J M Gatell

Hospital Clínic de Barcelona, Barcino, Catalonia, Spain

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Publications (361)1828.92 Total impact

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    ABSTRACT: Gene expression studies of subcutaneous adipose tissue may help to better understand the mechanisms underneath body fat changes in HIV-infected patients who initiate antiretroviral therapy (ART). Here we evaluated early changes in adipose tissue gene expression and their relationship with fat changes in ART-naïve HIV-infected patients randomly assigned to initiate therapy with emtricitabine/tenofovir plus efavirenz (EFV) or ritonavir-boosted lopinavir (LPV/r). This was a substudy of a randomized clinical trial (LIPOTAR-NCT00759070). Patients had abdominal subcutaneous adipose tissue biopsies at baseline and week 16 and dual-energy-X-ray absorptiometry at baseline, week 16 and 48. mRNA changes of eleven genes involved in adipogenesis, lipid and glucose metabolism, mitochondrial energy and inflammation were assessed through RT-qPCR. Additionally, correlations between gene expression changes and fat changes were evaluated. Fat increased preferentially in the trunk with EFV and in the limbs with LPV/r (p<0.05). After 16 weeks of exposure to the drug regimen, transcripts of CEBP/A, ADIPOQ, GLUT4, LPL and COXIV were significantly down-expressed in EFV arm compared to LPV/r (p<0.05). Significant correlations were observed between LPL expression change and trunk fat change at week 16 in both arms, and CEBP/A or COXIV changes and trunk fat change at the same time-point only in EFV arm and not in LPV/r. When combined with emtricitabine/tenofovir as standard backbone therapy, EFV or LPV/r induced differential early expression of genes involved in adipogenesis and energy metabolism. Moreover, these mRNA expression changes correlated with trunk fat change in the EFV arm.
    Antimicrobial Agents and Chemotherapy 08/2014; · 4.57 Impact Factor
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    ABSTRACT: The virologic efficacy of switching from a boosted protease inhibitor (PI/r) to raltegravir (RAL) containing regimens remains controversial according to the results of SWITCHMRK and SPIRAL studies. The aim of this analysis is to assess the impact of prior resistance mutations to nucleos(t)ides and other potential factors on the virologic outcome.
    Antiviral therapy 06/2014; · 3.07 Impact Factor
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    ABSTRACT: Abstract OBJECTIVES: A relationship between obesity and intestinal bacterial translocation has been reported. Very little information is available with respect to the involvement of the bacterial translocation mechanistic pathway in HIV-1/highly active antiretroviral therapy (HAART)-associated lipodystrophy syndrome (HALS). We determined whether lipopolysaccharide (LPS)-binding protein (LBP), cluster of differentiation 14 (CD14), myeloid differentiation protein 2 (MD2) and toll-like receptor 4 (TLR4) single-nucleotide polymorphisms and LPS, LBP and soluble CD14 (sCD14) plasma levels are involved in HALS. PATIENTS AND METHODS: This cross-sectional multicentre study involved 558 treated HIV-1-infected patients, 240 with overt HALS and 318 without HALS. Anthropometric, clinical, immunovirological and metabolic variables were determined. Polymorphisms were assessed by genotyping. Plasma levels were determined by ELISA in 163 patients (81 with HALS and 82 without HALS) whose stored plasma samples were available. Student's t-test, one-way ANOVA, two-way repeated measures ANOVA, the χ2 test and Pearson and Spearman correlation analyses were carried out for statistical analysis. RESULTS: LBP rs2232582 T→C polymorphism was significantly associated with HALS (P = 0.01 and P = 0.048 for genotype and allele analyses, respectively). Plasma levels of LPS (P = 0.009) and LBP (P < 0.001) were significantly higher and sCD14 significantly lower (P < 0.001) in patients with HALS compared with subjects without HALS. LPS levels were independently predicted by triglycerides (P < 0.001) and hepatitis C virus (P = 0.038), LBP levels by HALS (P < 0.001) and sCD14 levels by age (P = 0.008), current HIV-1 viral load (P = 0.001) and protease inhibitor use (P = 0.018). CONCLUSIONS: HALS is associated with LBP polymorphism and with higher bacterial translocation.
    Journal of Antimicrobial Chemotherapy 02/2014; · 5.34 Impact Factor
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    ABSTRACT: BACKGROUND:: Latent HIV-1-infected cells generated early in the infection are responsible for viral persistence, and we hypothesized that addition of maraviroc to triple therapy in patients recently infected with HIV-1 could accelerate decay of the viral reservoir.METHODS:: Patients recently infected (<24 weeks) by chemokine receptor 5 (CCR5)-using HIV-1 were randomized to a raltegravir + tenofovir/emtricitabine regimen (control arm, n = 15) or the same regimen intensified with maraviroc (+MVC arm, n = 15). Plasma viral load, cell-associated HIV-1 DNA (total, integrated, and episomal), and activation/inflammation markers were measured longitudinally.RESULTS:: Plasma viral load decayed in both groups, reaching similar residual levels at week 48. Total cell-associated HIV-1 DNA also decreased in both groups during the first month, although subsequently at a slightly faster rate in the +MVC arm. The transient increase in two long terminal repeat (2-LTR) circles observed in both groups early after initiation of treatment decreased earlier in MVC-treated individuals. Early (week 12) increase of CD4 T-cell counts was higher in the +MVC arm. Conversely, CD8 T-cell counts and CD4 T-cell activation decreased slower in the +MVC arm. Absolute CD4 T-cell and CD8 T-cell counts, immune activation, CD4/CD8 T-cell ratio, and soluble inflammation markers were similar in both arms at the end of the study.CONCLUSION:: Addition of maraviroc in early integrase inhibitor-based treatment of HIV-1 infection results in faster reduction of 2-LTR newly infected cells and recovery of CD4 T-cell counts, and a modest reduction in total reservoir size after 48 weeks of treatment. Paradoxically, CCR5 blockade also induced a slower decrease in plasma viremia and immune activation
    AIDS 01/2014; 28:325-34. · 6.41 Impact Factor
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    ABSTRACT: Introducción El panel de expertos de GESIDA/Plan Nacional del Sida ha recomendado pautas preferentes (PP) y alternativas (PA) de tratamiento antirretroviral (TARV) como terapia de inicio en pacientes infectados por VIH para 2014. El objetivo de este estudio es evaluar los costes y la eficiencia de iniciar tratamiento con estas pautas. Métodos Evaluación económica de costes y eficiencia (coste/eficacia) mediante construcción de árboles de decisión. Se definió eficacia como la probabilidad de tener carga viral <50 copias/mL en la semana 48 en análisis por intención de tratar. Se definió coste de iniciar tratamiento con una pauta como los costes del TARV y de todas sus consecuencias (efectos adversos, cambios de pauta y estudio de resistencias) que se producen en las siguientes 48 semanas. Se utilizó la perspectiva del Sistema Nacional de Salud, considerando sólo costes directos diferenciales: fármacos (a precio oficial), manejo de efectos adversos, estudios de resistencias y determinación de HLA B*5701. El ámbito es España, con costes de 2014. Se realizó análisis de sensibilidad determinista construyendo tres escenarios para cada pauta: basal, más favorable y más desfavorable. Resultados En el escenario basal, los costes de iniciar tratamiento oscilaron entre 5.133 euros para ABC/3TC + EFV y 11.949 euros para TDF/FTC + RAL. La eficacia osciló entre 0,66 para ABC/3TC + LPV/r y ABC/3TC + ATV/r, y 0,89 para TDF/FTC/EVG/COBI. La eficiencia, en términos de coste/eficacia, osciló entre 7.546 y 13.802 euros por respondedor a las 48 semanas, para ABC/3TC + EFV y TDF/FTC + RAL, respectivamente. Conclusión Considerando el precio oficial del TARV, la pauta más eficiente fue ABC/3TC + EFV (PA), seguida de las PP que contienen no nucleósidos (TDF/FTC/RPV y TDF/FTC/EFV). El análisis de sensibilidad confirmó la robustez de estos hallazgos.
    Enfermedades Infecciosas y Microbiología Clínica 01/2014; · 1.48 Impact Factor
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    ABSTRACT: Whether critically ill human immunodeficiency virus (HIV)-infected patients are at risk of acquiring nosocomial infections and resistant or potentially resistant microorganisms (RPRMs) remains to be clarified. The aim was to compare the acquisition of RPRMs, infections and mortality in critically ill HIV-infected and non-infected patients. An observational, prospective cohort study of patients admitted to a medical intensive care unit (ICU) was undertaken. Swabbing of nares, pharynx and rectum, and culture of respiratory secretions were obtained within 48 h of admission and thrice weekly thereafter. Clinical samples were obtained as deemed necessary by the attending physician. Clinical variables, severity scores on admission and exposures during ICU stay were collected. Logistic regression was used to evaluate ICU mortality. Out of the 969 included patients, 64 (6.6 %) were HIV-infected. These patients had a higher Acute Physiology and Chronic Health Evaluation (APACHE) II score on admission (19.5 ± 6.6 vs. 21.1 ± 5.4, p = 0.02), stayed longer in the care unit and were more exposed to several invasive devices and antibiotics. There were no differences in the rate of acquisition of RPRMs and the only difference in ICU-acquired infections was a significantly higher incidence of catheter-related bacteraemia (3 % vs. 9 %, p = 0.03). The ICU-related mortality was similar in both groups (14 % vs. 16 %, p = 0.70) and in HIV-infected patients, it tended to be associated with a lower CD4 cell count (p = 0.06). Despite a longer ICU stay, critically ill HIV-infected patients did not show a higher rate of RPRMs acquisition. The rate of ICU-acquired infection was similar between HIV-infected and non-infected patients, except for catheter-related bacteraemia, which was higher in the HIV-infected population. Mortality was similar in both groups.
    European Journal of Clinical Microbiology 10/2013; · 3.02 Impact Factor
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    ABSTRACT: The aim of this study was to determine whether the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)- or Cockcroft-Gault (CG)-based estimated glomerular filtration rates (eGFRs) performs better in the cohort setting for predicting moderate/advanced chronic kidney disease (CKD) or end-stage renal disease (ESRD). A total of 9521 persons in the EuroSIDA study contributed 133 873 eGFRs. Poisson regression was used to model the incidence of moderate and advanced CKD (confirmed eGFR < 60 and < 30 mL/min/1.73 m(2) , respectively) or ESRD (fatal/nonfatal) using CG and CKD-EPI eGFRs. Of 133 873 eGFR values, the ratio of CG to CKD-EPI was ≥ 1.1 in 22 092 (16.5%) and the difference between them (CG minus CKD-EPI) was ≥ 10 mL/min/1.73 m(2) in 20 867 (15.6%). Differences between CKD-EPI and CG were much greater when CG was not standardized for body surface area (BSA). A total of 403 persons developed moderate CKD using CG [incidence 8.9/1000 person-years of follow-up (PYFU); 95% confidence interval (CI) 8.0-9.8] and 364 using CKD-EPI (incidence 7.3/1000 PYFU; 95% CI 6.5-8.0). CG-derived eGFRs were equal to CKD-EPI-derived eGFRs at predicting ESRD (n = 36) and death (n = 565), as measured by the Akaike information criterion. CG-based moderate and advanced CKDs were associated with ESRD [adjusted incidence rate ratio (aIRR) 7.17; 95% CI 2.65-19.36 and aIRR 23.46; 95% CI 8.54-64.48, respectively], as were CKD-EPI-based moderate and advanced CKDs (aIRR 12.41; 95% CI 4.74-32.51 and aIRR 12.44; 95% CI 4.83-32.03, respectively). Differences between eGFRs using CG adjusted for BSA or CKD-EPI were modest. In the absence of a gold standard, the two formulae predicted clinical outcomes with equal precision and can be used to estimate GFR in HIV-positive persons.
    HIV Medicine 10/2013; · 3.16 Impact Factor
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    ABSTRACT: The GESIDA and National AIDS Plan panel of experts have proposed "preferred regimens" of antiretroviral treatment (ART) as initial therapy in HIV infected patients for 2013. The objective of this study is to evaluate the costs and effectiveness of initiating treatment with these "preferred regimens". An economic assessment of costs and effectiveness (cost/effectiveness) was performed using decision tree analysis models. Effectiveness was defined as the probability of having viral load <50copies/mL at week48, in an intention-to-treat analysis. Cost of initiating treatment with an ART regime was defined as the costs of ART and its consequences (adverse effects, changes of ART regime and drug resistance analyses) during the first 48weeks. The perspective of the analysis is that of the National Health System was applied, only taking into account differential direct costs: ART (official prices), management of adverse effects, resistance studies, and determination of HLA B*5701. The setting is Spain and the costs are those of 2013. A sensitivity deterministic analysis was performed, constructing three scenarios for each regimen: baseline, most favourable, and most unfavourable cases. In the baseline case scenario, the cost of initiating treatment ranges from 6,747euros for TDF/FTC+NVP to 12,059euros for TDF/FTC+RAL. The effectiveness ranges between 0.66 for ABC/3TC+LPV/r and ABC/3TC+ATV/r, and 0.87 for TDF/FTC+RAL and ABC/3TC+RAL. Effectiveness, in terms of cost/effectiveness, varies between 8,396euros and 13,930euros per responder at 48weeks, for TDF/FTC/RPV and TDF/FTC+RAL, respectively. Taking ART at official prices, the most effective regimen was TDF/FTC/RPV, followed by the rest of non-nucleoside containing regimens. The sensitivity analysis confirms the robustness of these findings.
    Enfermedades Infecciosas y Microbiología Clínica 08/2013; · 1.48 Impact Factor
  • Ref. No: WO/2013/127976, Year: 06/2013
  • AIDS Research and Human Retroviruses 03/2013; · 2.71 Impact Factor
  • AIDS 03/2013; · 6.41 Impact Factor
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    ABSTRACT: BACKGROUND:: Detection of episomal HIV cDNA has been associated with greater levels of CD8 and CD4 T-cell activation in HIV-1-infected HAART-suppressed individuals. However, HAART intensification exclusively reduced CD8 T cell activation. METHODS:: We evaluated activation markers 12 weeks after raltegravir withdrawal in a previously described 48-week raltegravir-intensification study. Subjects (n=34) were subgrouped into 2-LTR (n=12) or 2-LTR (n=22) subgroups according to delectability of 2-LTR episomes during intensification period. RESULTS:: The initial differences in CD8 T-cell activation between subgroups were lost after intensification. Linear mixed models revealed significant reductions in CD8 T-cell activation in both 2-LTR and 2-LTR subgroups, suggesting that raltegravir impacts subjects irrespective of 2-LTR detection. Remarkably, a partial rebound in CD8 activation markers after raltegravir discontinuation was observed in the 2-LTR subgroup. This restored the differences between subgroups observed at study entry, particularly in terms of CD38 expression within CD8 memory T-cells. Conversely, CD4 T-cell activation remained unchanged in both subgroups during the study period, although an early and transient CD45RA CD4 T-cells redistribution from tissues was apparent. CONCLUSION:: CD8 T-cell activation undergoes reversible changes during raltegravir intensification and discontinuation in patients showing detectable 2-LTR circles. The general decrease in CD8 T-cell activation and a transient CD45RA CD4 T-cell redistribution in intensified individuals may reflect residual viral replication during apparently suppressive HAART.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 02/2013; · 4.65 Impact Factor
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    ABSTRACT: Combination antiretroviral therapy (cART) greatly improves survival and quality of life of HIV-1-infected patients; however, cART must be continued indefinitely to prevent viral rebound and associated disease progression. Inducing HIV-1-specific immune responses with a therapeutic immunization has been proposed to control viral replication after discontinuation of cART as an alternative to "cART for life." We report safety, tolerability, and immunogenicity results associated with a control of viral replication for a therapeutic vaccine using autologous monocyte-derived dendritic cells (MD-DCs) pulsed with autologous heat-inactivated whole HIV. Patients on cART with CD4(+) >450 cells/mm(3) were randomized to receive three immunizations with MD-DCs or with nonpulsed MD-DCs. Vaccination was feasible, safe, and well tolerated and shifted the virus/host balance. At weeks 12 and 24 after cART interruption, a decrease of plasma viral load setpoint ≥1 log was observed in 12 of 22 (55%) versus 1 of 11 (9%) and in 7 of 20 (35%) versus 0 of 10 (0%) patients in the DC-HIV-1 and DC-control groups, respectively. This significant decrease in plasma viral load observed in immunized recipients was associated with a consistent increase in HIV-1-specific T cell responses. These data suggest that HIV-1-specific immune responses elicited by therapeutic DC vaccines could significantly change plasma viral load setpoint after cART interruption in chronic HIV-1-infected patients treated in early stages. This proof of concept supports further investigation of new candidates and/or new optimized strategies of vaccination with the final objective of obtaining a functional cure as an alternative to cART for life.
    Science translational medicine 01/2013; 5(166):166ra2. · 10.76 Impact Factor
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    ABSTRACT: Introduction The GESIDA and National AIDS Plan panel of experts have proposed “preferred regimens” of antiretroviral treatment (ART) as initial therapy in HIV infected patients for 2013. The objective of this study is to evaluate the costs and effectiveness of initiating treatment with these “preferred regimens”. Methods An economic assessment of costs and effectiveness (cost/effectiveness) was performed using decision tree analysis models. Effectiveness was defined as the probability of having viral load < 50 copies/mL at week 48, in an intention-to-treat analysis. Cost of initiating treatment with an ART regime was defined as the costs of ART and its consequences (adverse effects, changes of ART regime and drug resistance analyses) during the first 48 weeks. The perspective of the analysis is that of the National Health System was applied, only taking into account differential direct costs: ART (official prices), management of adverse effects, resistance studies, and determination of HLA B*5701. The setting is Spain and the costs are those of 2013. A sensitivity deterministic analysis was performed, constructing three scenarios for each regimen: baseline, most favourable, and most unfavourable cases. Results In the baseline case scenario, the cost of initiating treatment ranges from 6,747 euros for TDF/FTC + NVP to 12,059 euros for TDF/FTC + RAL. The effectiveness ranges between 0.66 for ABC/3TC + LPV/r and ABC/3TC + ATV/r, and 0.87 for TDF/FTC + RAL and ABC/3TC + RAL. Effectiveness, in terms of cost/effectiveness, varies between 8,396 euros and 13,930 euros per responder at 48 weeks, for TDF/FTC/RPV and TDF/FTC + RAL, respectively. Conclusions Taking ART at official prices, the most effective regimen was TDF/FTC/RPV, followed by the rest of non-nucleoside containing regimens. The sensitivity analysis confirms the robustness of these findings.
    Enfermedades Infecciosas y Microbiología Clínica 01/2013; 31(9):568–578. · 1.48 Impact Factor
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    ABSTRACT: OBJECTIVE:: The impact of host genetics factors on the incidence of dyslipidemia in antiretroviral-naïve HIV patients starting antiretroviral therapy(ART) is not clear. We assessed the role of SNPs identified from previous GWAS studies adjusting for the contribution of non-genetic factors. METHODS:: We assessed 192 SNPs in an HIV-cohort who started ART(1997-2008) including a protease inhibitor(PI) or a non-nucleoside reverse transcriptase(NNRTI). Patients had fasting plasma lipids Total-Chol,LDL-C,HDL-C and TG measured prior to their ART initiation and after one year. A logistic regression model was constructed and multiple-test was corrected using 10%FDR. Haplotypes and gene interactions were analyzed. RESULTS:: A total of 727 individuals were successfully genotyped(n = 381_PI-group;n = 346_NNRTI-group). Age and HCVco-infection were associated with increases and decreases respectively in T-Chol and LDL-C(p < 0.01). PI-containing ART showed an unfavourable association with T-Chol(p < 0.01) and TG(p = 7.4E-4) and NNRTI-containing ART was favourably associated with HDL-C(p < 0.01). Moreover, SNPs in APOB were associated with an increase of LDL-C(rs10495712[p = 3.18E-4];rs754524[p = 1.26E-3]). Six SNPs in three genes showed association with a favourable effect on HDL-C levels when ART included NNRTI:ABCA1(rs4149313,p = 2.97E-4),LIPC(rs1800588,p = 2.13E-3;rs473224,p = 3.06E-4;rs261336,p = 2.23E-3) and CETP(rs173539,p = 2.96E-3; rs3764261,p = 1.52E-3). After 10%FDR correction for multipletesting,one and six SNPs displayed significant associations with LDL-C and HDL-C respectively. CONCLUSIONS:: In HIV infected patients staring ART, one SNP in APOBwas associated with an increase of LDL-C. SNPs in ABCA1/LIPC/CETP were favourably associated with HDL-C when ART included NNRTI. However, an unfavourable effect on T-Chol and TG levels was observed when ART included PI. The risk of hypercholesterolaemia increasedwith age and decreased with HCVco-infection. These findings might help to individualize the selection of ART.
    AIDS (London, England) 12/2012; · 4.91 Impact Factor
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    ABSTRACT: BACKGROUND: Several potential immunological benefits have been observed during treatment with the CC chemokine receptor 5 (CCR5) antagonist maraviroc, in addition to its antiviral effect. Our objective was to analyse the in vitro effects of CCR5 blockade on T lymphocyte function and homeostasis. METHODS: Peripheral blood mononuclear cells (PBMCs) from both HIV-negative (n = 28) and treated HIV-positive (n = 27) individuals were exposed in vitro to different concentrations of maraviroc (0.1-100 μM). Effects on T cell activation were analysed by measuring the expression of the CD69, CD38, HLA-DR and CD25 receptors as well as CCR5 density using flow cytometry. Spontaneous and chemokine-induced chemotaxis were measured by transwell migration assays, and polyclonal-induced proliferation was assessed by a lymphoproliferation assay and carboxyfluorescein succinimidyl ester staining. RESULTS: Maraviroc increases CCR5 surface expression on activated T cells, even at low doses (0.1 μM). Slight differences were detected in the frequency and mean fluorescence intensity of activation markers at high concentrations of maraviroc. Expression of CD25, CD38 and HLA-DR tended to decrease in both CD4+ and CD8+ T lymphocytes, whereas expression of CD69 tended to increase. Maraviroc clearly inhibits T cell migration induced by chemokines in a dose-dependent manner. Moreover, at 100 μM, maraviroc tends to inhibit T cell proliferation. CONCLUSIONS: These data showed that in vitro exposure to maraviroc decreases some activation expression markers on T lymphocytes and also migration towards chemoattractants. These results support the additional immunological effects of CCR5 blockade and suggest that maraviroc might have potential capacity to inhibit HIV-associated chronic inflammation and activation, both by directly affecting T cell activation and by reducing entrapment of lymphocytes in lymph nodes.
    Journal of Antimicrobial Chemotherapy 11/2012; · 5.34 Impact Factor
  • Enfermedades Infecciosas y Microbiología Clínica 10/2012; 30(8):511–512. · 1.48 Impact Factor
  • Enfermedades Infecciosas y Microbiología Clínica 10/2012; 30(8):511-2. · 1.48 Impact Factor
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    ABSTRACT: To analyze the effect of switching the ritonavir-boosted protease inhibitor (PI/r) in a stable combined antiretroviral therapy (cART) regimen to raltegravir on low-density lipoprotein (LDL) particles, and lipoprotein-associated phospholipase A2 (Lp-PLA2). Substudy of a multicenter randomized trial that compared the efficacy of switching a PI/r to raltegravir-based cART in stable HIV-infected patients. LDL size and phenotype (by gel-gradient electrophoresis), Lp-PLA2 (by 2-thio-PAF [Cayman]), proprotein convertase subtilisin/kexin type 9 (PCSK9) (by ELISA), and standard lipid parameters were measured at baseline and week 48. Eighty-one (PI/r n = 41 and raltegravir n = 40) patients were evaluated. No differences in baseline demographic and metabolic variables between arms were found except in apolipoprotein (Apo) B (p = 0.042). At week 48, total cholesterol (TC) (p < 0.001), LDL-c (p = 0.023), non-high density lipoprotein cholesterol non-high-density lipoprotein cholesterol (non-HDL-c) (p < 0.001), TC/HDL (p = 0.026), triglyceride (p < 0.001), Apo B (p < 0.001), Apo A-I (p = 0.004) and Lp (a) (p = 0.005) decreased in raltegravir arm compared to PI/r arm. At week 48, a shift from LDL phenotype B to the less atherogenic phenotype A was observed only in raltegravir arm (p < 0.001). LDL size increased (PI/r 2.1 nm, p = 0.019; raltegravir 3.8 nm, p = 0.001) and cholesterol content in small and dense LDL subfractions (LDL 4,5,6) decreased (PI/r p = 0.007, raltegravir p = 0.006) at week 48 in both arms. Total Lp-PLA2 activity (PI/r p = 0.037 and raltegravir p = 0.051) and PCSK9 plasma concentration decreased in both arms (PI/r p = 0.034 and raltegravir p < 0.001). Switching a PI/r to a raltegravir-based cART in virologically suppressed HIV-infected patients was associated with an overall improvement in lipid profile, including a shift to a less atherogenic LDL phenotype.
    Atherosclerosis 09/2012; 225(1):200-7. · 3.71 Impact Factor
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    Retrovirology 09/2012; 9(2). · 5.66 Impact Factor

Publication Stats

7k Citations
1,828.92 Total Impact Points

Institutions

  • 1982–2014
    • Hospital Clínic de Barcelona
      • • Servicio de Farmacia
      • • Servicio de Enfermedades Infecciosas
      Barcino, Catalonia, Spain
  • 2011–2013
    • TAISS - Técnicas Avanzadas de Investigación en Servicios de Salud
      Madrid, Madrid, Spain
    • Instituto de Salud Carlos III
      Madrid, Madrid, Spain
    • The Global Fund to Fight AIDS, Tuberculosis and Malaria
      Genève, Geneva, Switzerland
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
    • Hospital Universitari de Bellvitge
      l'Hospitalet de Llobregat, Catalonia, Spain
  • 2004–2013
    • University College London
      • • Department of Infection and Population Health
      • • Royal Free Hospital
      Londinium, England, United Kingdom
  • 1982–2013
    • University of Barcelona
      • • Department of Medicine
      • • Unitat de Bioestadistica
      • • Facultad de Medicina
      Barcino, Catalonia, Spain
  • 2012
    • IDIBELL Bellvitge Biomedical Research Institute
      Barcino, Catalonia, Spain
    • University of Copenhagen
      • Copenhagen HIV Programme (CHIP)
      Copenhagen, Capital Region, Denmark
  • 2010–2011
    • Hospital Universitari Germans Trias i Pujol
      • Department of Clinical Pharmacology
      Badalona, Catalonia, Spain
  • 1999–2010
    • IDIBAPS August Pi i Sunyer Biomedical Research Institute
      Barcino, Catalonia, Spain
    • Universitat Rovira i Virgili
      • Faculty of Medicine and Science of Health
      Tarragona, Catalonia, Spain
  • 1984–2008
    • Southern Medical Clinic
      San Fernando, City of San Fernando, Trinidad and Tobago
  • 1996–2007
    • Hospital Universitari Joan XXIII de Tarragona
      Tarraco, Catalonia, Spain
  • 2003
    • Hospital Universitario Fundacion Alcorcon
      Madrid, Madrid, Spain
  • 2000
    • Karolinska University Hospital
      • Department of Infectious Diseases
      Stockholm, Stockholm, Sweden
  • 1998
    • Hospital General Universitario Morales Meseguer
      Murcia, Murcia, Spain
    • Hospital Universitario Virgen del Rocío
      Hispalis, Andalusia, Spain
  • 1994
    • Université Libre de Bruxelles
      Bruxelles, Brussels Capital Region, Belgium
    • Copenhagen University Hospital Hvidovre
      • Department of Infectious Diseases
      Hvidovre, Capital Region, Denmark