Abstract:
Background:Coagulation activity among persons with HIV is associated with end-organ disease risk, but the pathogenesis is not well characterized. We tested a hypothesis that hypercoagulation contributes to disease risk, in part, via upregulation of inflammation. Methods:Treatment effects of edoxaban (30 mg), a direct factor Xa inhibitor, vs placebo were investigated in a randomized, double-blind crossover trial among participants with HIV and viral suppression and D-dimer levels ≥100 ng/mL. During each 4-month crossover period, blood measures of coagulation, inflammation, and immune activation were assessed. Analyses of change on edoxaban vs change on placebo used linear mixed models. Results:Forty-four participants were randomized, and 40 completed at least 1 visit during each study period. The mean age was 49 years, and the CD4+ count was 739 cells/mm3. Edoxaban treatment led to declines in D-dimer (44%) and thrombin-antithrombin complex (26%) but did not lower inflammatory or immune activation measures. More bruising or bleeding events occurred during edoxaban (n = 28) than during placebo or no drug periods (n = 15). Conclusions:The direct factor Xa inhibitor edoxaban led to a substantial reduction in coagulation but no effect on inflammation or immune activation. These results do not support that hypercoagulation contributes to ongoing inflammation during chronic antiretroviral therapy-treated HIV disease.
journal_name
Open Forum Infect Disjournal_title
Open forum infectious diseasesauthors
Baker JV,Wolfson J,Peterson T,Mooberry M,Gissel M,Mystakelis H,Henderson MW,Garcia-Myers K,Rhame FS,Schacker TW,Brummel-Ziedins KE,Sereti I,Key NS,Tracy RPdoi
10.1093/ofid/ofaa026subject
Has Abstractpub_date
2020-02-01 00:00:00pages
ofaa026issue
2issn
2328-8957pii
ofaa026journal_volume
7pub_type
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