Juan G Abraldes

University of Alberta, Edmonton, Alberta, Canada

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Publications (178)1500.73 Total impact

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    ABSTRACT: Non-selective β-blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence on response to β-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to β-blockers according to such stage, we performed a prospective, multicenter (tertiary care setting), cross sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis, before and after i.v. propranolol (0.15 mg/Kg). 194 patients had an HVPG ≥10 mmHg (clinically significant PHT: CSPH), either with no-varices (n= 80) or small varices (n= 114), and 79 had an HVPG >5 and <10 mmHg (subclinical-PHT). Patients with CSPH had higher liver stiffness (P< 0.001), worse MELD score (P<0.001), more porto-systemic collaterals (P= 0.01) and splenomegaly (P= 0.01) on ultrasound and lower platelet count (P<0.001) than those with subclinical-PHT. Patients with CSPH had lower systemic vascular resistance (1336±423 vs 1469±335 dyne.s.cm−5, P<0.05) and higher cardiac index (3.3±0.9 vs 2.8±0.4 L/min/m2, P<0.01). After propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with CSPH (-16±12% vs -8±9%, P<0.01). The HVPG decreased ≥10% from baseline in 69% of patients with CSPH vs 36% with sub-clinical-PHT (P<0.001) and decreased ≥20% in 40% vs 12%, respectively (P=0.001). Conclusion: Patients with subclinical-PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute β-blockade than those with CSPH. This suggests that β-blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than in earlier stages. This article is protected by copyright. All rights reserved.
    Hepatology 09/2015; DOI:10.1002/hep.28264 · 11.06 Impact Factor
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    ABSTRACT: Non-selective beta-blockers (NSBB) are widely used since they have been proved effective in the prophylaxis of acute variceal bleeding (AVB). However, still a significant proportion of patients experience AVB whilst on treatment with NSBB and their impact on prognosis of AVB is unknown. The present study aimed at assessing the effect of being on prophylactic therapy with NSBB on 5-day failure and 6-week mortality of cirrhotic patients admitted with AVB. 142 patients were included: 49 patients were receiving prophylactic therapy with NSBB (NSBB group) and 93 patients were not (control group). There were some differences in the baseline characteristics between the groups: higher proportion of alcoholic etiology and active alcoholism (37% vs. 10%), higher platelets count and lower hematocrit at admission in the control group. However, the severity of AVB and initial treatment were similar. 5-day failure occurred in 20% of patients (14% in NSBB vs. 24% in controls; p = 0.27). The adjusted OR for 5-day failure under NSBB was 2.46; 95% CI: 0.53-11.37; p=0.25. Nineteen patients (13%) died and 2 had liver transplantation within 6-weeks. The probability of survival at 6 weeks was 96% in the NSBB group and 82% in the control group (p=0.02). After adjusting by propensity score and model for end-stage liver disease (MELD) score, the NSBB adjusted OR for 6-week mortality was 0.38; 95% CI: 0.05- 2.63; p=0.32. The estimated association between NSBB with both 5-day failure and 6-week mortality was homogenous across all MELD spectrums. Our study indicates that being under prophylactic NSBB treatment is not a negative prognostic indicator for the short-term survival of cirrhotic patients admitted with AVB. This article is protected by copyright. All rights reserved. © 2015 by the American Association for the Study of Liver Diseases.
    Hepatology 09/2015; DOI:10.1002/hep.28151 · 11.06 Impact Factor
  • Juan G Abraldes · Puneeta Tandon ·
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    ABSTRACT: Variceal bleeding is the most serious complication of portal hypertension. All cirrhotic patients should be screened endoscopically for varices which are present in about 30% of compensated and 60% of decompensated patients at diagnosis. In patients without varices, endoscopy surveillance should be continued every 2 years. Patients with high-risk varices (moderate or large in size, or with red color signs, or in Child-Pugh C patients) should be treated with a nonselective β-blocker to prevent bleeding (propranolol, nadolol or carvedilol). Endoscopic banding ligation is also effective for the prevention of first bleeding, and it is the first choice in patients with contraindications or intolerance to β-blockers. Acute variceal hemorrhage still has a high mortality rate (around 15%) and requires intensive care management and conservative blood transfusion policy. Treatment is based on the combined use of vasoactive drugs, endoscopic band ligation and prophylactic antibiotics. Failures are best managed by transjugular intrahepatic portosystemic shunt (TIPS). Balloon tamponade or specifically designed covered esophageal stents can be used as a bridge to definitive therapy in unstable patients. Early, preemptive TIPS might be the first choice in patients at high risk of failure (Child-Pugh B with active bleeding or Child-Pugh C up to 13 points). Patients surviving a variceal bleeding are at high risk of rebleeding. A combination of β-blockers and endoscopic band ligation is the most effective therapeutic approach. Preliminary data suggest that the addition of simvastatin increases survival in these patients. © 2015 S. Karger AG, Basel.
    Digestive Diseases 07/2015; 33(4):524-33. DOI:10.1159/000374101 · 2.18 Impact Factor
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    Journal of Hepatology 06/2015; 63(3). DOI:10.1016/j.jhep.2015.06.010 · 11.34 Impact Factor

  • Journal of Hepatology 04/2015; 62:S198-S199. DOI:10.1016/S0168-8278(15)30025-8 · 11.34 Impact Factor

  • Journal of Hepatology 04/2015; 62:S354. DOI:10.1016/S0168-8278(15)30360-3 · 11.34 Impact Factor
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    ABSTRACT: Unlabelled: Alcoholic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death. However, the driving factors are largely unknown. At admission, patients with AH often show criteria of systemic inflammatory response syndrome (SIRS) even in the absence of an infection. We hypothesize that the presence of SIRS may predispose to MOF and death. To test this hypothesis, we studied a cohort including 162 patients with biopsy-proven AH. The presence of SIRS and infections was assessed in all patients, and multivariate analyses identified variables independently associated with MOF and 90-day mortality. At admission, 32 (19.8%) patients were diagnosed with a bacterial infection, while 75 (46.3%) fulfilled SIRS criteria; 58 patients (35.8%) developed MOF during hospitalization. Short-term mortality was significantly higher among patients who developed MOF (62.1% versus 3.8%, P < 0.001). The presence of SIRS was a major predictor of MOF (odds ratio = 2.69, P = 0.025) and strongly correlated with mortality. Importantly, the course of patients with SIRS with and without infection was similar in terms of MOF development and short-term mortality. Finally, we sought to identify serum markers that differentiate SIRS with and without infection. We studied serum levels of high-sensitivity C-reactive protein, procalcitonin, and lipopolysaccharide at admission. All of them predicted mortality. Procalcitonin, but not high-sensitivity C-reactive protein, serum levels identified those patients with SIRS and infection. Lipopolysaccharide serum levels predicted MOF and the response to prednisolone. Conclusion: In the presence or absence of infections, SIRS is a major determinant of MOF and mortality in AH, and the mechanisms involved in the development of SIRS should be investigated; procalcitonin serum levels can help to identify patients with infection, and lipopolysaccharide levels may help to predict mortality and the response to steroids. (Hepatology 2015;62:762-772).
    Hepatology 03/2015; 62(3). DOI:10.1002/hep.27779 · 11.06 Impact Factor
  • Juan G. Abraldes · Puneeta Tandon ·
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    ABSTRACT: Non-selective beta-blockers (NSBBs) have been used for over 30 years in the treatment of portal hypertension in patients with cirrhosis. They have proven efficacy in preventing first variceal bleeding and rebleeding and in reducing mortality. NSBBs might additionally reduce the risk of infections in cirrhosis. Recent data suggest that patients with refractory ascites or that have experienced a spontaneous bacterial peritonitis might have an increased mortality if they are treated with NSBBs. The lack of randomized trials, and the conflicting results from observational studies, makes it difficult to reach a definitive conclusion. In this article, we review the current evidence on the benefits and harms of NSBBs in cirrhosis and provide recommendations for their use in special populations.
    03/2015; 14(1). DOI:10.1007/s11901-015-0256-8
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    ABSTRACT: Background: For patients awaiting liver transplantation, we aimed to determine the prevalence and predictors of insufficient protein intake as well as to determine whether very low protein intake was an independent predictor of malnutrition and mortality. Materials and Methods: Adults with cirrhosis who were activated on our local liver transplant waiting list between January 2000 and October 2009 were included. Estimated protein intake was derived from dietary records. Patients with incomplete dietary records were excluded. Multivariable logistic regression and competing risk analysis were used. Results: Of 742 potential patients, 112 were excluded due to insufficient data, leaving 630 patients for evaluation. Mean protein intake was 1.0 ± 0.36 g/kg/d and only 24% of patients met the expert consensus recommended threshold of > 1.2 g/kg of protein per day. Very low protein intake (< 0.8 g/kg/d) was associated with worse liver disease severity (as measured by Child-Pugh or MELD). Protein intake below 0.8 g/kg/d was an independent predictor both of malnutrition as measured by the subjective global assessment (adjusted odds ratio [95% confidence interval (CI)]: 2.0 [1.3-3.0]) and of transplant waiting list mortality (adjusted hazard ratio [95% CI]: 1.8 [1.2-2.7]). Conclusion: In this large cohort of liver transplant waitlisted patients, very low protein intake was prevalent and independently associated with malnutrition and mortality. Unlike many other prognostic factors, protein intake is potentially modifiable. Prospective studies are warranted to evaluate the effect of targeted protein repletion on clinically relevant outcomes such as muscle mass, muscle function, immune function, and mortality. © 2015 American Society for Parenteral and Enteral Nutrition.
    Nutrition in Clinical Practice 02/2015; 30(4). DOI:10.1177/0884533614567716 · 2.40 Impact Factor
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    ABSTRACT: The late and fast developments in the field of viral hepatitis were highly expected in the 2014 AASLD Liver Meeting. Several combinations using direct acting antivirals (DAAs) showed high rates of sustained virological response (∼ 95%). Importantly, high cure rates were also demonstrated in patients with previous treatment failures, decompensated cirrhosis and hepatitis C recurrence after transplantation, making it clear that the interferon era is over (not so clear for ribavirin, which might still have a role in difficult-to-treat populations). Importantly, sustained virological response was associated with an improvement in liver function (MELD and Child-Pugh scores) in patients with advanced liver disease. In the field of liver cirrhosis, there were relevant data assessing the optimal empirical antibiotic therapy in patients with spontaneous bacterial peritonitis (SBP) and high risk of resistant bacteria, as well as studies evaluating the role of terlipresin in type I hepatorenal syndrome and in septic shock. Regarding hepatic encephalopathy, two randomized trials suggest that the manipulation of the microbioma in patients with cirrhosis may have a role in the management of this complication. Some novel data on NASH support the beneficial effect of bariatric surgery (after failure of life-style intervention) in morbid obese patients with such diagnosis: clinical and histological improvements after surgery were evident in most patients with sufficient follow-up. A few controlled studies focused on the treatment of severe acute alcoholic hepatitis. Finally, several studies on hepatocellular carcinoma (HCC) were presented in the Liver Meeting, covering topics such as ultrasound screening in cirrhosis, cryoablation treatment of early HCC and the relevance of downstaging in patients with HCC awaiting liver transplantation. Copyright © 2015. Published by Elsevier B.V.
  • J.G. Abraldes · P. Sarlieve · P. Tandon ·
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    ABSTRACT: Hepatic venous pressure gradient (HVPG) measurement is one of the most useful techniques in the field of hepatology. The HVPG is close to the best surrogate marker in chronic liver diseases. It reflects disease severity and has strong prognostic value with regard to survival and decompensation in patients with compensated cirrhosis, during acute bleeding and before liver resection surgery. Furthermore, repeat measurements of the HVPG provide unique information on the response to the medical treatment of portal hypertension and represent an invaluable tool for developing new drugs for this syndrome. Transjugular liver biopsy adds very little time or complications to an HVPG procedure, and allows adequate liver sampling in several circumstances in which the percutaneous approach is contraindicated. The use of automated cutting needles, as compared to aspiration needles, is associated with better quality samples.
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    ABSTRACT: Real-time shear wave elastography (RT-SWE) might be useful to assess the severity of portal hypertension; reliability criteria for measurement are needed. We prospectively included 88 consecutive patients undergoing hepatic venous pressure gradient measurement (HVPG, reference standard) for portal hypertension. Liver stiffness (LS) was measured by RT-SWE and by transient elastography (TE). Spleen stiffness (SS) was measured by RT-SWE. Reliability criteria for RT-SWE were searched, and the accuracy of these techniques to identify HVPG⩾10 mmHg (clinically significant portal hypertension, CSPH) was tested and internally validated by bootstrapping analysis. LS and SS by RT-SWE were feasible respectively in 87 (99%) and 58 (66%) patients. Both correlated with HVPG (LS: R=0.611, p<0.0001 and SS: R=0.514,p<0.0001). LS performed well for diagnosing CSPH (optimism corrected AUROC 0.858). Reliability of measurements was influenced by standard deviation (SD)/median ratio and depth. SD/median ⩽0.10 and depth of measurement <5.6 cm were associated to 96.3% well classified for CSPH, while when one or none of the criteria were fulfilled the rated was, respectively, 76.4% and 44.4%. Measurements fulfilling at least one criterion were considered acceptable; in these patients RT-SWE performance to detect CSPH was excellent (AUROC 0.939; 95%CI: 0.865-1.000;p<0.0001; best cut-off: 15.4 kPa). LS by RT-SWE and by TE were strongly correlated (R=0.795,p<0.0001) and performed similarly both in "per protocol" and in "intention-to-diagnose" analysis after applying reliability criteria. Data CONCLUSIONS: LS by RT-SWE is an accurate method to diagnose CSPH if reliability criteria (SD/median ⩽0.10 and/or depth <5.6 cm) are fulfilled. Copyright © 2014. Published by Elsevier B.V.
    Journal of Hepatology 12/2014; 62(5). DOI:10.1016/j.jhep.2014.12.007 · 11.34 Impact Factor
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    ABSTRACT: In the liver, the transcription factor, Kruppel-like factor 2 (KLF2), is induced early during progression of cirrhosis to lessen the development of vascular dysfunction; nevertheless, its endogenous expression results insufficient to attenuate establishment of portal hypertension and aggravation of cirrhosis. Herein, we aimed to explore the effects and the underlying mechanisms of hepatic KLF2 overexpression in in vitro and in vivo models of liver cirrhosis. Activation phenotype was evaluated in human and rat cirrhotic hepatic stellate cells (HSC) treated with the pharmacological inductor of KLF2 simvastatin, with adenovirus codifying for this transcription factor (Ad-KLF2), or vehicle, in presence/absence of inhibitors of KLF2. Possible paracrine interactions between parenchymal and non-parenchymal cells overexpressing KLF2 were studied. Effects of in vivo hepatic KLF2 overexpression on liver fibrosis and systemic and hepatic haemodynamics were assessed in cirrhotic rats. KLF2 upregulation profoundly ameliorated HSC phenotype (reduced α-smooth muscle actin, procollagen I and oxidative stress) partly via the activation of the nuclear factor (NF)-E2-related factor 2 (Nrf2). Coculture experiments showed that improvement in HSC phenotype paracrinally ameliorated liver sinusoidal endothelial cells probably through a vascular endothelial growth factor-mediated mechanism. No paracrine interactions between hepatocytes and HSC were observed. Cirrhotic rats treated with simvastatin or Ad-KLF2 showed hepatic upregulation in the KLF2-Nrf2 pathway, deactivation of HSC and prominent reduction in liver fibrosis. Hepatic KLF2 overexpression was associated with lower portal pressure (-15%) due to both attenuations in the increased portal blood flow and hepatic vascular resistance, together with a significant improvement in hepatic endothelial dysfunction. Exogenous hepatic KLF2 upregulation improves liver fibrosis, endothelial dysfunction and portal hypertension in cirrhosis. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Gut 12/2014; 64(9). DOI:10.1136/gutjnl-2014-308338 · 14.66 Impact Factor
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    ABSTRACT: Antibiotics are frequently overused and associated with serious adverse events in patients with cirrhosis. However, these drugs are recommended for all patients presenting with acute variceal hemorrhage (AVH). We investigated whether patients should be stratified for antibiotic prophylaxis based on Child-Pugh scores, to estimate risks of bacterial infection, rebleeding, and mortality, and whether antibiotics have equal effects on patients of all Child Pugh classes. We performed sensitivity analysis using model for end-stage liver disease (MELD) scores. In a retrospective study, we analyzed data from 381 adult patients with cirrhosis and AVH (70% male; mean age, 56 years), admitted from 2000 through 2009 to 2 tertiary care hospitals in Edmonton, Alberta. We excluded patients with bacterial infection on the day of AVH. The association between antibiotic prophylaxis and outcomes was adjusted by liver disease severity and by a propensity score. The patients included in the study had mean MELD scores of 16, and 54% received antibiotic prophylaxis. Overall, antibiotic therapy was associated with lower risks of infection (adjusted odds ratio, 0.37; 95% confidence interval, 0.91-0.74) and mortality (adjusted odds ratio, 0.63; 95% confidence interval, 0.31-1.29). Among patients of Child-Pugh class A given antibiotics, only 2% developed infections and mortality was 0.4%. Among patients of Child-Pugh class B given antibiotics, 6% developed infections, compared to 14% of patients who did not receive antibiotics; antibiotics did not affect mortality. Administration of antibiotics to patients of Child-Pugh class C reduced infections and mortality by ∼50%, compared to patients who did not receive antibiotics. The MELD was not as useful as Child-Pugh class in identifying patients at risk for infection. Based on a retrospective analysis of patients with cirrhosis and AVH, those of Child-Pugh class A have lower rates of bacterial infection and lower mortality, in the absence of antibiotic prophylaxis, than patients of classes B or C. The recommendation for routine antibiotic prophylaxis for this subgroup requires further evaluation. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
    Clinical Gastroenterology and Hepatology 11/2014; 13(6). DOI:10.1016/j.cgh.2014.11.019 · 7.90 Impact Factor
  • Juan G. Abraldes · Puneeta Tandon · Jason Yap ·
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    ABSTRACT: Watch a video presentation of this articleWatch the interview with the authorAnswer questions and earn CME
    Clinical Liver Disease 10/2014; 4(4). DOI:10.1002/cld.423
  • Juan G Abraldes · Puneeta Tandon ·

    Hepatology 10/2014; 61(3). DOI:10.1002/hep.27583 · 11.06 Impact Factor
  • Annalisa Berzigotti · Maria Reig · Juan G. Abraldes · Jaume Bosch · Jordi Bruix ·
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    ABSTRACT: Unlabelled: Whether preoperative clinically significant portal hypertension (CSPH) has or not an impact on the outcome of surgery for hepatocellular carcinoma (HCC) in patients with compensated cirrhosis is debated. This systematic review assesses the impact of CSPH on the outcome of HCC in patients with compensated cirrhosis treated with surgery. We performed a systematic search of the MEDLINE database (articles published in full in English language from 1996 to October 2013) and related bibliography for studies reporting on the postoperative outcomes (3- and 5-year mortality and/or early clinical decompensation) of patients with HCC and compensated cirrhosis treated with surgery according to the presence or absence of CSPH. Independent extraction of articles by two authors using predefined data fields, including study quality indicators, was used; pooled analyses were based on random-effects models. Eleven studies in total met our inclusion criteria (eight studies for 3- and 5-year postoperative mortality and eight for postoperative clinical decompensation). Moderate heterogeneity among studies for both outcomes was observed, which disappeared after pooling studies using similar methods to assess CSPH. The presence of CSPH increased the risk of 3- and 5-year mortality versus absence of CSPH (pooled odds ratio [OR] for 3-year mortality: 2.09; 95% confidence interval [CI]: 1.52-2.88; for 5-year mortality: 2.07; 95% CI: 1.51-2.84). CSPH also increased the risk of postoperative clinical decompensation (pooled OR: 3.04; 95% CI: 2.02-4.59). Conclusions: CSPH (evaluated by any method) significantly increases the risk of 3- and 5-year mortality and of clinical decompensation after surgery for HCC.
    Hepatology 09/2014; 61(2). DOI:10.1002/hep.27431 · 11.06 Impact Factor
  • Juan G. Abraldes · Philippe Sarlieve · Puneeta Tandon ·
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    ABSTRACT: Portal pressure is estimated through measuring the hepatic venous pressure gradient (HVPG). The main clinical applications of HVPG measurements include diagnosis, classification, and monitoring of portal hypertension, risk stratification, identification of candidates for liver resection, and monitoring efficacy of β-adrenergic blockers. Clinically significant portal hypertension is defined as an HVPG of 10 mm Hg or greater. Patients who experience a reduction in the HVPG of 20% or greater or to lower than 12 mm Hg in response to β-blocker therapy have a markedly decreased risk of bleeding (or rebleeding), ascites, and spontaneous bacterial peritonitis, resulting in improved survival rates. Copyright © 2014 Elsevier Inc. All rights reserved.
    Clinics in Liver Disease 08/2014; 18(4). DOI:10.1016/j.cld.2014.07.002 · 3.66 Impact Factor
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    ABSTRACT: Patients with cirrhosis have reduced exercise tolerance, measured objectively as decreased peak exercise oxygen uptake (peak VO2). Reduced peak VO2 is associated with decreased survival time. The effect of aerobic exercise training on peak VO2 has not been well studied in patients with cirrhosis. We evaluated the safety and efficacy of 8 weeks of supervised exercise on peak VO2, quadriceps muscle thickness, and quality of life. In a prospective pilot study, stable patients (79% male, 57.6±6.7 years old) with Child Pugh class A or B cirrhosis (mean model for end-stage liver disease [MELD]score, 10±2.2) were randomly assigned to groups that received exercise training (n=9) or usual care (controls, n=10) at the University of Alberta Hospital in Canada, from February through June 2013. Supervised exercise was performed on a cycle ergometer 3 days/week for 8 weeks at 60% to 80% of baseline peak VO2. Peak VO2, quadriceps muscle thickness (measured by ultrasound), thigh circumference, answers from chronic liver disease questionnaires (CLDQs), EQ-visual analog scores (VAS), 6-minute walk distance, and MELD scores were evaluated at baseline and at week 8. Analysis of covariance was used to compare variables. At week 8, peak VO2 was 5.3 ml/kg/min higher exercise group compared with controls (95% confidence interval, 2.9-7.8; P=.001). Thigh circumference (P=.001), thigh muscle thickness (P=.01), and EQ-VAS determined self-perceived health status (P=.01) were also significantly higher in the exercise group compared with controls at week 8; fatigue subscores of the CLDQ were lower in the exercise group compared with controls (P=.01). No adverse events occurred during cardiopulmonary exercise testing or training. In a controlled prospective pilot trial, 8 weeks of supervised aerobic exercise training increased peak VO2 and muscle mass and reduced fatigue in patients with cirrhosis. No relevant adverse effects were observed. Larger trials are needed to evaluate the effects of exercise in patients with cirrhosis. Clinicaltrials.gov number, NCT01799785.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 04/2014; 12(11). DOI:10.1016/j.cgh.2014.04.016 · 7.90 Impact Factor

  • Journal of Hepatology 04/2014; 60(1):S525. DOI:10.1016/S0168-8278(14)61462-8 · 11.34 Impact Factor

Publication Stats

5k Citations
1,500.73 Total Impact Points


  • 2014-2015
    • University of Alberta
      • Division of Gastroenterology
      Edmonton, Alberta, Canada
  • 2010-2015
    • Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas
      Barcino, Catalonia, Spain
  • 2002-2014
    • IDIBAPS August Pi i Sunyer Biomedical Research Institute
      Barcino, Catalonia, Spain
  • 2000-2014
    • Hospital Clínic de Barcelona
      • Servicio de Hepatología
      Barcino, Catalonia, Spain
  • 2002-2013
    • University of Barcelona
      • Department of Medicine
      Barcino, Catalonia, Spain
  • 2011
    • Instituto de Salud Carlos III
      Madrid, Madrid, Spain
  • 2008-2010
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
  • 2009
    • Centro de Investigación Biomédica Esther Koplowitz
      Barcino, Catalonia, Spain
    • Hospital Universitario Ramón y Cajal
      • Departamento de Medicina Interna
      Madrid, Madrid, Spain
  • 2007
    • Hospital Medica Sur
      Ciudad de México, Mexico City, Mexico
    • Hospital General Universitario de Alicante
      Alicante, Valencia, Spain
  • 2006
    • Hospital General Universitario Gregorio Marañón
      Madrid, Madrid, Spain
  • 2004-2006
    • Yale University
      • • Section of Digestive Diseases
      • • Department of Internal Medicine
      New Haven, Connecticut, United States
  • 2005
    • Azienda Ospedaliero Universitaria Careggi
      • Department of Hematology
      Firenzuola, Tuscany, Italy