V Arroyo

Instituto de Salud Carlos III, Madrid, Madrid, Spain

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Publications (516)3525.38 Total impact

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    ABSTRACT: Abstract BACKGROUND & AIMS: Acute-on Chronic Liver Failure (ACLF) is a frequent syndrome (30% prevalence) characterized by acute decompensation of cirrhosis, organ failure(s) and high short-term mortality. This study develops and validates a specific prognostic score for ACLF patients. METHODS: Data from 1,349 patients included in the CANONIC study were used. First, a simplified organ function scoring system (CLIF-Consortium Organ Failure score, CLIF-C OFs) to diagnose ACLF was developed using data from all patients. Subsequently, in 275 patients with ACLF, CLIF-C OFs and two other independent predictors of mortality (age and white-cell count) were combined to develop a specific prognostic score for ACLF (CLIF CONSORTIUM score for ACLF, CLIF-C ACLFs). Concordance index (C-index) was used to compare the discrimination abilities of CLIF-C ACLFs, MELD (MELDs), MELD-Sodium (MELD-Nas) and Child-Pugh (CPs) scores. CLIF-C ACLFs was validated in an external cohort and assessed for sequential use. RESULTS: CLIF-C ACLFs showed a significantly higher predictive accuracy than MELDs, MELD-Nas and CPs, reducing (19-28%) the corresponding prediction error rates at all the main time-points after ACLF diagnosis (28, 90, 180 and 365 days) in both the CANONIC and the external validation cohort. CLIF-C ACLFs computed at 48 hours, 3-7 days and 8-15 days after ACLF diagnosis predicted 28-day mortality significantly better than at diagnosis. CONCLUSIONS: CLIF-C ACLFs at ACLF diagnosis is superior to MELDs and MELD-Nas in predicting mortality. CLIF-C ACLFs is a clinically relevant, validated scoring system that can be used sequentially to stratify the risk of mortality in ACLF patients.
    Journal of Hepatology 06/2014; · 9.86 Impact Factor
  • Vicente Arroyo, Richard Moreau
    Nature medicine 05/2014; 20(5):467-9. · 27.14 Impact Factor
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    ABSTRACT: Human serum albumin (HSA) is one of the most frequent treatments in patients with decompensated cirrhosis. Prevention of paracentesis-induced circulatory dysfunction, prevention of type-1 HRS associated to bacterial infections and treatment of type-1 hepatorenal syndrome are the main indications. In these indications treatment with HSA is associated to improvement in survival. Albumin is a stable and very flexible molecule with a heart shape, 585 residues and three domains of similar size, each one containing two sub-domains. Many of the physiological functions of HSA rely on its ability to bind an extremely wide range of endogenous and exogenous ligands, to increase their solubility in plasma, to transport them to specific tissues and organs or to dispose of them when they are toxic. The chemical structure of albumin can be altered by some specific processes (oxidation, glication) leading to rapid clearance and catabolism. An outstanding feature of HSA is its capacity to bind lypopolysaccharide and other bacterial producs (lypoteichoic acid and peptidoglican), reactive oxygen species, nitric oxide and other nitrogen reactive species and prostaglandins. Binding to NO and prostaglandins are reversible, so they can be transferred to other molecules at different sites from their synthesis. Through these functions, HSA modulates the inflammatory reaction. Decompensated cirrhosis is a disease associated systemic inflammation, which plays an important role in the pathogenesis of organ or system dysfunction/failure. Although, the beneficial effects of HAS have been traditionally attributed to plasma volume expansion, they could also relate to its effects modulating systemic and organ inflammation.
    Journal of Hepatology 04/2014; · 9.86 Impact Factor
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  • Richard Moreau, Vicente Arroyo
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    ABSTRACT: Patients hospitalized for an acute complication of cirrhosis who also have organ failure(s) are at high risk of short-term death. The term Acute-on-Chronic Liver Failure (ACLF) is used to characterize these patients. Until recently there was no evidence-based definition of ACLF. It is now the case because results of a large prospective observational European study called "chronic liver failure (CLIF) Acute-on-Chronic Liver Failure in Cirrhosis (CANONIC)" study have been published in 2013 establishing diagnostic criteria for ACLF in a large series of hospitalized patients who had an acute complication of cirrhosis. In addition, this study described the natural history of ACLF. According to the CANONIC study ACLF is now considered as a new clinical entity because it is distinct from "mere", traditional decompensated cirrhosis, based not only on the presence of organ failure(s) and high mortality rate but also on younger age, alcoholic etiology of cirrhosis, higher prevalence of some precipitating events (bacterial infections, active alcoholism), and higher level of systemic inflammation. ACLF is a new entity also because it cannot be entirely explained by severe sepsis or severe alcoholic hepatitis, a large proportion of cases being of "unknown" origin. ACLF should be considered as a whole that includes subcategories such as severe sepsis, severe alcoholic hepatitis and others which require to be defined. ACLF is a relatively common syndrome since it occurs in 31% of hospitalized patients with cirrhosis who have an acute complication of their liver disease. In these patients ACLF is the most common cause of death.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 02/2014; · 5.64 Impact Factor
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    ABSTRACT: We previously showed that severe liver diseases are characterized by expansion of liver progenitor cells (LPC), which correlates with disease severity. However, the origin and role of LPC in liver physiology and in hepatic injury remains a contentious topic. We found that ductular reaction cells in human cirrhotic livers express HNF1β. However, HNF1β expression was not present in newly generated EpCAM-positive hepatocytes. In order to investigate the role of HNF1β-expressing cells we have used a tamoxifen-inducible Hnf1βCreER/R26R(Yfp/LacZ) mouse to lineage-trace Hnf1β(+) biliary duct cells and to assess their contribution to LPC expansion and hepatocyte generation. Lineage tracing demonstrated no contribution of HNF1β(+) cells to hepatocytes during liver homeostasis in healthy mice or after loss of liver mass. After acute acetaminophen or carbon tetrachloride injury no contribution of HNF1β(+) cells to hepatocyte was detected. We next assessed the contribution of Hnf1β(+) -derived cells following two liver injury models with LPC expansion, diethoxycarbonyl-1,4-dihydro-collidin (DDC)-diet and choline-deficient ethionine-supplemented (CDE)-diet. Contribution of Hnf1β(+) cells to liver regeneration was dependent on the liver injury model. While no contribution was observed after DDC-diet treatment, mice fed with CDE-diet showed a small population of hepatocytes derived from Hnf1β(+) cells that were expanded to 1.86% of total hepatocytes after injury recovery. Genome-wide expression profile of Hnf1β(+) -derived cells from DDC and CDE models indicated that no contribution of LPC to hepatocytes was associated to LPC expression of genes related to telomere maintenance, inflammation and chemokine signaling pathways. Conclusion: HNF1β(+) biliary duct cells are the origin of LPC. HNF1β(+) cells do not contribute to hepatocyte turnover in the healthy liver, but after certain liver injury, they can differentiate to hepatocytes contributing to liver regeneration. (Hepatology 2014;).
    Hepatology 02/2014; · 12.00 Impact Factor
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    ABSTRACT: Bacterial infections are very common and represent one of the most important reasons of progression of liver failure, development of liver-related complications, and mortality in patients with cirrhosis. In fact, bacterial infections may be a triggering factor for the occurrence of gastrointestinal bleeding, hypervolemic hyponatremia, hepatic encephalopathy, kidney failure, and development of acute-on-chronic liver failure. Moreover, infections are a very common cause of repeated hospitalizations, impaired health-related quality of life, and increased healthcare costs in cirrhosis. Bacterial infections develop as a consequence of immune dysfunction that occurs progressively during the course of cirrhosis. In a significant proportion of patients, infections are caused by gramnegative bacteria from intestinal origin, yet grampositive bacteria are a frequent cause of infection, particularly in hospitalized patients. In recent years, infections caused by multidrug-resistant bacteria are becoming an important clinical problem in many countries. The reduction of the negative clinical impact of infections in patients with cirrhosis may be achieved by a combination of prophylactic measures, such as administration of antibiotics, to reduce the occurrence of infections in high-risk groups together with early identification and management of infection once it has developed. Investigation on the mechanisms of altered gut microflora, translocation of bacteria, and immune dysfunction may help develop more effective and safe methods of prevention compared to those that are currently available. Moreover, research on biomarkers of early infection may be useful in early diagnosis and treatment of infections. The current manuscript reports and in-depth review and a position statement on bacterial infections in cirrhosis.
    Journal of Hepatology 02/2014; · 9.86 Impact Factor
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    ABSTRACT: Terlipressin and albumin is the standard of care for classical type-1 Hepatorenal syndrome (HRS) not associated with active infections. However, there is no information on efficacy and safety of this treatment in patients with type-1 HRS associated with sepsis. Study aim was to investigate the effects of early treatment with terlipressin and albumin on circulatory and kidney function in patients with type-1 HRS and sepsis and assess factors predictive of response to therapy. Prospective study in 18 consecutive patients with type-1 HRS associated with sepsis. Treatment was associated with marked improvement in arterial pressure and suppression of the high levels of plasma renin activity and norepinephrine. Response to therapy (serum creatinine<1.5 mg/dL) was achieved in 12/18 patients (67%) and was associated with improved 3-month survival compared to patients without response. Non-responders had significantly lower baseline heart rate, poor liver function tests, slightly higher serum creatinine, and higher Child-Pugh and MELD scores compared to responders. Interestingly, non-responders had higher values of CLIF-SOFA score compared to responders (14±3 vs 8±01,respectively p<0.001), indicating greater severity of acute-on-chronic liver failure (ACLF). A CLIF-SOFA score ⩾11 had 92% sensitivity and 100% specificity in predicting no response to therapy. No significant differences were observed between responders and non-responders in baseline urinary kidney biomarkers. Treatment was safe and no patient required withdrawal of terlipressin. Early treatment with terlipressin and albumin in patients with type-1 HRS associated with sepsis is effective and safe. Patients with associated severe ACLF are unlikely to respond to treatment.
    Journal of Hepatology 01/2014; · 9.86 Impact Factor
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    ABSTRACT: There is no histologic classification system to determine prognoses of patients with alcoholic hepatitis (AH). We identified histologic features associated with disease severity and created a histologic scoring system to predict short-term (90 day) mortality. We analyzed data from 121 patients admitted to the Liver Unit (Hospital Clinic, Barcelona, Spain) from January 2000 through January 2008 with features of AH, and developed a histologic scoring system to determine risk of death using logistic regression. The system was tested and updated in a test set of 96 patients from 5 academic centers in the US and Europe, and a semi-quantitative scoring system was developed, called the alcoholic hepatitis histologic score (AHHS). The system was validated in an independent set of 109 patients. Inter-observer agreement was evaluated by weighted κ statistic analysis. Degree of fibrosis, neutrophil infiltration, type of bilirubinostasis, and presence mega-mitochondria were independently associated with 90 day mortality. We used these 4 parameters to develop the AHHS to identify patients with low (0-3 points), moderate (4-5 points), and high (6-9 points) risks of death within 90 days (3%, 19%, and 51%, respectively; P<.0001). The AHHS estimated 90 day mortality in the training and test sets with an area under the receiver operating characteristic value of 0.77 (95% confidence interval, 0.71-0.83). Inter-rate agreement values were 0.65 for fibrosis, 0.86 for bilirubinostasis, 0.60 for neutrophil infiltration, and 0.46 for megamitochondria. Interestingly, the type of bilirubinostasis predicted the development of bacterial infections. We identified histologic features associated with severity of AH and developed a patient classification system that might be used in clinical decision making.
    Gastroenterology 01/2014; · 12.82 Impact Factor
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    ABSTRACT: Chemokines are known to play an important role in the pathophysiology of alcoholic hepatitis (AH), a form of acute-on-chronic liver injury frequently mediated by gut derived lipopolysaccharide (LPS). In our study, we hypothesise that chemokine CCL20, one of the most upregulated chemokines in patients with AH, is implicated in the pathogenesis of AH by mediating LPS induced liver injury. CCL20 gene expression and serum levels and their correlation with disease severity were assessed in patients with AH. Cellular sources of CCL20 and its biological effects were evaluated in vitro and in vivo in chronic, acute and acute-on-chronic experimental models of carbon tetrachloride and LPS induced liver injury. RNA interference technology was used to knockdown CCL20 in vivo. CCL20 hepatic and serum levels were increased in patients with AH and correlated with the degree of fibrosis, portal hypertension, endotoxaemia, disease severity scores and short term mortality. Moreover, CCL20 expression was increased in animal models of liver injury and particularly under acute-on-chronic conditions. Macrophages and hepatic stellate cells (HSCs) were identified as the main CCL20 producing cell types. Silencing CCL20 in vivo reduced LPS induced aspartate aminotransferase and lactate dehydrogenase serum levels and hepatic proinflammatory and profibrogenic genes. CCL20 induced proinflammatory and profibrogenic effects in cultured primary HSCs. Our results suggest that CCL20 upregulation is strongly associated with LPS and may not only represent a new potential biomarker to predict outcome in patients with AH but also an important mediator linking hepatic inflammation, injury and fibrosis in AH.
    Gut 01/2014; · 10.73 Impact Factor
  • Gastroenterology 01/2014; 147(1):4–10. · 12.82 Impact Factor
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    ABSTRACT: Background & Aims Infections in cirrhosis are frequently complicated by kidney dysfunction that entails a poor prognosis. Urinary biomarkers may be of potential clinical usefulness in this setting. We aimed at assessing the value of urinary neutrophil gelatinase-associated lipocalin (uNGAL), a biomarker overexpressed in kidney tubules during kidney injury, in predicting clinical outcomes in cirrhosis with infections. Methods One-hundred and thirty-two consecutive patients hospitalized with infections were evaluated prospectively. Acute kidney injury (AKI) was defined according to AKIN criteria. uNGAL was measured at infection diagnosis and at days 3 and 7 (ELISA, Bioporto,DK). Results Patients with AKI (n = 65) had significantly higher levels of uNGAL compared to patients without AKI (203 ± 390 vs 79 ± 126 μg/gr creatinine,p<0.001). Moreover, uNGAL levels were significantly higher in patients who developed persistent AKI (n = 40), compared to those with transient AKI (n = 25) (281 ± 477 vs 85 ± 79 μg/gr creatinine, p<0.001). Among patients with persistent AKI, uNGAL was able to discriminate type-1 HRS from other causes of AKI (59 ± 46 vs 429 ± 572 μg/gr creatinine, respectively; p<0.001). Moreover, the time course of uNGAL was markedly different between the two groups. Interestingly, baseline uNGAL levels also predicted the development of a second infection during hospitalization. Overall, 3-month mortality was 34%. Independent predictive factors of 3-month mortality were MELD score, serum sodium, and uNGAL levels at diagnosis, but not presence or stage of AKI. Conclusions In patients with cirrhosis and infections, measurement of urinary NGAL at infection diagnosis is useful in predicting important clinical outcomes, specifically persistency and type of AKI, development of a second infection, and 3-month mortality.
    Journal of Hepatology 01/2014; · 9.86 Impact Factor
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    ABSTRACT: Insulin resistance and nonalcoholic steatohepatitis (NASH), characterized by hepatic steatosis combined with inflammation, are major sequelae of obesity. Currently, lifestyle modification (i.e., weight loss) is the first-line therapy for NASH. However, weight loss resolves steatosis but not inflammation. In this study, we tested the ability of resolvin D1 (RvD1), an anti-inflammatory and proresolving molecule, to promote the resolution initiated by calorie restriction in obese mice with NASH. Calorie restriction reduced adipose and liver weight (-56 and -13%, respectively; P<0.001), serum leptin and resistin levels, hepatic steatosis, and insulin resistance. In addition to these, mice receiving RvD1 during the dietary intervention showed increased adiponectin expression at both the mRNA and protein levels and reduced liver macrophage infiltration (-15%, P<0.01). Moreover, RvD1 skewed macrophages from an M1- to an M2-like anti-inflammatory phenotype, induced a specific hepatic miRNA signature (i.e., miR-219-5p and miR-199a-5p), and reduced inflammatory adipokine mRNA and protein expression and macrophage innate immune response. In precision-cut liver slices (PCLSs), which override the influence of circulating factors, RvD1 attenuated hypoxia-induced mRNA and protein expression of COX-2, IL-1β, IL-6, and CCR7. Of note, RvD1 anti-inflammatory actions were absent in macrophage-depleted PCLSs. In summary, RvD1 acts as a facilitator of the hepatic resolution process by reducing the inflammatory component of obesity-induced NASH.-Rius, B., Titos, E., Morán-Salvador, E., López-Vicario, C., García-Alonso, V., González-Périz, A., Arroyo, V., Clària, J. Resolvin D1 primes the resolution process initiated by calorie restriction in obesity-induced steatohepatitis.
    The FASEB Journal 11/2013; · 5.70 Impact Factor
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    ABSTRACT: In spite of the high incidence of hepatic encephalopathy (HE) in cirrhosis, there are few observational studies. We performed an analysis to define the characteristics of HE and associated features using the database of the Canonic Study. Clinical, laboratory and survival data of 1348 consecutive cirrhotic patients admitted with an acute decompensation were compared according to the presence (n= 406) or absence of HE and of acute-on-chronic liver failure (ACLF) (n=301). HE development was independently associated with previous HE episodes; survival probabilities worsen in relation to the presence and grade of HE. There were marked differences between HE associated (n=174) and not associated (n=286) to ACLF. HE not associated with ACLF occurred in older cirrhotics, inactive drinkers, without severe liver failure or systemic inflammatory reaction and in relation to diuretic use. In contrast, HE associated with ACLF occurred in younger cirrhotics, more frequently alcoholics, with severe liver failure and systemic inflammatory reaction and in relation to bacterial infections, active alcoholism and/or dilutional hyponatremia. Prognosis was relatively preserved in the first and extremely poor in the second group. Independent risk factors of mortality in patients with HE were age, bilirubin, INR, creatinine, sodium and HE grade. In cirrhosis, previous HE identifies a subgroup of patients that is especially vulnerable for developing new episodes of HE. The course of HE appears to be different according to the presence of ACLF.
    Journal of Hepatology 10/2013; · 9.86 Impact Factor
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    ABSTRACT: Type-1 hepatorenal syndrome is a common complication of bacterial infections in cirrhosis, but its natural history remains undefined. To assess the outcome of kidney function and survival of patients with type-1HRS associated with infections, 70 patients diagnosed during a 6-yr period were evaluated prospectively. Main outcomes were no reversibility of type-1HRS during treatment of the infection and 3-month survival. Twenty-three (33%) of the 70 patients had no reversibility of type-1HRS during treatment of the infection. The main predictive factor of no reversibility of type-1HRS was absence of infection resolution (no reversibility: 96% vs 48% in patients without and with resolution of the infection; p<0.001). Independent predictive factors of no reversibility of type-1HRS were age, high baseline serum bilirubin, nosocomial infection, and reduction in serum creatinine <0.3 mg/dL at day 3 of antibiotic treatment. No reversibility was also associated with severity circulatory dysfunction, as indicated my more marked activity of the vasoconstrictor systems. In the whole series, 3-month probability of survival was only 21%. Factors associated with poor prognosis were baseline serum bilirubin, no reversibility of type-1 HRS, lack of resolution of the infection, and development of septic shock after diagnosis of type-1HRS. Conclusion: type-1 HRS associated with infections is not reversible in two-thirds of patients only with treatment of infection. No reversibility of type-1 HRS is associated with lack of resolution of the infection, age, high bilirubin, and no early improvement of kidney function and implies a poor prognosis. These results may help advance the management of patients with type-1 HRS associated with infections. (Hepatology 2013;).
    Hepatology 08/2013; · 12.00 Impact Factor
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    ABSTRACT: Peroxisome proliferator-activated receptor (PPAR)γ is a ligand-activated nuclear receptor and a master regulator of adipogenesis. Microsomal prostaglandin E (PGE) synthase-1 (mPGES-1) is an inducible enzyme that couples with cyclooxygenase-2 (COX-2) for the biosynthesis of PGE2. In this study, we demonstrate the existence of a coordinate functional interaction between PPARγ and mPGES-1 in controlling the process of pre-adipocyte differentiation in white adipose tissue (WAT). Adipocyte-specific PPARγ knockout mice carrying an aP2 promoter-driven Cre recombinase transgene showed a blunted response to the adipogenic effects of a high-fat diet. Pre-adipocytes from these knockout mice showed loss of PPARγ and were resistant to rosiglitazone-induced WAT differentiation. In parallel, WAT from these mice showed increased expression of uncoupling protein 1 (UCP1), a mitochondrial enzyme that dissipates chemical energy as heat. Adipose tissue from mice lacking PPARγ also showed mPGES-1 up-regulation and increased PGE2 levels. In turn, PGE2 suppressed PPARγ expression and blocked rosiglitazone-induced pre-adipocyte differentiation toward white adipocytes while directly elevating UCP1 expression and pre-adipocyte differentiation into mature beige/brite adipocytes. Consistently, pharmacological mPGES-1 inhibition directed pre-adipocyte differentiation toward white adipocytes while suppressing differentiation into beige/brite adipocytes. This browning effect was reproduced in knock-down experiments using a siRNA directed against mPGES-1. The effects of PGE2 on pre-adipocyte differentiation were not seen in mice lacking PPARγ in adipose tissue and were not mirrored by other eicosanoids (i.e. leukotriene B4). Taken together, these findings identify PGE2 as a key regulator of white-to-brown adipogenesis and suggest the existence of a coordinate regulation of adipogenesis between PPARγ and mPGES-1.
    Journal of Biological Chemistry 08/2013; · 4.65 Impact Factor
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    ABSTRACT: PPARγ plays an essential role in the transcriptional regulation of genes involved in lipid and glucose metabolism, insulin sensitivity and inflammation. We recently demonstrated that PPARγ plays a causative role in hepatocyte lipid deposition, contributing to the pathogenesis of hepatic steatosis. In this study, we investigated the role of PPARγ in the inflammatory and fibrogenic response of the liver. Heterozygous floxed/null Cre/LoxP mice with targeted deletion for PPARγ in either hepatocytes (Alb-Cre), macrophages (LysM-Cre) or hepatic stellate cells (HSCs) (aP2-Cre), were submitted to carbon tetrachloride (CCl4) liver injury. Further analysis were performed in precision-cut liver slices (PCLS) and primary cultures of hepatocytes, macrophages and HSCs. LysM-Cre mice displayed an exacerbated response to chronic CCl4 injury and showed higher necroinflammatory injury, lipid peroxidation, inflammatory infiltrate, cleaved-caspase-3 and caspase 3/7 activity, and COX-2, TNF-α, CXCL2 and IL-1β expression than Alb-Cre and control mice. The deleterious effects of PPARγ disruption in liver macrophages were confirmed in an acute model of CCl4 injury as well as in PCLS incubated with LPS. Moreover, LysM-Cre mice showed an aggravated fibrogenic response to CCl4, as revealed by more prominent Sirius Red and Masson's trichrome staining, elevated hydroxyproline content and induced α-SMA and TIMP-1 expression. Importantly, aP2-Cre mice with specific disruption of PPARγ in HSCs, as confirmed by immunocytochemical analysis of individual liver cells, also showed exacerbated liver damage and fibrogenic response to CCl4. These data unveil antiinflammatory and antifibrogenic roles for PPARγ in non-parenchymal liver cells.
    Journal of Hepatology 07/2013; · 9.86 Impact Factor
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    Vicente Arroyo, Javier Fernández
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    Clinical Liver Disease. 06/2013; 2(3).
  • Javier Fernandez, Vicente Arroyo
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    Clinical Liver Disease. 06/2013; 2(3).
  • Richard Moreau, Vicente Arroyo
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    Clinical Liver Disease. 06/2013; 2(3).

Publication Stats

18k Citations
3,525.38 Total Impact Points

Institutions

  • 2009–2014
    • Instituto de Salud Carlos III
      Madrid, Madrid, Spain
  • 2008–2014
    • Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas
      Barcino, Catalonia, Spain
    • Hospital General Universitario Gregorio Marañón
      Madrid, Madrid, Spain
    • The Andalusian School of Public Health
      Granata, Andalusia, Spain
  • 1998–2014
    • IDIBAPS August Pi i Sunyer Biomedical Research Institute
      Barcino, Catalonia, Spain
  • 1975–2014
    • University of Barcelona
      • • Department of Medicine
      • • Biomedical Research Centre Esther Koplowitz
      • • Departament d'Obstetrícia i Ginecologia, Pediatria, Radiologia i Anatomia
      • • Facultad de Medicina
      Barcino, Catalonia, Spain
  • 2008–2013
    • Centro de Investigación Biomédica Esther Koplowitz
      Barcino, Catalonia, Spain
  • 2012
    • Complutense University of Madrid
      • Departamento de Medicina
      Madrid, Madrid, Spain
  • 2003–2012
    • University College London
      • Centre for Rheumatology
      Londinium, England, United Kingdom
  • 2011
    • University of Toronto
      • Department of Medicine
      Toronto, Ontario, Canada
    • Mayo Foundation for Medical Education and Research
      • Division of Gastroenterology and Hepatology
      Scottsdale, AZ, United States
  • 1989–2011
    • Hospital Clínic de Barcelona
      • • Servicio de Hepatología
      • • Servicio de Bioquímica y Genética Molecular
      Barcino, Catalonia, Spain
  • 2010
    • Aarhus University Hospital
      • Department of Hepatology and Gastroenterology
      Aarhus, Central Jutland, Denmark
  • 2004–2009
    • Beth Israel Deaconess Medical Center
      • Division of Gastroenterology
      Boston, MA, United States
  • 2007
    • University of Milan
      • Department of Internal Medicine
      Milano, Lombardy, Italy
  • 2005–2007
    • Fundació Puigvert
      Barcino, Catalonia, Spain
    • University of Colorado Hospital
      Denver, Colorado, United States
    • University of Alcalá
      Cómpluto, Madrid, Spain
    • University of Padova
      • Department of Medicine - DIMED
      Padova, Veneto, Italy
  • 1997–2003
    • Hospital Universitario Ramón y Cajal
      Madrid, Madrid, Spain
  • 2000
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
  • 1991–1997
    • Hospital Universitari Germans Trias i Pujol
      Badalona, Catalonia, Spain
  • 1994
    • Autonomous University of Barcelona
      Cerdanyola del Vallès, Catalonia, Spain
  • 1985
    • Hospital Universitari Mutua de Terrassa
      Terrassa, Catalonia, Spain