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ID
Source
Brief title
Health condition
HIV, thrombophilia
Sponsors and support
Intervention
Outcome measures
Primary outcome
Plasma levels of following markers:
- FVIII
- Anti-thrombin
- Protein C antigen
- Protein S antigen
- Free protein S
- Fibrinogen
- Lupus anticoagulans
- Von Willebrand factor
- D-dimer
Secondary outcome
- Lipid plasma levels (including cholesterol, HDL- and LDL cholesterol and triglycerides)
- The occurrence of cardiovascular events (including myocardial infarction, cerebrovascular accidents, peripheral arterial disease, arterial thrombosis) and venous thrombosis at any site
Background summary
Epidemiological studies have demonstrated that people living with hiv have an increased risk of developing venous thrombosis and cardiovascular disease than the general population. The pathophysiology of thrombosis is a complex and multifactorial process, in which the balance of procoagulant and anticoagulant activity is disturbed causing a thrombophilic state. Several factors in hiv-infection contribute to a procoagulant state. Earlier studies have demonstrated a decrease in anticoagulant factors, e.g. protein S en C, and an increase in procoagulant factors, e.g. D-dimer, fibrinogen and von Willebrand factor (vWF). However, the pathophysiology of this thrombophilic state in hiv-infection remains to be elucidated. Several studies have demonstrated that the thrombotic risk in hiv-infection is associated with chronic immune-activation and inflammation. On the other hand, combination antiretroviral therapy (cART) is also associated with an increased risk of venous thrombosis and cardiovascular disease. It is unclear whether the hiv-infection itself and its treatment could contribute to the thrombophilic state seen in hiv-infected patients.
In 2010, the INF-BEAST study was performed to evaluate the effect of cART in cART-naive hiv-infected. At start of cART, elevated levels of procoagulant factors and decreased levels of anticoagulant factors were found. After a year of cART, a subtle decrease in procoagulant and increase in anticoagulant factors were seen. Despite the initiation of cART therapy, the effect of persistent immune-activation and inflammation could not be ruled out, as suppression of immune activation is yet not achieved after one year of cART use. Currently no data is available on the long-term effect of cART on the thrombophilic state in hiv patients. In this study we aim to determine the thrombophilic state in the INF-BEAST patient population after almost eight years of treatment with cART.
Study objective
The procoagulant state seen in patients with hiv can be a result of the immune activation due to the hiv infection itself or combination antiretroviral therapy (cART). In case the acquired thrombophilia is a result of immune activation, the progcoagulant state should resolve after long term (cART).
Study design
time of inclusion
Intervention
Questionnaire and blood sampling
Inclusion criteria
Inclusion in the original INF-BEAST study
Exclusion criteria
Declining informed consent to participate in the INF-BEAST2 study
Design
Recruitment
IPD sharing statement
Followed up by the following (possibly more current) registration
No registrations found.
Other (possibly less up-to-date) registrations in this register
No registrations found.
In other registers
Register | ID |
---|---|
NTR-new | NL7884 |
Other | METC Groningen : METC2019/086 |