Valantin MA, Bittar R, de Truchis P, Bollens D, Slama L, Giral P, et al. Switching the nucleoside reverse transcriptase inhibitor backbone to tenofovir disoproxil fumarate + emtricitabine promptly improves triglycerides and low-density lipoprotein cholesterol in dyslipidaemic patients

Department of Infectious Diseases, AP-HP, Pitié-Salpêtrière Hospital, Paris, France.
Journal of Antimicrobial Chemotherapy (Impact Factor: 5.31). 03/2010; 65(3):556-61. DOI: 10.1093/jac/dkp462
Source: PubMed


To assess the impact of switching to tenofovir disoproxil fumarate + emtricitabine on lipid parameters.
HIV-infected patients with plasma viral load <400 copies/mL, fasted triglycerides from 2.3 to 11.4 mmol/L and/or fasted low-density lipoprotein (LDL)-cholesterol >4.1 mmol/L were randomized to switch the nucleoside reverse transcriptase inhibitor (NRTI) backbone to fixed-dose combination tenofovir disoproxil fumarate + emtricitabine or to maintain the baseline antiretroviral regimen (the control group). The study has been registered with under the identifier NCT00323492.
Ninety-one patients were included in the intent-to-treat (ITT) analysis with triglycerides 2.4 mmol/L and LDL-cholesterol 4.0 mmol/L (median values). At week 12, the median changes from baseline of triglycerides were -0.5 mmol/L (-25%; n = 46) and -0.1 mmol/L (-6%; n = 45) in the tenofovir disoproxil fumarate + emtricitabine and control groups, respectively, indicating a difference of -0.4 mmol/L (P = 0.034) [95% confidence interval (CI): -0.9 to -0.0]. Similarly for LDL-cholesterol, changes of -0.4 mmol/L (-9%) and -0.1 mmol/L (-1%) were observed in the tenofovir disoproxil fumarate + emtricitabine and control groups, respectively, indicating a difference of -0.4 mmol/L (P = 0.031) [95% CI: -0.7 to -0.0]. The proportion of patients with LDL-cholesterol >4.1 mmol/L decreased from 48% at baseline to 26% at week 12 in the tenofovir disoproxil fumarate + emtricitabine group versus no change in the control group. No virological failure was observed during the study.
Switching to tenofovir disoproxil fumarate + emtricitabine in dyslipidaemic HIV-infected patients improves triglycerides and LDL-cholesterol.

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    • "The effect of tenofovir (TDF) containing regimen indicates a lipid lowering action of this NRTI which is different from other ARV drugs in the same class. In randomised trials conducted in France (Valantin et al., 2010) and Spain (Saumoy et al., 2011 "
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    ABSTRACT: Studies on dyslipidaemia in human immunodeficiency virus (HIV) infected people have reported on lipoproteins and lipoprotein subclass profiles. Lipoprotein subclasses are regarded as more accurate measures of cardiovascular disease (CVD) risk than levels of lipoproteins. In this review, the primary objective was to compare and contrast the distribution patterns of lipoprotein and lipoprotein subclasses in highly active antiretroviral therapy (HAART) naïve people and those on HAART based on available literature. PubMed, Science Direct and Google were searched using a combination of various keywords, and relevant English language articles were selected. HIV infection is associated with a decrease of high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), total cholesterol (TC), with increased triglycerides (TG) accompanied by noticeable decreases in total HDL-particles (HDL-p), small dense HDL-p, total LDL-particles (LDL-p) and small dense LDL-p. Acquired immunodeficiency syndrome (AIDS) is associated with increase in small dense LDL-p and decreased HDL-p. HAART, especially protease inhibitor (PI)-based, is associated with increase in lipoprotein levels and levels of total LDL-p and small dense LDL-p, while the non-nucleoside reverse transcriptase inhibitors (NNRTI)-based HAART is associated with smaller increase in lipoprotein levels and significant increase in HDL-p. In addition to a predominance of small dense LDL-p, patients on HAART, especially PI-based have low HDL-p levels. This subclass pattern increases the risk of CVD in HIV-infected people. The use of NNRTI-based HAART or newer PI drugs such as atazanavir, associated with a less atherogenic subclass profile could defer premature CVD in HIV-infected people. As most studies were conducted in Western countries and in people whose ethnicity is different from the ethnicity of people from sub-Saharan Africa, there is a need to analyse lipoprotein subclasses in HIV- infected people, especially in sub-Saharan Africa where HIV infection is most prevalent
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    • "Switches to tenofovir from thymidine analogues [39], mainly stavudine [34, 79–81], have showed some good changes in the lipid profile. In particular, a study on 352 HIV-infected subjects followed for 48 weeks found a sustained reduction in median TC (−17.5 mg/dL; P < .001), "
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    ABSTRACT: Many infections favor or are directly implicated with lipid metabolism perturbations and/or increased risk of coronary heart disease (CHD). HIV itself has been shown to increase lipogenesis in the liver and to alter the lipid profile, while the presence of unsafe habits, addiction, comorbidities, and AIDS-related diseases increases substantially the risk of cardiovascular disease (CVD) in the HIV-infected population. Antiretroviral therapy reduces such stimuli but many drugs have intrinsic toxicity profiles impacting on metabolism or potential direct cardiotoxicity. In a moment when the main guidelines of HIV therapy are predating the point when to start treating, we mean to highlight the contribution of HIV-1 to lipid alteration and inflammation, the impact of antiretroviral therapy, the decisions on what drugs to use to reduce the probability of having a cardiovascular event, the increasing use of statins and fibrates in HIV-1 infected subjects, and finally the switch strategies, that balance effectiveness and toxicity to move the decision to change HIV drugs. Early treatment might reduce the negative effect of HIV on overall cardiovascular risk but may also evidence the impact of drugs, and the final balance (reduction or increase in CHD and lipid abnormalities) is not known up to date.
    Cholesterol 10/2010; 2010(2090-1283):271504. DOI:10.1155/2010/271504

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