J M Gatell

IDIBAPS August Pi i Sunyer Biomedical Research Institute, Barcino, Catalonia, Spain

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Publications (378)1930.53 Total impact

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    ABSTRACT: Background: Although virus-specific responses are rarely detected by conventional approaches, we report here the detection of T-cell responses in HESN by two distinct assays. Methods: HIV-specific T cell responses were analyzed by ELISPOT in PBMC from HESN after a 48h-co-culture with boosted dendritic cells (bDC). Additionally, a boosted flow cytometry approach was used to capture anti-viral T cell responses. Host genetic factors and T cell activation were also analyzed to assess their implication on HIV exposure. Results: Of 45 HESN individuals tested, up to 11 (24,4%) showed at least one response to peptide pools covering HIV Gag and Nef. A positive correlation was observed between the intensity (p=0.0022) and magnitude (p=0.0174) of the response detected in the HESN and the viral load of the HIV+ partner. Moreover, the result from the boosted flow and cytomix analyses showed a dominant Th1- like response pattern against HIV antigens, especially in CD8 T cell population. Conclusions: The combined use of our bDC technique with a boosted flow cytometric approach allows us both to detect specific HIV positive responses in a higher percentage of HESN and to define specific effector function profiles. This study contributes to a better understanding of resistance to HIV infection.
    AIDS 05/2015; · 6.56 Impact Factor
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    ABSTRACT: Ex vivo analysis of mitochondrial function may reveal HIV progression and the impact of ART. We propose a mitochondrial and apoptotic in vitro model using Jurkat T cells incubated with plasma. The objectives of this study were to evaluate mitochondrial and apoptotic lesions in this model in relation to HIV progression, and to assess the effect of >1 year of standard non-thymidine-containing therapy. This was a cross-sectional comparison among three age- and gender-matched groups (n = 19 × 3): healthy non-HIV-infected participants, HIV-infected long-term non-progressors (LTNPs) and standard antiretroviral-naive chronically infected patients [standard progressors (Sps)], longitudinally evaluated before (Sp1) and after (Sp2) >1 year of efavirenz + tenofovir + emtricitabine therapy. We analysed mitochondrial DNA content by RT-PCR, mitochondrial function by spectrophotometry, mitochondrial protein synthesis by western blot analysis, mitochondrial dynamics by western blot analysis (MFN2), apoptotic transition pore formation by western blot analysis (VDAC-1) and mitochondrial membrane potential and annexin V/propidium iodide fluorescence by flow cytometry. There was a decreasing non-significant trend towards lower mitochondrial parameters for HIV-infected values with respect to uninfected control reference values. HIV progression (LTNP versus Sp1) was associated with decreased mitochondrial genetic, functional and translational parameters, which partially recovered after treatment intervention (Sp2). Mitochondrial fusion showed a trend to decrease non-significantly in Sp patients compared with LTNP patients, especially after therapy. All apoptotic parameters showed a trend to increase in Sp1 with respect to LTNP, followed by recovery in Sp2. We proposed an in vitro model for mitochondrial and apoptotic assessment to test the effects of HIV infection and its therapy, resembling in vivo conditions. This model could be useful for clinical research purposes. © The Author 2015. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
    Journal of Antimicrobial Chemotherapy 04/2015; DOI:10.1093/jac/dkv101 · 5.44 Impact Factor
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    ABSTRACT: Very little information is available on the involvement of newly-characterized adipokines in HIV/HAART-associated lipodystrophy syndrome (HALS). Our aim was to determine whether apelin, apelin receptor, omentin, RBP4, vaspin and visfatin genetic variants and plasma levels are associated with HALS. We performed a cross-sectional multi-centre study that involved 558 HIV-1-infected patients treated with a stable HAART regimen, 240 of those with overt HALS and 318 without HALS. Epidemiological and clinical variables were determined. Polymorphisms in the apelin, omentin, RBP4, vaspin and visfatin genes were assessed by genotyping. Plasma apelin, apelin receptor, omentin, RBP4, vaspin and visfatin levels were determined by ELISA in 163 patients (81 with HALS and 82 without HALS) from whom stored plasma samples were available. Student's t-test, one-way ANOVA, χ(2) test, Pearson and Spearman correlations, and linear regression analysis were used for statistical analyses. There were no associations between the different polymorphisms assessed and the HALS phenotype. Circulating RBP4 was significantly higher (p<0.001) and plasma omentin was significantly lower (p=0.001) in patients with HALS compared with those without HALS; differences in plasma levels of the remaining adipokines were non-significant between groups. Circulating RBP4 concentration was predicted independently by the presence of HALS. Apelin and apelin receptor levels were independently predicted by body mass index. Visfatin concentration was predicted independently by the presence of AIDS. HALS is associated with higher RBP4 and lower omentin in plasma. These two adipokines, particularly RBP4, may be a link between HIV/HAART and fat redistribution syndromes. Copyright © 2015. Published by Elsevier Ltd.
    Clinical Microbiology and Infection 04/2015; DOI:10.1016/j.cmi.2015.04.002 · 5.20 Impact Factor
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    ABSTRACT: A proportion of patients who spontaneously control viral load (controllers) experienced clinical progression. We hypothesized that microbial translocation would independently determine the rate of disease progression in controllers. sCD14, lipopolysaccharide-binding protein (LBP) and EndoCab levels were assessed in 114 antiretroviral-naive patients with CD4 T cells above 500 cells/μl (including 63 controllers and 51 noncontrollers). The independent predictive value of these markers on time to progression to the combined endpoint of AIDS, non-AIDS event, initiation of combination antiretroviral therapy (cART) or CD4 cell count less than 500 cells/μl was assessed using a Cox regression model. Most of the patients progressed to a combined endpoint (60%). Clinical progression in controllers was significantly lower than in noncontrollers (P = 0.02). Controllers with lower than the median baseline CD4 T-cell count and higher than the median baseline viral load, sCD14 and EndoCab levels had a worse prognosis (P < 0.0001, P = 0.007, P = 0.05 and P = 0.012), while noncontrollers with higher than the median baseline LBP level also had a worse prognosis (P = 0.019). sCD14 and LBP increased and EndoCab decreased over time [from baseline (median values: 1486, 17604 ng/ml and 68 MMU/ml, respectively, to the date of event or the last determination (median values: 1663, 20230 ng/ml and 49 MMU/ml), respectively] in controllers (P = 0.04, 0.08 and 0.0006, respectively). Microbial translocation seems to be an important determinant of clinical progression in HIV-infected controllers independently of viremia. Measures to improve the intestinal mucosa damage or decrease translocation could influence the outcome in these patients.
    AIDS 02/2015; 29(6). DOI:10.1097/QAD.0000000000000596 · 6.56 Impact Factor
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    ABSTRACT: a Background: A proportion of patients who spontaneously control viral load (controllers) experienced clinical progression. We hypothesized that microbial translocation would independently determine the rate of disease progression in controllers. Methods: sCD14, lipopolysaccharide-binding protein (LBP) and EndoCab levels were assessed in 114 antiretroviral-naive patients with CD4 þ T cells above 500 cells/ml (including 63 controllers and 51 noncontrollers). The independent predictive value of these markers on time to progression to the combined endpoint of AIDS, non-AIDS event, initiation of combination antiretroviral therapy (cART) or CD4 þ cell count less than 500 cells/ml was assessed using a Cox regression model. Results: Most of the patients progressed to a combined endpoint (60%). Clinical progression in controllers was significantly lower than in noncontrollers (P ¼ 0.02). Controllers with lower than the median baseline CD4 þ T cell count and higher than the median baseline viral load, sCD14 and EndoCab levels had a worse prognosis (P < 0.0001, P ¼ 0.007, P ¼ 0.05 and P ¼ 0.012), while noncontrollers with higher than the median baseline LBP level also had a worse prognosis (P ¼ 0.019). sCD14 and LBP increased and EndoCab decreased over time [from baseline (median values: 1486, 17604 ng/ml and 68 MMU/ml, respectively, to the date of event or the last determination (median values: 1663, 20230 ng/ml and 49 MMU/ml), respectively] in controllers (P ¼ 0.04, 0.08 and 0.0006, respectively). Conclusion: Microbial translocation seems to be an important determinant of clinical progression in HIV-infected controllers independently of viremia. Measures to improve the intestinal mucosa damage or decrease translocation could influence the outcome in these patients.
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    ABSTRACT: HIV-1 infection increases plasma levels of inflammatory markers. Combination antiretroviral therapy (cART) does not restore inflammatory markers to normal levels. Since intensification of cART with raltegravir reduced CD8 T-cell activation in the Discor-Ral and IntegRal studies, we have evaluated the effect of raltegravir intensification on several soluble inflammation markers in these studies. Longitudinal plasma samples (0-48 weeks) from the IntegRal (n = 67, 22 control and 45 intensified individuals) and the Discor-Ral studies (44 individuals with CD4 T-cell counts<350 cells/µl, 14 control and 30 intensified) were assayed for 25 markers. Mann-Whitney, Wilcoxon, Spearman test and linear mixed models were used for analysis. At baseline, different inflammatory markers were strongly associated with HCV co-infection, lower CD4 counts and with cART regimens (being higher in PI-treated individuals), but poorly correlated with detection of markers of residual viral replication. Although raltegravir intensification reduced inflammation in individuals with lower CD4 T-cell counts, no effect of intensification was observed on plasma markers of inflammation in a global analysis. An association was found, however, between reductions in immune activation and plasma levels of the coagulation marker D-dimer, which exclusively decreased in intensified patients on protease inhibitor (PI)-based cART regimens (P = 0.040). The inflammatory profile in treated HIV-infected individuals showed a complex association with HCV co-infection, the levels of CD4 T cells and the cART regimen. Raltegravir intensification specifically reduced D-dimer levels in PI-treated patients, highlighting the link between cART composition and residual viral replication; however, raltegravir had little effect on other inflammatory markers.
    PLoS ONE 12/2014; 9(12):e114142. DOI:10.1371/journal.pone.0114142 · 3.53 Impact Factor
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    ABSTRACT: Fixed-dose combination antiretroviral therapy administered as a single-tablet regimen (STR) may improve virologic suppression rates. The effect of STRs on development of resistance when virologic failure occurs on STRs is not known. To compare the rate of emergent drug resistance mutations (DRMs) on first-line therapy with coformulated tenofovir disoproxil fumarate (TDF)/emtricitabine (FTC)/efavirenz (EFV) as an STR versus TDF, lamivudine (3TC) or FTC, and EFV given as non-STR. Patients from eight cohorts and four randomized clinical trials who received first-line antiretroviral therapy with Atripla (STR group) or with TDF + FTC/3TC + EFV (non-STR group) were eligible if a genotypic resistance test was available immediately after the first episode of viral failure. The DRM list from the 2013 version of IAS-USA was used. One hundred and eighty-six patients were included in the final analysis, 122 (65.6%) from eight cohorts and 64 (34.1%) from four randomized clinical trials. The overall proportion of patients with at least one DRM at viral failure was 67.7%, including 53.4% (31 of 58) in the STR group vs. 74.2% (95 of 128) in the non-STR group (P = 0.005). Among patients exclusively from cohorts, at least one DRM was detected in 53.4% (31 of 58) in the STR group vs. 78.1% (50 of 64) in the non-STR group (P = 0.004). DRMs for individual drugs were: TDF, 15.5 vs. 16.4% (P = 0.87); 3TC/FTC, 31 vs. 35.2% (P = 0.58); and NNRTI, 51.7 vs. 65.6% (P = 0.07). The proportion of patients with an M184V/I among the 128 patients who received FTC was 32.8 vs. 36.2% among the 58 treated with 3TC (P = 0.65). Compared to patients receiving the STR-Atripla, those receiving the same components individually in a non-STR regimen have a statistically significantly increased risk of selecting for DRMs associated with their drugs on failure.
    AIDS 11/2014; 28(17):1. DOI:10.1097/QAD.0000000000000424 · 6.56 Impact Factor
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    ABSTRACT: Doravirine (DOR) is an investigational NNRTI (aka MK-1439) that retains activity against common NNRTI-resistant mutants. We have previously reported the Part 1 results from a two-part, randomized, double-blind, Phase IIb study in ART-naïve HIV-1-positive patients (1). At doses of 25, 50, 100 and 200 mg qd, DOR plus open-label tenofovir/emtricitabine (TDF/FTC) demonstrated potent antiretroviral activity comparable to EFV 600 mg qhs plus TDF/FTC and was generally well tolerated at week 24. DOR 100 mg was selected for use in patients continuing in Part 1 and those newly enrolled in Part 2.
    Journal of the International AIDS Society 11/2014; 17(4 Suppl 3):19532. DOI:10.7448/IAS.17.4.19532 · 4.21 Impact Factor
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    ABSTRACT: Purpose Very scarce information has been published to date with the combination of ABC/3TC/NVP but it is currently being used in clinical practice in Spain and Portugal. Our aim was to present the clinical experience with this regimen in a cohort of adult HIV-infected antiretroviral (ARV)-naïve patients. Methods Retrospective, multicentre, cohort study. Consecutive adult HIV-infected ARV-naïve HLA-B*5701-negative patients, who started ABC/3TC/NVP between 2005-2013, with at least one follow-up visit, were included. Demographic, clinical and laboratory variables were assessed at baseline, month 1, and every three–four months thereafter. The primary end point was HIV-1 viral load (VL)<40 c/mL at 48 weeks. Data were analyzed by intent-to-treat (ITT) (switch=failure, and missing=failure) and on treatment (OT) analyses. Results 78 patients were included. Median follow up was 26 (0.1-84) months. 86% were male, median age 41 (23-69) years, 9% had AIDS, 8% were HCV+, baseline CD4 was 275 (10-724) cells/µL and median VL 4.58 (3.02-6.92) log. After 48 weeks, VL was<40 c/mL in 89.8% (OT), 79.7% (M=F) and 65.4% (S=F) and at 96 weeks in 88.5%, 78.9% and 61.6%, respectively. CD4 increased +246 (p<0.001) and +292 (p<0.001) cells/uL after 48 and 96 weeks, respectively. One or more drugs of the regimen were discontinued in 33 (42.3%) patients. In 15 (19.2%) patients (13 NVP, 2 ABC/3TC) therapy was stopped due to toxicity after a median of one month (in only two cases after six months of follow up): 80% of them had rash/liver toxicity. Six (7.7%) patients discontinued ART due to virologic failure, five (6.4%) because of other reasons and seven (9%) were lost to follow-up. ALT but not AST significantly increased (+0.07 ukat/L at 96 weeks, p=0.033). A significant increase of 25%, 26% and 42% in total cholesterol, LDLc and HDLc, respectively, and a significant decrease in TC/HDL ratio (6%, p=0.008) was observed after 96 weeks. Conclusions Despite a considerable proportion of patients had to stop therapy due to toxicity (most associated with NVP), those initially tolerating this regimen presented a high virologic and immunologic response after 96 weeks, as well as a favourable lipid profile. ABC/3TC/NVP may be a suitable alternative first regimen, mainly in countries with economic constraints.
    Journal of the International AIDS Society 11/2014; 17(4(Suppl 3)):19773. DOI:10.7448/IAS.17.4.19773 · 4.21 Impact Factor
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    ABSTRACT: The National AIDS Plan and the Spanish AIDS study group (GESIDA) proposes "preferred regimens" (PR) of antiretroviral treatment (ART) as initial therapy in HIV-infected patients. In 2013, the recommended regimens were all triple therapy regimens. The Gardel Study assessed the efficacy of a dual therapy (DT) combination of lopinavir/ritonavir (LPV/r) plus lamivudine (3TC). Our objective is to evaluate the GESIDA PR and the DT regimen LPV/r+3TC cost/efficacy ratios. Decision tree models were built. Efficacy: probability of having viral load <50 copies/mL at week 48. ART regime cost: costs of ART, adverse effects, and drug resistance tests during the first 48 weeks. Cost/efficacy ratios varied between 5,817 and 13,930 euros per responder at 48 weeks, for the DT of LPV/r+3TC and tenofovir DF/emtricitabine+raltegravir, respectively. Taking into account the official Spanish prices of ART, the most efficient regimen was DT of LPV/r+3TC, followed by the triple therapy with non-nucleoside containing regimens. Copyright © 2015 Elsevier España, S.L.U. y Sociedad Española de Enfermedades Infecciosas y Microbiología Clínica. All rights reserved.
    Journal of the International AIDS Society 11/2014; 17(4 Suppl 3):19603. DOI:10.7448/IAS.17.4.19603 · 4.21 Impact Factor
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    ABSTRACT: Introduction Monotherapy with protease-inhibitors (MPI) may be an alternative to cART for HIV treatment. We assessed the impact of this strategy on immune activation, bacterial translocation and inflammation. Methods We performed a cross-sectional study comparing patients on successful MPI (n=40) with patients on cART (n=20). Activation, senescence, exhaustion and differentiation stage in CD4+ and CD8+ T lymphocyte subsets, markers of monocyte activation, microbial translocation, inflammation, coagulation and low-level viremia were assessed. Results CD4+ or CD8+ T lymphocyte subset parameters were not significantly different between both groups. Conversely, as compared with triple cART, MPI patients showed a higher proportion of activated monocytes (CD14+ CD16−CD163+ cells, p=0.031), soluble markers of monocyte activation (sCD14 p=0.004, sCD163 p=0.002), microbial translocation (lipopolysaccharide (LPS)-binding protein; LBP p=0.07), inflammation (IL-6 p=0.04) and low-level viremia (p=0.035). In a multivariate model, a higher level of CD14+ CD16−CD163+ cells and sCD14, and presence of very low-level viremia were independently associated with MPI. Monocyte activation was independently associated with markers of inflammation (IL-6, p=0.006), microbial translocation (LBP, p=0.01) and low-level viremia (p=0.01). Conclusions Patients on MPI showed a higher level of monocyte activation than patients on standard therapy. Microbial translocation and low-level viremia were associated with the high level of monocyte activation observed in patients on MPI. The long-term clinical consequences of these findings should be assessed.
    Journal of the International AIDS Society 09/2014; 17(1):19246. DOI:10.7448/IAS.17.1.19246 · 4.21 Impact Factor
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    ABSTRACT: Since recent data suggest that nanoparticles and modified vaccinia ankara (MVA) vectors could play a pivotal role in HIV-1 therapeutics and vaccine design, in an ex vivo model of human monocyte-derived dendritic cells (MDDCs), we compared two different loading strategies with HIV-1 vaccine vehicles, either viral or synthetic derived. We used polylactic acid (PLA) colloidal biodegradable particles, coated with HIV Gag antigens (p24), and MVA expressing Gag (rMVA-gag and rMVA-gag/trans membrane) or Tat, Nef and Rev genes (rMVA tat+rev and rMVA nef). PLA-p24 captured by MDDCs from HIV-1 individuals induced a slight degree of MDDC maturation, cytokine and chemokine secretion and migration towards a gradient of CCL19 chemokine and highly increased HIV-specific CD8+ T-cell proliferation compared with p24 alone. After complete maturation induction of PLA-p24-pulsed MDDCs, maximal migration towards a gradient of CCL19 chemokine and induction of HIV-specific T-cell proliferation (two-fold higher for CD4+ than CD8+) and cytokine secretion (IFN-γ and IL-2) in the co-culture were observed. Upon exposure to MVA-gag, MDDCs produced cytokines and chemokines and maintained their capacity to migrate to a gradient of CCL19. MDDCs infected with MVA-gag and MVA-gag trans-membrane were able to induce HIV-specific CD8+ proliferation and secretion of IFN-γ, IL-2, IL-6 and TNF-α. We conclude that both HIV antigens loading strategies (PLA-p24 nanoparticles or MVA expressing HIV genes) induce HIV-1-specific T-cell responses, which are able to kill autologous gag-expressing cells. Thus, they are plausible candidates for the development of anti-HIV vaccines.
    Vaccine 09/2014; 32(47). DOI:10.1016/j.vaccine.2014.09.010 · 3.77 Impact Factor
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    ABSTRACT: Objetivo Describir la incidencia, la etiología y el pronóstico de la infección de las vías respiratorias bajas (IVRB) en los pacientes VIH, que acudieron a un Servicio de Urgencias (SU), durante el período del 2000–2010. Diseño del estudio Estudio prospectivo de 10 años de evolución. Métodos Se recogió únicamente el primer episodio del paciente que acude al SU por IRVB (definida según la European Respiratory Society). Se analizaron una serie de variables epidemiológicas y de laboratorio, así como la necesidad de ingreso en una unidad de cuidados intensivos (UCI). Se estudió la etiología de la IRVB y la incidencia. Finalmente se analizaron la influencia de las variables con la mortalidad a 30 días. Resultados Se incluyeron un total de 131 pacientes. La edad media fue de 39 ± 9 años. El 72% de los pacientes eran varones y el 18% de los pacientes requirieron ingreso en la UCI. La IRVB más frecuente fue la neumonía por P. jirovecci, seguida de la neumonía bacteriana en 27 y la tuberculosis pulmonar en 20. La incidencia de IRVB se ha ido reduciendo gradualmente de forma significativa, 6,13 × 1.000 pacientes/año en 2000 a 0,23 × 1.000 pacientes/año en 2010 (p < 0,05). El análisis de regresión logística mostró que la única variable que predijo mortalidad fue el ingreso en UCI (p < 0,05; OR: 73,01). Conclusión La IRVB es una enfermedad cuya incidencia y etiología han ido disminuyendo y cambiando respectivamente, probablemente en relación con la utilización generalizada del TAR. Sin embargo, todavía presenta una mortalidad nada despreciable, que es mayor cuando el paciente requiere ingreso en la UCI.
    Enfermedades Infecciosas y Microbiología Clínica 09/2014; 33(4). DOI:10.1016/j.eimc.2014.06.002 · 1.88 Impact Factor
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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; 58(11). DOI:10.1128/AAC.03481-14 · 4.45 Impact Factor
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    ABSTRACT: To evaluate the results of the treatment with pegylated interferon and ribavirin for recurrence of hepatitis C after liver transplantation in HCV/HIV-coinfected patients.
    Journal of Hepatology 08/2014; DOI:10.1016/j.jhep.2014.07.034 · 10.40 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 08/2014; DOI:10.1016/j.eimc.2014.05.016 · 1.88 Impact Factor
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    ABSTRACT: To evaluate the association of host genetics with changes in limb or trunk fat in a group of antiretroviral therapy (ART)-naive HIV-infected patients prospectively followed up according to the initiation and the type of ART.
    Journal of Antimicrobial Chemotherapy 07/2014; 69(11). DOI:10.1093/jac/dku266 · 5.44 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; DOI:10.3851/IMP2812 · 3.14 Impact Factor

Publication Stats

8k Citations
1,930.53 Total Impact Points

Institutions

  • 1999–2014
    • IDIBAPS August Pi i Sunyer Biomedical Research Institute
      Barcino, Catalonia, Spain
  • 1982–2014
    • Hospital Clínic de Barcelona
      • Servicio de Enfermedades Infecciosas
      Barcino, Catalonia, Spain
    • University of Barcelona
      • • Department of Medicine
      • • Facultad de Medicina
      Barcino, Catalonia, Spain
  • 2011–2013
    • TAISS - Técnicas Avanzadas de Investigación en Servicios de Salud
      Madrid, Madrid, Spain
    • Instituto de Salud Carlos III
      • National Center of Microbiology (CNM)
      Madrid, Madrid, Spain
    • Hospital Universitari de Bellvitge
      • Department of Infectious Diseases
      l'Hospitalet de Llobregat, Catalonia, Spain
  • 2011–2012
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
  • 1984–2008
    • Southern Medical Clinic
      San Fernando, City of San Fernando, Trinidad and Tobago
  • 2007
    • Granollers General Hospital
      Granollers, Catalonia, Spain
    • Hospital Universitari Joan XXIII de Tarragona
      Tarraco, Catalonia, Spain
  • 2005
    • Deutsche Gesellschaft für Sportmedizin und Prävention e.V.
      Germany
  • 2004
    • Parc de Salut Mar
      Barcino, Catalonia, Spain
  • 2001
    • University of Hamburg
      Hamburg, Hamburg, Germany
  • 2000
    • Odense University Hospital
      Odense, South Denmark, Denmark
    • Hospital Universitari Germans Trias i Pujol
      Badalona, Catalonia, Spain
  • 1998
    • Hospital General Universitario Morales Meseguer
      Murcia, Murcia, Spain
    • Hospital Universitario Virgen del Rocío
      Hispalis, Andalusia, Spain
  • 1996
    • University of Milan
      Milano, Lombardy, Italy
  • 1994
    • Université Libre de Bruxelles
      Bruxelles, Brussels Capital Region, Belgium
    • Copenhagen University Hospital Hvidovre
      • Department of Infectious Diseases
      Hvidovre, Capital Region, Denmark