C Tural

Hospital Universitari Germans Trias i Pujol, Badalona, Catalonia, Spain

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Publications (64)403.04 Total impact

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    ABSTRACT: HIV-infected individuals with a history of transmission via injection drug use (IDU) have poorer survival than other risk groups. The extent to which higher rates of hepatitis C (HCV) infection in IDU explain survival differences is unclear. Adults who started antiretroviral therapy (ART) between 2000-2009 in 16 European and North American cohorts with >70% complete data on HCV status were followed for 3 years. We estimated unadjusted and adjusted [for age, sex, baseline CD4 count and HIV-1 RNA, AIDS diagnosis prior to ART, and stratified by cohort] mortality hazard ratios (HR) for IDU (versus non-IDU) and for HCV-infected (versus HCV-uninfected). Of 32,703 patients 3,374 (10%) were IDU; 4,630 (14%) HCV+; 1,116 (3.4%) died. Mortality was higher in IDU compared with non-IDU (adjusted HR 2.71; 95% CI 2.32,3.16) and in HCV+ compared with HCV- (2.65; 2.31,3.04). The effect of IDU was substantially attenuated (1.57; 1.27,1.94) after adjustment for HCV, while attenuation of the effect of HCV was less substantial (2.04; 1.68,2.47) after adjustment for IDU. Both IDU and HCV were strongly associated with liver-related mortality (10.89; 6.47,18.3 for IDU and 14.0; 8.05,24.5 for HCV) with greater attenuation of the effect of IDU (2.43; 1.24,4.78) than for HCV (7.97; 3.83,16.6). Rates of CNS, respiratory and violent deaths remained elevated in IDU after adjustment for HCV. A substantial proportion of the excess mortality in HIV-infected IDU is explained by HCV co-infection. These findings underscore the potential impact on mortality of new treatments for HCV in HIV-infected people.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 04/2015; 69(3). DOI:10.1097/QAI.0000000000000603 · 4.39 Impact Factor
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    ABSTRACT: Chronic kidney disease (CKD) is a major health issue for HIV-positive individuals, associated with increased morbidity and mortality. Development and implementation of a risk score model for CKD would allow comparison of the risks and benefits of adding potentially nephrotoxic antiretrovirals to a treatment regimen and would identify those at greatest risk of CKD. The aims of this study were to develop a simple, externally validated, and widely applicable long-term risk score model for CKD in HIV-positive individuals that can guide decision making in clinical practice. A total of 17,954 HIV-positive individuals from the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study with ≥3 estimated glomerular filtration rate (eGFR) values after 1 January 2004 were included. Baseline was defined as the first eGFR > 60 ml/min/1.73 m2 after 1 January 2004; individuals with exposure to tenofovir, atazanavir, atazanavir/ritonavir, lopinavir/ritonavir, other boosted protease inhibitors before baseline were excluded. CKD was defined as confirmed (>3 mo apart) eGFR ≤ 60 ml/min/1.73 m2. Poisson regression was used to develop a risk score, externally validated on two independent cohorts. In the D:A:D study, 641 individuals developed CKD during 103,185 person-years of follow-up (PYFU; incidence 6.2/1,000 PYFU, 95% CI 5.7-6.7; median follow-up 6.1 y, range 0.3-9.1 y). Older age, intravenous drug use, hepatitis C coinfection, lower baseline eGFR, female gender, lower CD4 count nadir, hypertension, diabetes, and cardiovascular disease (CVD) predicted CKD. The adjusted incidence rate ratios of these nine categorical variables were scaled and summed to create the risk score. The median risk score at baseline was -2 (interquartile range -4 to 2). There was a 1:393 chance of developing CKD in the next 5 y in the low risk group (risk score < 0, 33 events), rising to 1:47 and 1:6 in the medium (risk score 0-4, 103 events) and high risk groups (risk score ≥ 5, 505 events), respectively. Number needed to harm (NNTH) at 5 y when starting unboosted atazanavir or lopinavir/ritonavir among those with a low risk score was 1,702 (95% CI 1,166-3,367); NNTH was 202 (95% CI 159-278) and 21 (95% CI 19-23), respectively, for those with a medium and high risk score. NNTH was 739 (95% CI 506-1462), 88 (95% CI 69-121), and 9 (95% CI 8-10) for those with a low, medium, and high risk score, respectively, starting tenofovir, atazanavir/ritonavir, or another boosted protease inhibitor. The Royal Free Hospital Clinic Cohort included 2,548 individuals, of whom 94 individuals developed CKD (3.7%) during 18,376 PYFU (median follow-up 7.4 y, range 0.3-12.7 y). Of 2,013 individuals included from the SMART/ESPRIT control arms, 32 individuals developed CKD (1.6%) during 8,452 PYFU (median follow-up 4.1 y, range 0.6-8.1 y). External validation showed that the risk score predicted well in these cohorts. Limitations of this study included limited data on race and no information on proteinuria. Both traditional and HIV-related risk factors were predictive of CKD. These factors were used to develop a risk score for CKD in HIV infection, externally validated, that has direct clinical relevance for patients and clinicians to weigh the benefits of certain antiretrovirals against the risk of CKD and to identify those at greatest risk of CKD.
    PLoS Medicine 03/2015; 12(3):e1001809. DOI:10.1371/journal.pmed.1001809 · 14.00 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
  • Gastroenterology 05/2014; 146(5):S-978. DOI:10.1016/S0016-5085(14)63553-8 · 13.93 Impact Factor
  • Journal of Hepatology 04/2014; 60(1):S469. DOI:10.1016/S0168-8278(14)61317-9 · 10.40 Impact Factor
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    ABSTRACT: The growing number of cases of acute hepatitis C (AHC) infections among human immunodeficiency virus type 1 (HIV-1)-positive men who have sex with men (MSM) in the last 10 years has promoted the search for predictors of AHC clearance as well as for epidemiological networks of viral transmission. We characterized the diversity and catalytic efficiency of HCV NS3/4A protease quasispecies in AHC patients coinfected with HIV-1. Plasma samples obtained at HCV diagnosis from 18 MSM HIV-coinfected patients with AHC were studied. Five HCV monoinfected patient samples with AHC were also investigated. An average of 39 clones from each sample was analysed. The catalytic efficiency of the dominant quasispecies (i.e. the most abundant) from each quasispecies was also assayed for mitochondrial antiviral signalling protein (MAVS) cleavage. Phylogenetic analysis identified two clusters of patients with highly related viruses, suggesting a common source of HCV infection. None of the 18 MSM HIV-coinfected patients spontaneously cleared HCV, although 78% of the treated patients achieved a sustained virological response after early treatment with pegylated interferon (pegIFN) plus ribavirin (RBV). The synonymous-nonsynonymous (ds/dn) mutation ratio, a marker of selective pressure, was higher in AHC compared to 26 HIV-1-infected men with genotype 1a chronic hepatitis C (CHC) (P < 0.0001). NS3/4A proteases from AHC patients also exhibited higher catalytic efficiency compared to CHC patients (P < 0.0001). No differences were found when ds/dn mutation ratios and NS3/4A protease catalytic efficiencies from AHC HIV-coinfected patients were compared with AHC monoinfected patients. The presence of epidemiological networks of HCV transmission was confirmed among HIV-1-positive MSM. In addition, substantial genetic diversity was demonstrated in AHC. NS3/4A protease efficiency cleaving MAVS may be associated with virus transmission and response to pegIFN/RBV treatment.
    Journal of Viral Hepatitis 03/2014; 21(6). DOI:10.1111/jvh.12254 · 3.31 Impact Factor
  • Zeitschrift für Gastroenterologie 01/2014; 52(01). DOI:10.1055/s-0033-1361025 · 1.67 Impact Factor
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    ABSTRACT: The aim of the study was to assess the progression of liver fibrosis in HIV/hepatitis C virus (HCV)-coinfected patients with no or mild-to-moderate fibrosis (stages F0-F2). Liver fibrosis was reassessed by transient elastometry (TE) between January 2009 and November 2011 in HIV/HCV-coinfected patients with stage F0-F2 fibrosis in a liver biopsy performed between January 1997 and December 2007. Patients with liver stiffness at the end of follow-up < 7.1 kPa were defined as nonprogressors, and those with values ≥ 9.5 kPa or who died from liver disease were defined as progressors. Cirrhosis was defined as a cut-off of 14.6 kPa. The follow-up period was the time between liver biopsy and TE. Cox regression models adjusted for age, gender and liver fibrosis stage at baseline were applied. The median follow-up time was 7.8 years [interquartile range (IQR) 5.5-10 years]. The study population comprised 162 patients [115 (71%) nonprogressors and 47 (29%) progressors; 19 patients (11.7%) had cirrhosis]. The median time from the diagnosis of HCV infection to the end of follow-up was 20 years (IQR 16.3-23.1 years). Three progressors died from liver disease (1.8%). The variables associated with a lower risk of progression were age ≤ 38 years (hazard ratio (HR) 0.32; 95% confidence interval (CI) 0.16-0.62; P = 0.001], having received interferon (HR 2.18; 95% CI 1.14-4.15; P = 0.017), being hepatitis B virus surface antigen (HBsAg) negative (HR 0.20; 95% CI 0.04-0.92; P = 0.039), and baseline F0-F1 (HR 0.43; 95% CI 0.28-0.86; P = 0.017). A high proportion of patients with stage F0-F2 fibrosis progress to advanced liver fibrosis. Advanced liver fibrosis must be included in the list of diseases associated with aging. Our results support the recommendation to offer HCV antiviral therapy to HIV/HCV-coinfected patients at early stages of liver fibrosis.
    HIV Medicine 11/2013; DOI:10.1111/hiv.12105 · 3.45 Impact Factor
  • Cristina Tural, Ramon Planas
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    ABSTRACT: Triple combination therapy with pegylated interferon, ribavirin and telaprevir is currently considered the gold standard for the treatment of chronic hepatitis C virus (HCV) infection. The most important features are an increase in rates of sustained viral response (74-79% vs 46% with pegylated interferon and ribavirin), as well as the possibility of early cessation of ineffective therapy due to the application of futility rules at weeks 4 and 12 (HCV-RNA > 1,000UI/ml), and the possibility of selecting candidates for the shortest treatments due to the clinical significance of extended rapid viral response (undetectable HCV-RNA at weeks 4 and 12 of triple therapy). Treatment length is mainly based on the stage of fibrosis and prior response to pegylated interferon and ribavirin. Thus, in both treatment-naïve patients and patients with recurrence after pegylated interferon therapy, the duration of treatment is 24 or 48 weeks (unless cirrhosis is present), depending on the presence of extended rapid viral response, while in cirrhotic patients and null responders, treatment length is 48 weeks. The main adverse effects of telaprevir therapy are anemia and skin rash. If these effects occur, the main measures that should be adopted are reduction of the ribavirin dose in anemia, and close monitoring and treatment cessation in skin rash, depending on its spread and severity.
    Enfermedades Infecciosas y Microbiología Clínica 07/2013; 31 Suppl 3:19-25. DOI:10.1016/S0213-005X(13)70120-4 · 1.88 Impact Factor
  • Journal of Hepatology 04/2013; 58:S9. DOI:10.1016/S0168-8278(13)60022-7 · 10.40 Impact Factor
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    ABSTRACT: Purpose of the study: Our aim was to evaluate factors associated with progression to AIDS/death in HIV-infected naïve pts initiating cART with low CD4 counts. Methods: Adult HIV-infected ARV-naïve pts with CD4 <200 who initiated NNRTI or PI-containing regimens between 1998 and 2009, were included. Primary end point was progression to AIDS (a first episode or a new AIDS-defining condition in pts with prior AIDS) or death. Kaplan-Meier curves were used to determine progression-free survival and multivariate Cox regression models were used to identify independent predictive factors of progression to AIDS/death. Summary of results: We included 1427 patients (80% men, median age 38 years, 25% IDU, 37% AIDS, 20% HCV) between 1998 and 2009. At baseline (BL), median (range) CD4 and viral load (VL) was 77 (1-199) cells/µL and 170,000 (19-8,750,000) copies/mL, respectively. After a median follow-up 4.6 years, 70% of pts reached CD4>200/µL, 65.2% reached undetectable VL and 268 (19%) pts progressed to AIDS/death during follow-up. The probability of AIDS/death at 5 years was 76%, 34%, 3% and 3%, in pts with BL CD4<100/VL>5 log and CD4<200/VL detectable during FU, BL CD4<100/ VL>5 log and CD4<200/VL undetectable during FU, BL CD4<100 and/or VL>5 log and CD4>200/VL undetectable during FU and BL CD4>100/ VL<5 log and CD4>200/VL undetectable during FU, respectively. In the multivariate analysis, several variables were associated with AIDS/death: CD4< 200 during FU (HR 10.89, p<0.001), detectable VL during FU (HR 3.49, p<0.001), age>50 years (HR 1.75, p=0.001), prior AIDS (HR 1.71, p<0.001) and BL VL>5 log (HR 1.45, p=0.011). If only pts without prior AIDS (n=895) were analyzed, the variables independently associated with AIDS/death were: CD4<200 during FU (HR 9.90, p<0.001), detectable VL during FU (HR 2.78, p<0.001) and BL VL>5 log (HR 1.62, p=0.016). Conclusions: In immunosuppressed patients initiating cARV therapy, not reaching CD4>200/µL during FU was the strongest variable associated with progression to AIDS/death. VL at BL and mainly at follow up also played a role in patient outcome.
    Journal of the International AIDS Society 11/2012; 15(6):18148. DOI:10.7448/IAS.15.6.18148 · 4.21 Impact Factor
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    ABSTRACT: Clin Microbiol Infect ABSTRACT: In this prospective, multicentre cohort study, we analysed specific prognostic factors and the impact of timing of highly active antiretroviral therapy (HAART) on disease progression and death among 625 human immunodeficiency virus (HIV)-1-infected, treatment-naïve patients diagnosed with an AIDS-defining disease. HAART was classified as early (<30 days) or late (30-270 days). Deferring HAART was significantly associated with faster progression to a new AIDS-defining event/death overall (p 0.009) and in patients with Pneumocystis jiroveci pneumonia (p 0.017). In the multivariate analysis, deferring HAART was associated with a higher risk of a new AIDS-defining event/death (p 0.002; hazard ratio 1.83; 95% CI 1.25-2.68). Other independent risk factors for poorer outcome were baseline diagnosis of AIDS-defining lymphoma, age >35 years, and low CD4(+) count (<50 cells/μL).
    Clinical Microbiology and Infection 07/2012; 19(7). DOI:10.1111/j.1469-0691.2012.03991.x · 5.20 Impact Factor
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    ABSTRACT: Information regarding liver retransplantation in HIV-infected patients is scant. Data from 14 HIV-infected patients retransplanted between 2002 and 2011 in Spain (6% retransplantation rate) were analyzed and compared with those from 157 matched HIV-negative retransplanted patients. In HIV-infected patients, early (≤30 days) retransplantation was more frequently indicated (57% vs. 29%; p = 0.057), and retransplantation for HCV recurrence was less frequently indicated (7% vs. 37%; p = 0.036). Survival probability after retransplantation in HIV-positive patients was lower than in HIV-negative patients, 42% versus 64% at 3 years, although not significantly (p = 0.160). Among HIV-infected patients, those with undetectable HCV RNA at retransplantation and those with late (>30 days) retransplantation showed better 3-year survival probability (80% and 67%, respectively), similar to that in their respective HIV-negative counterparts (72% and 70%). In HIV-infected and HIV-negative patients, 3-year survival probability in those with positive HCV RNA at retransplantation was 22% versus 65% (p = 0.008); in those with early retransplantation, 3-year survival probability was 25% versus 56% (p = 0.282). HIV infection was controlled with antiretroviral therapy after retransplantation. In conclusion, HIV-infected patients taken as a whole have unsatisfactory survival after liver retransplantation, although patients with undetectable HCV RNA at retransplantation or undergoing late retransplantation show a more favorable outcome.
    American Journal of Transplantation 06/2012; 12(9):2465-76. DOI:10.1111/j.1600-6143.2012.04142.x · 6.19 Impact Factor
  • Value in Health 11/2011; 14(7). DOI:10.1016/j.jval.2011.08.272 · 2.89 Impact Factor
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    ABSTRACT: Minority drug-resistant hepatitis C virus (HCV) variants may go undetected yet be clinically important. NS3/4A protease resistance substitutions V36A and A156S/T/V were selected in patients treated with protease inhibitors. The aim of this study was to investigate whether these substitutions pre-existed in HCV infected patients. An allele-specific PCR protocol that detected the NS3/4A protease resistance substitutions V36A and A156S/T/V was used to determine the prevalence of naturally occurring variants in 45 patients. All patient samples were infected with HCV of genotype 1b and were naïve for pegIFNα/ribavirin treatment. Thirty samples (67%) had at least one HCV PI-resistant variant. A156T (23, 51%) was detected more frequently than A156V (13, 29%) or A156S (1, 2%). V36A was detected in 12 samples (27%). These results demonstrate the high prevalence of minority drug-resistant NS3/4 protease resistance substitutions. Our results also demonstrate that allele-specific PCR can be used to detect minor HCV NS3 protease resistant variants in pretreatment samples and to study in detail the evolution of mutant viruses during targeted antiviral therapy.
    Journal of Viral Hepatitis 10/2011; 18(10):e578-82. DOI:10.1111/j.1365-2893.2011.01490.x · 3.31 Impact Factor
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    ABSTRACT: We examined whether determinants of disease progression and causes of death differ between injecting drug users (IDUs) and non-IDUs who initiate combination antiretroviral therapy (cART). The ART Cohort Collaboration combines data from participating cohort studies on cART-naïve adults from cART initiation. We used Cox models to estimate hazard ratios for death and AIDS among IDUs and non-IDUs. The cumulative incidence of specific causes of death was calculated and compared using methods that allow for competing risks. Data on 6269 IDUs and 37 774 non-IDUs were analysed. Compared with non-IDUs, a lower proportion of IDUs initiated cART with a CD4 cell count <200 cells/μL or had a prior diagnosis of AIDS. Mortality rates were higher in IDUs than in non-IDUs (2.08 vs. 1.04 per 100 person-years, respectively; P<0.001). Lower baseline CD4 cell count, higher baseline HIV viral load, clinical AIDS at baseline, and later year of cART initiation were associated with disease progression in both groups. However, the inverse association of baseline CD4 cell count with AIDS and death appeared stronger in non-IDUs than in IDUs. The risk of death from each specific cause was higher in IDUs than non-IDUs, with particularly marked increases in risk for liver-related deaths, and those from violence and non-AIDS infection. While liver-related deaths and deaths from direct effects of substance abuse appear to explain much of the excess mortality in IDUs, they are at increased risk for many other causes of death, which may relate to suboptimal management of HIV disease in these individuals.
    HIV Medicine 08/2011; 13(2):89-97. DOI:10.1111/j.1468-1293.2011.00940.x · 3.45 Impact Factor
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    ABSTRACT: Progression of liver fibrosis is associated with the risk of cirrhosis and end-stage liver disease. We aimed to evaluate fibrosis of the liver using three non-invasive indexes (FIB-4, Forns, and Pohl score) and its association with mortality of HCV-monoinfected and HCV/HIV-coinfected drug users. Patients and methods: longitudinal study in patients admitted to substance abuse treatment between 1994 and 2006. Socio-demographic data, drug use characteristics, blood samples for laboratory tests, and serology for HIV and hepatitis C virus infections were collected at admission. Patients were followed-up until December 2006 and mortality was ascertained through hospital charts and death certificates. Results: Four hundred and ninety-seven patients were included (83.1% men); median age at admission was 31 years (IQR: 27-35). The main drugs of abuse were opiates (89.5%) and cocaine (8.3%). Thirty-two percent of patients reported daily alcohol consumption. The estimated prevalence of advanced liver fibrosis (ALF) was higher among HCV/HIV-coinfected patients (9.2% to 17.3% depending on the index analyzed) than among the HCV-monoinfected patients (3% to 3.5%). Odds ratio (OR) for ALF were 3.3 to 6.0 times higher in coinfected patients as compared to the HCV-monoinfected. After a median follow-up time of 7.7 years (IQR: 4.1-9.9 years), almost 20% of patients had died. The estimated ALF at admission was associated with an increased risk of death (RR 1.85 to 3.89 depending on the index). Among those with ALF, mortality rates were similar in HCV-monoinfected and HCV/HIV-coinfected patients, as determined by the FIB-4 and Forns indexes. Conclusions: Estimation of liver fibrosis using serum markers may help with clinical decisions to facilitate access to treatment of chronic hepatitis C in this population.
    Current HIV research 06/2011; 9(4):256-62. DOI:10.2174/157016211796320298 · 2.14 Impact Factor
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    ABSTRACT: Most clinical guidelines recommend that AIDS-free, HIV-infected persons with CD4 cell counts below 0.350 × 10(9) cells/L initiate combined antiretroviral therapy (cART), but the optimal CD4 cell count at which cART should be initiated remains a matter of debate. To identify the optimal CD4 cell count at which cART should be initiated. Prospective observational data from the HIV-CAUSAL Collaboration and dynamic marginal structural models were used to compare cART initiation strategies for CD4 thresholds between 0.200 and 0.500 × 10(9) cells/L. HIV clinics in Europe and the Veterans Health Administration system in the United States. 20, 971 HIV-infected, therapy-naive persons with baseline CD4 cell counts at or above 0.500 × 10(9) cells/L and no previous AIDS-defining illnesses, of whom 8392 had a CD4 cell count that decreased into the range of 0.200 to 0.499 × 10(9) cells/L and were included in the analysis. Hazard ratios and survival proportions for all-cause mortality and a combined end point of AIDS-defining illness or death. Compared with initiating cART at the CD4 cell count threshold of 0.500 × 10(9) cells/L, the mortality hazard ratio was 1.01 (95% CI, 0.84 to 1.22) for the 0.350 threshold and 1.20 (CI, 0.97 to 1.48) for the 0.200 threshold. The corresponding hazard ratios were 1.38 (CI, 1.23 to 1.56) and 1.90 (CI, 1.67 to 2.15), respectively, for the combined end point of AIDS-defining illness or death. Limitations: CD4 cell count at cART initiation was not randomized. Residual confounding may exist. Initiation of cART at a threshold CD4 count of 0.500 × 10(9) cells/L increases AIDS-free survival. However, mortality did not vary substantially with the use of CD4 thresholds between 0.300 and 0.500 × 10(9) cells/L.
    Annals of internal medicine 04/2011; 154(8):509-15. DOI:10.1059/0003-4819-154-8-201104190-00001 · 16.10 Impact Factor
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    ABSTRACT: To provide detailed information about the natural history of HIV-hepatitis C virus (HCV)-coinfected patients with cirrhosis. Prospective cohort including 340 HIV-HCV-coinfected patients with compensated (n = 248) or decompensated (n = 92) cirrhosis. We evaluated predictors of survival and of first hepatic decompensation. The mortality rate for patients with decompensated and compensated cirrhosis was 27.14 deaths per 100 person-years [95% confidence interval (CI) 18.93-35.35] and 3.98 deaths per 100 person-years (95% CI 2.42-5.54), respectively. Rate of first hepatic decompensation in patients with compensated cirrhosis was 4.62 per 100 persons-years (95% CI 2.91-6.33). In the complete cohort, permanent HAART interruption during follow-up, CD4 cell count nadir and baseline Child-Pugh score (CPS) B or C were significantly associated with shorter survival. In patients with compensated cirrhosis factors significantly associated with decreased survival were having the first hepatic decompensation during follow-up, permanent HAART discontinuation, and CPS B and C at baseline. For patients with compensated cirrhosis, time since diagnosis of HCV infection, CPS B and C and permanent HAART discontinuation were significantly associated with the risk of first hepatic decompensation. Sustained viral response to anti-HCV therapy was not independently associated with better survival in patients with compensated cirrhosis. HIV-HCV-coinfected patients with cirrhosis have a relatively good 3-year survival (87%). In contrast, 2-year survival of patients with decompensated liver cirrhosis is only 50%. Three-year survival was mostly impacted by liver-related factors and HAART maintenance.
    AIDS (London, England) 02/2011; 25(7):899-904. DOI:10.1097/QAD.0b013e3283454174 · 6.56 Impact Factor
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Publication Stats

1k Citations
403.04 Total Impact Points


  • 2000–2014
    • Hospital Universitari Germans Trias i Pujol
      • • Department of Clinical Pharmacology
      • • Department of Internal Medicine
      Badalona, Catalonia, Spain
  • 1989–2013
    • Autonomous University of Barcelona
      • Department of Medicine
      Cerdanyola del Vallès, Catalonia, Spain
  • 2008
    • Universidad Autónoma de Madrid
      Madrid, Madrid, Spain