Venous and arterial thrombosis in patients with HIV infection

Micieli, Evy; Dentali, Francesco; Giola, Massimo; Grossi, Paolo; Venco, Achille; Ageno, Walter

doi:10.1097/mbc.0b013e32808738a3

Cited by 16 publications

(11 citation statements)

References 35 publications

(47 reference statements)

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“…Some studies have found a high prevalence of hyperlipidemia; nonetheless, its role in the pathogenesis of clot formation has not been demonstrated10, 11. Our study did not find a relationship between lipid levels (total cholesterol, triglycerides, HDL, or LDL) and an increased risk of VTEs.…”

Section: Discussioncontrasting

confidence: 79%

“…Two studies have found that the incidence of VTEs increased sharply since the introduction of PIs8, 33, yet, another study reported no significant increase40. Some case reports and series described a temporal relationship between PI initiation and clot development32, 33 , while others did not11 . One large study showed that indinavir was predictive of VTEs, but not other PIs9.…”

Section: Discussionmentioning

confidence: 99%

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Review:Thromboses among HIV-Infected Patients during the Highly Active Antiretroviral Therapy Era

Crum-Cianflone

Weekes²,

Bavaro³

2008

AIDS Patient Care and STDs

100

148

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Venous thrombotic events (VTEs) may occur at higher rates among HIV patients; some studies suggest that HAART may increase the risk for these potentially life-threatening events. We performed a retrospective study among HIV patients to evaluate the incidence and risk factors for VTEs during the HAART era. A literature review was performed examining VTEs in the pre-and post HAART eras. Seventeen (3.7%) of 465 HIV patients experienced a VTE. The overall incidence rate of deep VTEs among HIV positive persons was 377 cases/100,000 person-years, a four-fold higher rate compared to age-matched males in the general population. The median age at VTE was 36 years (range 27-68). Patients with a thrombosis compared to those without had significantly lower current CD4 (153 vs. 520 cells/mm 3 , p<0.001) and nadir (76 vs. 276 cells/mm 3 , p<0.001) CD4 counts, higher viral loads (3.6 vs. 1.7 log 10 copies/ml, p=0.003), and more likely to have a diagnosis of AIDS (76% vs. 32%, p<0.001); there were no differences in demographics, hyperlipidemia, current use of HAART, the duration of HAART or PI exposure. A review of the literature noted 129 VTE cases; mean age was 40 years, mean CD4 count was 181 cells/mm 3 , the majority of patients were not receiving HAART, and the most common risk factor was an ongoing infection. Thrombotic events are occurring among HIV patients despite their relatively young ages. Advanced HIV disease is a risk factor for development of thromboses, possibly due to an increased inflammatory state or the presence of concurrent comorbidities such as infections. HAART or PI therapy does not appear to play a significant role in the occurrence of VTEs.

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Section: Discussioncontrasting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Review:Thromboses among HIV-Infected Patients during the Highly Active Antiretroviral Therapy Era

Crum-Cianflone

Weekes²,

Bavaro³

2008

AIDS Patient Care and STDs

100

148

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“…The variation in observed incidences between studies is probably related to the nature of these studies, mostly retrospective, the difference in diagnostic criteria and cohort characteristics such as immune status of patients. An increasing amount of evidence in the literature supports the notion that HIV status is associated with increased risk on myocardial infarction, stroke and venous thrombo-embolism (Micieli et al, 2007). With the aging of HIV cohorts and related increased exposure to cART, it remains important to re-evaluate this incidence rate.…”

Section: Discussionmentioning

confidence: 89%

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

et al. 2015

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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.

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“…[1][2][3][4] In general, shared risk factors for atherothrombosis are suggested, such as age, obesity, infections, diabetes mellitus, and metabolic syndrome. Hypercoagulability is likely to be the pathogenic mechanism linking venous and arterial disease.…”

Section: Introductionmentioning

confidence: 99%

The Hemostatic Balance in HIV-Infected Patients with and without Antiretroviral Therapy: Partial Restoration with Antiretroviral Therapy

Jong

Louw²,

Meijers³

et al. 2009

AIDS Patient Care and STDs

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The incidence of arterial and venous thrombosis in HIV-infected patients is increased compared to healthy controls. In this cross-sectional analysis we measured markers of endothelial cell activation, thrombin generation, fibrinolysis and anticoagulation combined with endogenous thrombin potential (ETP) and activated protein C sensitivity ratio (APCsr) as more global markers. We included 160 consecutive HIV-infected patients with a median age of 46 years (range, 27-77), of whom 92% were male, 74% Caucasian, 11% African American, 9% Hispanic, and 6% Asian. Homosexual contact was the main transmission mode. Seventy percent of patients were using combined antiretroviral therapy (cART). In 83% of patients laboratory markers outside the normal range for a non-HIV-infected population were observed. Significant lower levels of von Willebrand factor (vWF; p = 0.03), factor VIII (p < 0.0001), D-dimer (p = 0.01), and ETP (p = 0.01) were observed in HIV-infected patients on cART compared to patients not on cART. Significant lower levels of protein C (p = 0.05) and free protein S (p < 0.0001), and increased APCsr (p < 0.0001) were found in the HIV-infected patients not on cART. A single association was observed between raised levels of fibrinogen and use of a protease inhibitor (p = 0.002). No significant difference was observed in the percentage of patients with laboratory markers outside the normal range between patients using cART-regimens containing abacavir, stavudine, or didanosine and those with other nucleoside reverse transcriptase inhibitors. Although the prevalence of coagulation abnormalities was lower in HIV-infected patients using cART, a considerable proportion of HIV-infected patients on cART show endothelial cell activation and increased APCsr, suggestive of a persistent procoagulant state.

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Venous and arterial thrombosis in patients with HIV infection

Cited by 16 publications

References 35 publications

Review:Thromboses among HIV-Infected Patients during the Highly Active Antiretroviral Therapy Era

Review:Thromboses among HIV-Infected Patients during the Highly Active Antiretroviral Therapy Era

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

The Hemostatic Balance in HIV-Infected Patients with and without Antiretroviral Therapy: Partial Restoration with Antiretroviral Therapy

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