Low-Density Lipoprotein Size and Lipoprotein-Associated Phospholipase A2 in HIV-Infected Patients Switching to Abacavir or Tenofovir

Ordóñez-Llanos, Jordi; Martínez, Estebán; Barragán, Patricia; Ribera, Esteban; Bonet, Rosa; Knobel, Hernando; Negredo, Eugènia; Loncá, Montserrat; Curran, Adrían; Gatell, Josep M.; Podzamczer, Daniel; Team, Bicombo-met Substudy

doi:10.3851/imp1785

Cited by 22 publications

(10 citation statements)

References 35 publications

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“…Abacavir-lamivudine was recently compared to tenofoviremtricitabine, combined either with efavirenz or atazanavir- ritonavir, reporting higher lipid levels in the abacavir group but similar TC/HDL ratio [78], findings beings also reported in other studies [79][80][81]. However, decreases in TG and increases in HDL-C were greater with abacavir/ lamivudine than with tenofovir/emtricitabine when combined with raltegravir [82].…”

Section: Metabolic and Thrombotic Complications Associated With Cartmentioning

confidence: 70%

Risk of Cardiovascular Disease in an Aging HIV Population: Where Are We Now?

2015

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With more effective and widespread antiretroviral treatment, the overall incidence of AIDS- or HIV-related death has decreased dramatically. Consequently, as patients are aging, cardiovascular disease (CVD) has emerged as an important cause of morbidity and mortality in the HIV population. The incidence of CVD overall in HIV is relatively low, but it is approximately 1.5-2-fold higher than that seen in age-matched HIV-uninfected individuals. Multiple factors are believed to explain this excess in risk such as overrepresentation of traditional cardiovascular risk factors (particularly smoking), toxicities associated with cumulative exposure to some antiretroviral agents, together with persistent chronic inflammation, and immune activation associated with HIV infection. Tools are available to calculate an individual's predicted risk of CVD and should be incorporated in the regular follow-up of HIV-infected patients. Targeted interventions to reduce this risk must be recommended, including life-style changes and medical interventions that might include changes in antiretroviral therapy.

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Section: Metabolic and Thrombotic Complications Associated With Cartmentioning

confidence: 70%

Risk of Cardiovascular Disease in an Aging HIV Population: Where Are We Now?

2015

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“…The effect of ABC on Lp-PLA 2 has been evaluated previously over a shorter period (48 weeks) in another study, but did not change significantly in that time frame. 30 Our study is the first to report Lp-PLA 2 data with an unboosted ATV or ATV/r regimen.…”

Section: Discussionmentioning

confidence: 93%

“…Median Framingham risk scores did not change significantly over 144 weeks, which is consistent with the results of two shorter term studies (Bicombo-met and STEAL). 30,31 In these studies, when an ABC/3TC nucleoside backbone was compared to another nucleoside/nucleotide backbone, tenofovir/emtricitabine (TDF/FTC), no significant changes in median or mean Framingham 10-year CHD risk scores over 48 and 96 weeks were observed.…”

Section: Discussionmentioning

confidence: 97%

Inflammatory Biomarker Changes and Their Correlation with Framingham Cardiovascular Risk and Lipid Changes in Antiretroviral-Naive HIV-Infected Patients Treated for 144 Weeks with Abacavir/Lamivudine/Atazanavir with or without Ritonavir in ARIES

Young¹,

Squires

Ross

et al. 2013

AIDS Research and Human Retroviruses

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Propensity for developing coronary heart disease (CHD) is linked with Framingham-defined cardiovascular risk factors and elevated inflammatory biomarkers. Cardiovascular risk and inflammatory biomarkers were evaluated in ARIES, a Phase IIIb/IV clinical trial in which 515 antiretroviral-naive HIV-infected subjects initially received abacavir/lamivudine + atazanavir/ritonavir for 36 weeks. Subjects who were virologically suppressed by week 30 were randomized 1:1 at week 36 to either maintain or discontinue ritonavir for an additional 108 weeks. Framingham 10-year CHD risk scores (FRS) and risk category of <6% or ≥6%, lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hsCRP) were assessed at baseline, week 84, and week 144. Biomarkers were stratified by FRS category. When ritonavir-boosted/nonboosted treatment groups were combined, median hsCRP did not change significantly between baseline (1.6 mg/liter) and week 144 (1.4 mg/liter) in subjects with FRS <6% (p=0.535) or with FRS ≥6% (1.9 mg/liter vs. 2.0 mg/liter, respectively; p=0.102). Median IL-6 was similar for subjects with FRS <6% (p=0.267) at baseline (1.6 pg/ml) and week 144 (1.4 pg/ml) and for FRS ≥6% (2.0 pg/ml vs. 2.2 pg/ml, respectively; p=0.099). Median Lp-PLA(2) decreased significantly (p<0.001) between baseline (197 nmol/min/ml) and week 144 (168 nmol/min/ml) in subjects with FRS <6% and with FRS ≥6% (238 nmol/min/ml vs. 175 nmol/min/ml, respectively; p<0.001). In conclusion, in antiretroviral-naive subjects treated with abacavir-based therapy for 144 weeks, median inflammatory biomarker levels for hsCRP and IL-6 generally remained stable with no significant difference between baseline and week 144 for subjects with either FRS <6% or FRS ≥6%. Lp-PLA(2) median values declined significantly over 144 weeks for subjects in either FRS stratum.

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“…In particular, these patients, compared with healthy controls, presented with higher plasma sPLA 2 and Lp-PLA 2 levels or increased enzymatic activity, associated with an enhanced risk of cardiovascular disease [199][200][201][202][203][204]. The effect of different antiretroviral regimens on plasma Lp-PLA 2 levels was investigated by several groups [205][206][207][208][209][210][211]. Interestingly, the use of integrase inhibitors in some studies resulted in a greater decrease of Lp-PLA 2 levels as compared with treatment with either reverse-transcriptase or protease inhibitors, in conjunction with a more-favorable effect on other markers of immune activation [209,210].…”

Section: Plcs In Hiv-1 Infectionmentioning

confidence: 99%

Phospholipases: at the crossroads of the immune system and the pathogenesis of HIV-1 infection

Cecchetti

Spadaro

Gessani

et al. 2016

Journal of Leukocyte Biology

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Multiple host factors and their interactions with viral proteins contribute to the complexity of HIV-1 pathogenesis and disease progression. The virus exploits the cell-signaling networks to prepare the ground for viral replication, to affect functions of either infected or uninfected bystander cells, and to evade the immune response. These events are hallmarks of HIV-1 pathogenesis that lead toward AIDS. Phospholipases are essential mediators of intracellular and intercellular signaling. They function as phospholipid-hydrolyzing enzymes, generating many bioactive lipid mediators or second messengers, which control multiple cellular functions, thus regulating a variety of physiologic and pathophysiologic processes. These enzymes also represent important components of the cell-signaling networks exploited by HIV-1 and its proteins to favor viral replication and persistence, as well as immune response dysfunction. Although some individual phospholipases were studied in the context of HIV-1 infection, the mechanisms whereby they regulate diverse infection-associated processes, as well as the interaction among different phospholipases have yet to be fully elucidated. In this review, we discuss the principal aspects of the complex interaction between phospholipases, HIV-1, and the immune system. A thorough understanding of the signaling networks that involve phospholipases in both HIV-1-infected cells and individuals is essential to determine whether therapeutic targeting of these enzymes may represent a novel approach to control viral replication, as well as the associated inflammation and comorbidities.

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Low-Density Lipoprotein Size and Lipoprotein-Associated Phospholipase A2 in HIV-Infected Patients Switching to Abacavir or Tenofovir

Abstract: A more atherogenic LDL profile, including a decrease in LDL size, was found in the ABC group and not in TDF patients.

Cited by 22 publications

References 35 publications

Risk of Cardiovascular Disease in an Aging HIV Population: Where Are We Now?

Risk of Cardiovascular Disease in an Aging HIV Population: Where Are We Now?

Inflammatory Biomarker Changes and Their Correlation with Framingham Cardiovascular Risk and Lipid Changes in Antiretroviral-Naive HIV-Infected Patients Treated for 144 Weeks with Abacavir/Lamivudine/Atazanavir with or without Ritonavir in ARIES

Phospholipases: at the crossroads of the immune system and the pathogenesis of HIV-1 infection

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