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A prospective study showed no relevance of the number of antiretrovirals used to preserve neurocognitive function in aviremic human immunodeficiency virus (HIV)–positive patients, with important implications concerning HIV-associated neurocognitive disorders and the use of nucleoside-sparing regimens.Background. The evolution of neurocognitive performance in aviremic human immunodeficiency virus (HIV)–positive patients treated with <3 antiretrovirals is unknown.Methods. We prospectively included aviremic (≥1 year) HIV-positive patients, without concomitant major neurocognitive confounders, currently receiving boosted lopinavir or darunavir as monotherapy (n = 67) or triple antiretroviral therapy (ART) (n = 67) for ≥1 year. We evaluated neurocognitive function (7 domains) at baseline and after 1 year. We performed analysis of covariance to evaluate if 1 additional year of exposure to monotherapy compared with triple ART had an effect on Global Deficit Score (GDS) changes after adjustment for potential confounders. We also compared the evolution of neurocognitive performance and impairment rates.Results. Intention-to-treat analysis showed that monotherapy did not influence 1-year GDS change after adjustment for significant confounders (age, ethnicity, duration of therapy, hepatitis C virus status, and HOMA-IR index); the adjusted effect was −0.04 (95% confidence interval, −.14 to .05; P = .38). Neurocognitive stability was observed with monotherapy and triple therapy (GDS crude mean change, −0.09 [95% confidence interval, −.16 to −.01] vs −0.08 [−.14 to −.02]), after 1 year of follow-up, similar proportions of patients changed neurocognitive status from impaired to unimpaired (monotherapy, 4 of 18 [22.2%]; triple therapy, 4 of 19 [21.1%]; P = .91) and vice versa (monotherapy, 5 of 44 [10.2%] and triple therapy, 3 of 45 [6.3%]; P = .48). Similar results were observed in an on-treatment analysis and with use of clinical ratings instead of GDS changes.Conclusions. The number of antiretrovirals included in the ART regimen does not seem to influence the evolution of neurocognitive function in HIV-infected patients with suppressed plasma viremia. [ABSTRACT FROM AUTHOR]

It is unknown if, compared to a triple drug antiretroviral therapy, boosted protease inhibitor monotherapy leads to worse results in specific neuropsychological processes. In our study, we included patients virologically suppressed (≥1 year), on antiretroviral therapy, without concomitant major neurocognitive confounders, receiving boosted lopinavir or darunavir as monotherapy ( n = 96) or as triple therapy with two nucleoside reverse transcriptase inhibitors ( n = 95). All patients underwent a comprehensive neuropsychological test battery (14 neuropsychological measures, covering seven domains). Both groups were compared in average score distributions and rates of neuropsychological deficits. Similar comparisons were conducted only for patients with neurocognitive impairment. In the adjusted analysis, we found only small differences between groups in the entire sample: better verbal learning ( p = 0.02; d = 0.28) and verbal recall scores ( p < 0.01; d = 0.25) in patients on boosted protease inhibitor monotherapy and slightly better motor skills with dominant hand ( p = 0.02; d = 0.23) scores in patients on triple therapy. No greater proportion of deficits in the protease inhibitor monotherapy group was found in any neuropsychological measure. In neurocognitively impaired patients, we found similar outcomes in verbal learning, verbal recall, and motor skills with dominant hand but with larger effect sizes. Close similarities in the neurocognitive pattern between groups question the clinical relevance of the number of neuroactive drugs included in the regimen. These results also suggest that peripheral viral load control may be a good indicator of brain protection. [ABSTRACT FROM AUTHOR]

In a cross-sectional study of aviremic neurocognitively impaired patients receiving protease inhibitors as triple-drug therapy (n = 30) or as monotherapy (n = 22), we found no statistically significant differences in the types of cognitive domains involved or severity of cognitive deficit. Cerebrospinal fluid concentrations of total proteins, total tau, myelin basic protein, neuron-specific enolase, β2 microglobulin, S100B protein, or prevalence of cerebrospinal fluid HIV-RNA detection by standard (6.3% vs 7.1% P = 1) or ultrasensitive assays (50% vs 71.4%, P = 0.28) were similar in both groups. These results do not suggest important differences in the pattern of neurocognitive impairment between groups receiving very different antiretroviral strategies. [ABSTRACT FROM AUTHOR]