The role of extended-release niacin on immune activation and neurocognition in HIV-infected patients treated with antiretroviral therapy – CTN PT006: study protocol for a randomized controlled trial

The role of extended-release niacin on immune activation and neurocognition in HIV-infected patients treated with antiretroviral therapy – CTN PT006: study protocol for a randomized controlled trial

Trials, October 2014

25293882

Bertrand Lebouché, Mohammad-Ali Jenabian, Joel Singer, Gina M Graziani, Kim Engler, Benoit Trottier, Réjean Thomas, Marie-Josée Brouillette, Jean-Pierre Routy

Approximately 30% of HIV-1-infected patients receiving antiretroviral therapy who achieve virologic control have unsatisfactory immune reconstitution, with CD4+ T-cell counts persistently below 350 cells/muL. These patients are at elevated risk for clinical progression to AIDS and non-AIDS events. CD4+ T-cell depletion following infection and persistent immune activation can partially explain this low CD4+ T-cell recovery. Recent data suggest a link between the tryptophan oxidation pathway, immune activation and HIV disease progression based on overstimulation of the tryptophan oxidation pathway by HIV antigens and by interferon-gamma. This overstimulation reduces levels of circulating tryptophan, resulting in inflammation which has been implicated in the development of neurocognitive dysfunction. Niacin (vitamin B3) is able to control the excess tryptophan oxidation, correcting tryptophan depletion, and therefore represents an interesting strategy to improve CD4 recovery.We aim to design a crossover proof-of-concept study to assess supplementation with an extended-release form of niacin (Niaspan FCTTM) in combination with antiretroviral therapy, compared to antiretroviral therapy alone, on T-cell immune activation as defined by changes in the percentage of CD8 + CD38 + HLA-DR + T-cells.