Literature DB >> 30134289

A switch to a raltegravir containing regimen does not lower platelet reactivity in HIV-infected individuals.

Wouter A van der Heijden1, Reinout van Crevel1, Philip G de Groot1,2, Rolf T Urbanus2, Hans J P M Koenen3, Marjolein Bosch1, Monique Keuter1, Andre J van der Ven1, Quirijn de Mast1.   

Abstract

OBJECTIVE: Platelet hyperreactivity and increased platelet-monocyte aggregation (PMA) are associated with increased cardiovascular risk and inflammation. In a previous cross-sectional study, individuals using a raltegravir (RAL)-based regimen were found to have reduced platelet reactivity and PMA compared with other antiretroviral regimens. Our aim was to investigate whether switching from a nonintegrase inhibitor regimen to a RAL-based regimen reduces platelet reactivity or PMA.
DESIGN: An investigator initiated, single-centre, prospective randomized, open-label, blinded endpoint trial.
METHODS: Forty HIV-infected adults using a nonintegrase inhibitor containing regimen with undetectable viral load were randomized to either continue their regimen or switch to a RAL-based regimen for 10 weeks, continuing the same backbone. The primary outcome was the change in platelet reactivity at week 10, which was determined as the expression of the platelet activation marker P-selectin and binding of fibrinogen before and after ex-vivo stimulation with different platelet agonists. Secondary outcomes included PMA, plasma markers of platelet activation and markers of inflammation and immune cell activation.
RESULTS: Twenty-one participants were enrolled in the continuation group and 19 in the RAL group. Baseline characteristics were comparable between groups. There were no differences in the change in platelet reactivity to either platelet agonist at week 10, nor in plasma markers of platelet activation. PMA, C-reactive protein, T-cell activation (CD38HLA-DR) and monocyte (CD14CD16) subsets.
CONCLUSION: Switching a nonintegrase inhibitor containing regimen to a RAL-based regimen does not reduce platelet reactivity, platelet-leukocyte aggregation, inflammation and immune activation in virologically suppressed HIV-infected individuals. CLINICAL TRIAL NUMBER: NCT02383355.

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Year:  2018        PMID: 30134289     DOI: 10.1097/QAD.0000000000001993

Source DB:  PubMed          Journal:  AIDS        ISSN: 0269-9370            Impact factor:   4.177


  4 in total

1.  Functional changes in hemostasis during asexual and sexual parasitemia in a controlled human malaria infection.

Authors:  Shengshi Huang; Wouter van der Heijden; Isaie J Reuling; Jun Wan; Qiuting Yan; Romy M W de Laat-Kremers; Andre J Van der Ven; Philip G de Groot; Matthew McCall; Robert W Sauerwein; Teun Bousema; Mark Roest; Marisa Ninivaggi; Quirijn de Mast; Bas de Laat
Journal:  PLoS One       Date:  2022-07-15       Impact factor: 3.752

2.  Long-term treated HIV infection is associated with platelet mitochondrial dysfunction.

Authors:  Wouter A van der Heijden; Lisa van de Wijer; Martin Jaeger; Karin Grintjes; Mihai G Netea; Rolf T Urbanus; Reinout van Crevel; Lambertus P van den Heuvel; Maaike Brink; Richard J Rodenburg; Philip G de Groot; Andre J van der Ven; Quirijn de Mast
Journal:  Sci Rep       Date:  2021-03-18       Impact factor: 4.379

Review 3.  Interactions of HIV and Antiretroviral Therapy With Neutrophils and Platelets.

Authors:  Morris Madzime; Theresa M Rossouw; Annette J Theron; Ronald Anderson; Helen C Steel
Journal:  Front Immunol       Date:  2021-03-12       Impact factor: 7.561

4.  Increased biomarkers of cardiovascular risk in HIV-1 viremic controllers and low persistent inflammation in elite controllers and art-suppressed individuals.

Authors:  Monick Lindenmeyer Guimarães; Fernanda Heloise Côrtes; Diogo Gama Caetano; Marcelo Ribeiro-Alves; Eugênio Damaceno Hottz; Larissa Melo Vilela; Sandra Wagner Cardoso; Brenda Hoagland; Beatriz Grinsztejn; Valdilea Gonçalves Veloso; Mariza Gonçalves Morgado; Patrícia Torres Bozza
Journal:  Sci Rep       Date:  2022-04-21       Impact factor: 4.996

  4 in total

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