Down regulation of CD38 activation markers by atorvastatin in HIV patients with undetectable viral load

Wit, Stéphane De; Delforge, Marc; Necsoi, Coca; Clumeck, Nathan

doi:10.1097/qad.0b013e328347c083

Cited by 25 publications

(18 citation statements)

References 8 publications

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“…In contrast to the small, but significantly greater BMD at the hip and trochanter that we previously reported after 48 weeks, 7 the BMD in the rosuvastatin arm trended back toward baseline between weeks 48 and 96, and differences were no longer significant between study arms by week 96. Outside of a trend for increased LBM in the rosuvastatin arm, we were unable to detect significant differences in peripheral or central fat, CK, or physical activity between rosuvastatin and placebo.…”

Section: Discussioncontrasting

confidence: 43%

“…1,3,4 The antiinflammatory effect of HMG-CoA reductase inhibitors, or statins, has led to a growing interest in the use of statins to attenuate the low-grade inflammation and immune activation observed in treated HIV infection. [5][6][7] In addition to reductions in inflammation, cardiovascular events, and mortality, statins have been shown to have a beneficial effect on bone mineral density (BMD) 8,9 and lean body mass (LBM) 10,11 in some studies of older, HIV-uninfected cohorts. With the heightened inflammation and activation and lower BMD and LBM seen among HIVinfected persons, we hypothesized that rosuvastatin therapy would be associated with an improvement in BMD and gain in LBM compared to placebo.…”

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confidence: 99%

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Effects of 96 Weeks of Rosuvastatin on Bone, Muscle, and Fat in HIV-Infected Adults on Effective Antiretroviral Therapy

Erlandson¹,

Jiang

Debanne

et al. 2016

AIDS Research and Human Retroviruses

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Heightened inflammation and immune activation are associated with lower bone mineral density (BMD) and lean body mass (LBM) among HIV-infected persons. We hypothesized that a reduction in inflammation with rosuvastatin would be associated with improvements in BMD and LBM. HIV-infected participants on stable antiretroviral therapy without statin indication and with heightened immune activation ( ‡19% CD8T cells) or inflammation (hsCRP ‡2 mg/liter) were randomized to rosuvastatin 10 mg daily or placebo for 96 weeks. Among 72 participants randomized to rosuvastatin and 75 to placebo, there were no significant differences in the relative changes in BMD ( p > 0.29) or in fat ( p ‡ 0.19). A trend toward increased LBM ( p = 0.059) was seen in the rosuvastatin arm without differences in creatinine kinase or self-reported physical activity ( p ‡ 0.10). In a multivariable regression model, rosuvastatin was associated with a significant positive effect on LBM after adjusting for age, sex, race, smoking status, and detectable HIV-1 viral load. Higher baseline sCD163 correlated with increases in LBM from weeks 0 to 96 ( p = 0.023); greater changes in total and leg lean mass were seen among statin users with higher compared to lower baseline IP-10 levels (LBM 1.8 vs. -0.3%; p = 0.028 and leg lean mass 2.9 vs. -1.7%; p = 0.012). Rosuvastatin is associated with an absence of toxicity on BMD and a potential benefit on LBM over 96 weeks of therapy. The preservation of LBM in the rosuvastatin arm over the 2 years of the study is of major clinical relevance in delaying loss of muscle mass with aging.

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Section: Discussioncontrasting

confidence: 43%

mentioning

confidence: 99%

Effects of 96 Weeks of Rosuvastatin on Bone, Muscle, and Fat in HIV-Infected Adults on Effective Antiretroviral Therapy

Erlandson¹,

Jiang

Debanne

et al. 2016

AIDS Research and Human Retroviruses

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“…In the SATURN-HIV trial, rosuvastatin 10mg slowed progression of carotid intima-media thickness among 147 subjects with elevated hs-CRP and/or heightened CD8+ T-cell activation. Similar to HIV studies of atorvastatin[79-82], rosuvastatin reduced T-cell activation and exhaustion markers over 48 weeks in SATURN-HIV[83]. Markers of innate immune activation such as soluble CD14 and the proportion of tissue factor-positive non-classical (CD14 dim CD16 + ) monocytes were also reduced with rosuvastatin[83].…”

Section: Immune-based Strategies To Mitigate Riskmentioning

confidence: 72%

Immune activation and cardiovascular disease in chronic HIV infection

Longenecker

Sullivan

Baker³

2016

Current Opinion in HIV and AIDS

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Purpose of review To describe the potential contribution of immune activation in the pathogenesis of HIV-associated cardiovascular disease (CVD)—a leading cause of morbidity and mortality among HIV positive persons with access to antiretroviral therapy (ART). Recent findings We review recent literature that suggests abnormalities in both adaptive and innate immunity contributes to CVD risk among persons with HIV infection. In particular, potentially atherogenic T-cell mechanisms include persistent high-level T-cell activation (and associated pro-inflammatory mechanisms), as well as the presence of co-pathogens (e.g., CMV) providing an ongoing stimulus for cytotoxic T-cell responses. More recent data has then emphasized the potential impact of monocyte/macrophage-mediated inflammation and injury within atherosclerotic lesions. The pathology driving innate immune activation many not fully reverse with ART treatment, highlighting the need for interventions that target inflammation as a CVD prevention strategy. Summary Premature CVD among persons with HIV infection is due, in part, to persistent abnormalities in immune activation and systemic inflammation despite viral suppression. Prevention strategies for persons with HIV infection include those that target traditional CVD risk factors as well as newer candidate treatments with potential immunomodulatory benefits.

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“…The use of statins in HIV-infected patients on and off cART has reported variable changes in T-cell activation and highly sensitive C-reactive protein (hsCRP) levels [32–35] but no effect on CD4 T-cell counts [32,33,36]. However, in two large observational studies of cART-treated patients, the use of statins was associated with reduced mortality [37] and reduced incidence of non-Hodgkin lymphoma (NHL) [38].…”

Section: Strategies To Reduce Persistent Immune Activation In Hiv-infmentioning

confidence: 99%

Persistent immune activation in chronic HIV infection

Rajasuriar

Khoury

Kamarulzaman³

et al. 2013

Aids

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Down regulation of CD38 activation markers by atorvastatin in HIV patients with undetectable viral load

Cited by 25 publications

References 8 publications

Effects of 96 Weeks of Rosuvastatin on Bone, Muscle, and Fat in HIV-Infected Adults on Effective Antiretroviral Therapy

Effects of 96 Weeks of Rosuvastatin on Bone, Muscle, and Fat in HIV-Infected Adults on Effective Antiretroviral Therapy

Immune activation and cardiovascular disease in chronic HIV infection

Persistent immune activation in chronic HIV infection

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