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von Willebrand Factor is elevated in HIV patients with a history of thrombosis.

van den Dries LW, Gruters RA, Hövels-van der Borden SB, Kruip MJ, de Maat MP, van Gorp EC, van der Ende ME - Front Microbiol (2015)

Bottom Line: Arterial and venous thrombotic events are more prevalent in HIV infected individuals compared to the general population, even in the era of combination antiretroviral therapy.The incidence of venous thrombosis was two-fold higher in HIV infected patients compared to age-adjusted data from general population cohort studies.This could be a reason to prolong anti-thrombotic treatment in HIV patients with a history of thrombosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Viroscience, Erasmus MC, University Medical Center Rotterdam, Netherlands.

ABSTRACT

Background: Arterial and venous thrombotic events are more prevalent in HIV infected individuals compared to the general population, even in the era of combination antiretroviral therapy. Although the mechanism is not fully understood, recent evidence suggests a role for chronic immune activation.

Methods: We reviewed the Dutch National HIV registry database for HIV infected patients in Rotterdam with a history of arterial or venous thrombosis and calculated the incidence. We collected samples from patients with and without thrombosis and compared plasma levels of lipopolysaccharide (LPS), LPS binding protein (LBP), soluble CD14 (sCD14), and von Willebrand Factor antigen level (vWF).

Results: During a 10-year period, a total of 60 documented events in 14,026 person years of observation (PYO) occurred, resulting in an incidence rate of 2.50, 2.21, and 4.28 for arterial, venous and combined thrombotic events per 1000 PYO, respectively. The vWF was elevated in the majority of study subjects (mean 2.36 SD ± 0.88 IU/ml); we found a significant difference when comparing venous cases to controls (mean 2.68 SD ± 0.82 IU/ml vs. 2.20 SD ± 0.77 IU/ml; p = 0.024). This difference remained significant for recurrent events (mean 2.78 SD ± 0.75; p = 0.043). sCD14 was positively correlated with LPS (r = 0.255; p = 0.003).

Conclusion: The incidence of venous thrombosis was two-fold higher in HIV infected patients compared to age-adjusted data from general population cohort studies. We couldn't find a clear association between immune activation markers to either arterial or venous thrombotic events. We observed a marked increase in vWF levels as well as a correlation of vWF to first and recurrent venous thrombo-embolic events. These findings suggest that HIV infection is an independent risk factor for coagulation abnormalities and could contribute to the observed high incidence in venous thrombosis. This could be a reason to prolong anti-thrombotic treatment in HIV patients with a history of thrombosis.

No MeSH data available.


Related in: MedlinePlus

Plasma levels of LPS (N = 101), LBP (N = 130), sCD14 (N = 130), and vWF antigen (N = 93) in chronic HIV infected individuals with or without a history of arterial or venous thrombotic disease. Horizontal bar represents median for LPS, LBP, and sCD14; and mean in vWF. Cases had a significantly higher vWF antigen level as compared to controls. Gray, controls without a thrombotic event; red, arterial events; blue, venous events; green, both arterial and venous events. LPS, Lipopolysaccharide; LBP, LPS binding protein; sCD14, soluble CD14; vWF, von Willebrand Factor antigen level. *p = 0.024 for venous events vs. controls.
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Figure 2: Plasma levels of LPS (N = 101), LBP (N = 130), sCD14 (N = 130), and vWF antigen (N = 93) in chronic HIV infected individuals with or without a history of arterial or venous thrombotic disease. Horizontal bar represents median for LPS, LBP, and sCD14; and mean in vWF. Cases had a significantly higher vWF antigen level as compared to controls. Gray, controls without a thrombotic event; red, arterial events; blue, venous events; green, both arterial and venous events. LPS, Lipopolysaccharide; LBP, LPS binding protein; sCD14, soluble CD14; vWF, von Willebrand Factor antigen level. *p = 0.024 for venous events vs. controls.

Mentions: For patient characteristics of subjects that underwent analysis of sCD14, LPS, LBP, and vWF please see Supplementary Table 1. Patients with a thrombotic event in the past had a higher mean vWF antigen level when compared to controls (venous: 2.68 SD ± 0.82 IU/ml; arterial: 2.31 SD ± 1.10 IU/ml; both: 2.74 SD ± 0.90 IU/ml; controls: 2.20 SD ± 0.77 IU/ml). The difference in vWF antigen levels was significant in patients with a past venous event compared to controls (p = 0.024, Independent samples T-test) (Figure 2), which remained significant when comparing only recurrent events to controls (2.78 SD ± 0.75; p = 0.043 Independent Samples T-test, Figure 3). The significance of difference in vWF antigen level between cases combined vs. controls varied upon the applied statistical test (p = 0.047, Mann Whitney; p = 0.071 Independent samples T-test). There was no clear connection between time since thrombotic event and the level of vWF antigen (see Figure 4). There was no significant difference between cases and controls in sCD14 (median: 2.45 IQR ± 2.08 vs. 2.31 IQR ± 1.36; p = 0.341) and LBP (median: 20.19 IQR ± 17.56 vs. 16.63 IQR ± 15.05 μ/ml; p = 0.264) as well as LPS (median: 12.19 IQR ± 24.70 vs. 10.76 IQR ± 23.58) although values tended to be higher in cases (Figure 2).


von Willebrand Factor is elevated in HIV patients with a history of thrombosis.

van den Dries LW, Gruters RA, Hövels-van der Borden SB, Kruip MJ, de Maat MP, van Gorp EC, van der Ende ME - Front Microbiol (2015)

Plasma levels of LPS (N = 101), LBP (N = 130), sCD14 (N = 130), and vWF antigen (N = 93) in chronic HIV infected individuals with or without a history of arterial or venous thrombotic disease. Horizontal bar represents median for LPS, LBP, and sCD14; and mean in vWF. Cases had a significantly higher vWF antigen level as compared to controls. Gray, controls without a thrombotic event; red, arterial events; blue, venous events; green, both arterial and venous events. LPS, Lipopolysaccharide; LBP, LPS binding protein; sCD14, soluble CD14; vWF, von Willebrand Factor antigen level. *p = 0.024 for venous events vs. controls.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4356086&req=5

Figure 2: Plasma levels of LPS (N = 101), LBP (N = 130), sCD14 (N = 130), and vWF antigen (N = 93) in chronic HIV infected individuals with or without a history of arterial or venous thrombotic disease. Horizontal bar represents median for LPS, LBP, and sCD14; and mean in vWF. Cases had a significantly higher vWF antigen level as compared to controls. Gray, controls without a thrombotic event; red, arterial events; blue, venous events; green, both arterial and venous events. LPS, Lipopolysaccharide; LBP, LPS binding protein; sCD14, soluble CD14; vWF, von Willebrand Factor antigen level. *p = 0.024 for venous events vs. controls.
Mentions: For patient characteristics of subjects that underwent analysis of sCD14, LPS, LBP, and vWF please see Supplementary Table 1. Patients with a thrombotic event in the past had a higher mean vWF antigen level when compared to controls (venous: 2.68 SD ± 0.82 IU/ml; arterial: 2.31 SD ± 1.10 IU/ml; both: 2.74 SD ± 0.90 IU/ml; controls: 2.20 SD ± 0.77 IU/ml). The difference in vWF antigen levels was significant in patients with a past venous event compared to controls (p = 0.024, Independent samples T-test) (Figure 2), which remained significant when comparing only recurrent events to controls (2.78 SD ± 0.75; p = 0.043 Independent Samples T-test, Figure 3). The significance of difference in vWF antigen level between cases combined vs. controls varied upon the applied statistical test (p = 0.047, Mann Whitney; p = 0.071 Independent samples T-test). There was no clear connection between time since thrombotic event and the level of vWF antigen (see Figure 4). There was no significant difference between cases and controls in sCD14 (median: 2.45 IQR ± 2.08 vs. 2.31 IQR ± 1.36; p = 0.341) and LBP (median: 20.19 IQR ± 17.56 vs. 16.63 IQR ± 15.05 μ/ml; p = 0.264) as well as LPS (median: 12.19 IQR ± 24.70 vs. 10.76 IQR ± 23.58) although values tended to be higher in cases (Figure 2).

Bottom Line: Arterial and venous thrombotic events are more prevalent in HIV infected individuals compared to the general population, even in the era of combination antiretroviral therapy.The incidence of venous thrombosis was two-fold higher in HIV infected patients compared to age-adjusted data from general population cohort studies.This could be a reason to prolong anti-thrombotic treatment in HIV patients with a history of thrombosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Viroscience, Erasmus MC, University Medical Center Rotterdam, Netherlands.

ABSTRACT

Background: Arterial and venous thrombotic events are more prevalent in HIV infected individuals compared to the general population, even in the era of combination antiretroviral therapy. Although the mechanism is not fully understood, recent evidence suggests a role for chronic immune activation.

Methods: We reviewed the Dutch National HIV registry database for HIV infected patients in Rotterdam with a history of arterial or venous thrombosis and calculated the incidence. We collected samples from patients with and without thrombosis and compared plasma levels of lipopolysaccharide (LPS), LPS binding protein (LBP), soluble CD14 (sCD14), and von Willebrand Factor antigen level (vWF).

Results: During a 10-year period, a total of 60 documented events in 14,026 person years of observation (PYO) occurred, resulting in an incidence rate of 2.50, 2.21, and 4.28 for arterial, venous and combined thrombotic events per 1000 PYO, respectively. The vWF was elevated in the majority of study subjects (mean 2.36 SD ± 0.88 IU/ml); we found a significant difference when comparing venous cases to controls (mean 2.68 SD ± 0.82 IU/ml vs. 2.20 SD ± 0.77 IU/ml; p = 0.024). This difference remained significant for recurrent events (mean 2.78 SD ± 0.75; p = 0.043). sCD14 was positively correlated with LPS (r = 0.255; p = 0.003).

Conclusion: The incidence of venous thrombosis was two-fold higher in HIV infected patients compared to age-adjusted data from general population cohort studies. We couldn't find a clear association between immune activation markers to either arterial or venous thrombotic events. We observed a marked increase in vWF levels as well as a correlation of vWF to first and recurrent venous thrombo-embolic events. These findings suggest that HIV infection is an independent risk factor for coagulation abnormalities and could contribute to the observed high incidence in venous thrombosis. This could be a reason to prolong anti-thrombotic treatment in HIV patients with a history of thrombosis.

No MeSH data available.


Related in: MedlinePlus