement in the levels of positive and negative acute
phase reactants which may contribute to endothelial cell dysfunction thus
increasing thromboembolic risk.
This study aimed to evaluate acute phase reactants antithrombin and
plasminogen activator inhibitor-1 (PAI-1) as markers of increased
predisposition to thrombosis in HIV infected persons and comparing their
levels with D-dimer levels- a marker of fibrinolysis and with fibrinopeptides
A and B- markers of thrombogenesis. The presence (or not) of asymptomatic
thrombosis in both lower limbs of HIV infected persons using Doppler
ultrasonography was also determTo document the presence of asymptomatic
thrombosis in both lower limbs using Doppler ultrasound scan.
Patients and Methods
This was a cross-sectional study conducted on HIV infected participants and
HIV negative control population. A total of 240 participants were recruited in
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the study. This included 80 persons in the control group and 80 persons in the
HAART exposed and HAART naïve groups respectively. HAART exposed
group were virologically suppressed at the time of the study. Investigations
carried out included complete blood count, ALT, creatinine, CD4+ cell count,
HIV RNA load. Antithrombin, PAI-1, D-dimer, fibrinopeptides A and B were
measured using ELISA based technique.
Results
The mean antithrombin levels for the control (132.0±65.5ng/ml) was
significantly higher in the control group than the HAART exposed group
(111.6±49.8ng/ml) p=0.04. It was also higher in the control group than the HIV
infected treatment naïve group (119.0±48.55ng/ml) but the difference was not
significant. P=0.642. Antithrombin levels were low in 12% of the HIV infected
individuals as compared with 1.25% in the control subjects. (χ2=14.35;
p=0.002).
The mean PAI-1 level for the control population (26.15±7.06ng/ml) was not
significantly different from that obtained for the HAART exposed HIV
participants (27.29±6.36ng/ml) p=0.517 but it was significantly than the level
obtained the HAART naïve subjects. (32.41±6.27ng/ml) P=0.0000.
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PAI-1 was shown to be positively correlated with D-dimer levels (r=0.226;
p=0.002) while antithrombin deficiency showed a significant negative
correlation with D-dimer levels (r=-0.253, p=0.001).
Antithrombin deficiency was negatively correlated with fibrinopeptides A and
B levels but this did not reach significant levels (p>0.05). PAI-1 was positively
correlated with the fibrinopeptides.
Doppler studies showed no evidence of thrombosis in the HIV infected
participants.
Conclusion
This study has demonstrated raised levels firinopeptides A and B, raised level
of PAI 1 and reduced levels of antithrombin III in HIV infected subjects
indicating presence of thrombotic state. Failure to demonstrate sonographic
evidence of thrombosis coupled with raised levels of D-dimer suggest that the
prothrombotic state is mild and that any thrombus formed is lysed.