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The International Liver Congress™ 2014, 49th annual meeting of the European Association for the Study of the Liver
Venue and dates
April 9-13, 2014
London, United Kingdom
Course organisers
EASL, the European Association for the Study of the Liver,
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This video was produced by EASL (European Association for the Study of the Liver) to showcase the past/present and future of hepatology.

It was shown during the opening ceremony of the International Liver Congress™ (annual meeting of EASL), London 2014.

watch video in full screen or view our announcement and get notified link for ILC 2015

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International Liver congress2014 highlights

from Excel congress center, London, UK

The European Association for the Study of the Liver has selected the city of London for its 49th annual congress "The International Liver Congress™, which will take place April 9-13, 2014 at the International Convention Centre ExCeL.

ILC 2014 will build on its record breaking success by providing:

Multiple opportunities to:

  • Exchange Expertise
  • Network

State-of-the-art Scientific Programme, including:

  • Symposia
  • Workshops
  • Postgraduate Courses
  • Basic Science Seminar
  • Forums
  • Young Investigator Dedicated Sessions
  • Nurse & Associates Forum
  • Abdominal Sonography Course

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10 April 2014
SPEAKER: Len Verbeke
Presentation
OBETICHOLIC ACID, A FARNESOID-X RECEPTOR AGONIST, REDUCES BACTERIAL TRANSLOCATION AND RESTORES INTESTINAL PERMEABILITY IN A RAT MODEL OF CHOLESTATIC LIVER DISEASE (L. Verbeke, Belgium)
Question 1: Can you speculate on the efficacy of OCA in a cholestatic model, where endogenous competing bile acid ligands are markedly upregulated? Does obeticolic acid interfere with primary or secondary ba enterohepatic circulation
Answer 1: Our work has focused on the effects of FXR agonists on the integrity of the intestinal epithelial barrier and subsequent permeability and its specific interaction with intestinal inflammation and bacterial translocation in a model of extrahepatic cholestasis. Wheather an intermediate effect trough alteration of the bile acid pool (overload or altered composition at the serosal side, depletion at the mucosal side) under FXR stimulatory conditions is currrently being examined in our lab; in general it is not well understood to date. The changes in bile acid pool and composition in animal models of intra- and extrahepatic conditions by FXR agonists however, have been elegantly demonstrated by Modica et al. in Gastroenterology 2012, Feb;142(2):355-65. They observed a general reduction of the total bile acid pool by FXR agonists and an alteration of its composition by FXR stimulation.
SPEAKER: Willem Brouwer
Presentation
ADDING PEGINTERFERON TO ENTECAVIR INCREASES RESPONSE RATES IN HBEAG-POSITIVE CHRONIC HEPATITIS B PATIENTS: WEEK 96 RESULTS OF A GLOBAL MULTICENTER RANDOMISED TRIAL (ARES STUDY) (W.P. Brouwer, Netherlands)
Question 1: What is the best way to combine; NUC then PEG, NUC concomitant with PEG or PEG then NUC?

Answer 1: In this study we have shown that 24 weeks PEG-IFN add-on leads to higher response rates compared to ETV monotherapy, and that PEG-IFN add-on facilitates the discontinuation of ETV as the response to PEG-IFN is more durable after treatment cessation while HBeAg loss to ETV is not. We have seen that switching to 48 weeks PEG-IFN (Switch study, Ning et al) leads to high HBeAg loss rates, and HBeAg seroconversion rates that were comparable to the rates found in our study after 24 weeks of add-on.

It should be noted that the patients included in the switch study were selected on basis of a low HBeAg level at baseline. The HBeAg response rates are therefore difficult to compare to the results of our study; for this you should have a case matched analysis.

Compared to 52 weeks PEG-IFN monotherapy, 52 weeks of NUC concomitant with PEG-IFN leads to more on-treatment HBV DNA and HBsAg decline (Janssen, Lancet 2005), but not to more off-treatment HBeAg and HBsAg response. 24 weeks of PEG-IFN add-on seemed to lead to comparable HBeAg response rates, but again, in order to compare these response rates we have to match patients as the baseline characteristics are different across these studies, especially with regard to HBV genotype. Therefore on basis of these observations it is difficult to conclude which approach is most beneficial.

Question 2: Are there any histology data of these patients before treatment ?
Answer 2: Yes – the mean (SD) Ishak fibrosis score was 2.4 (1.3) for ETV monotherapy and 2.0 (1.3) for PEG-IFN add-on. 5% of patients had cirrhosis (8 in total, 3 in add-on and 5 in monotherapy).
SPEAKER: Stefan Zeuzem
Presentation
SAPPHIRE II: PHASE 3 PLACEBO-CONTROLLED STUDY OF INTERFERON-FREE, 12-WEEK REGIMEN OF ABT-450/R/ABT-267, ABT-333, AND RIBAVIRIN IN TREATMENT-EXPERIENCED ADULTS WITH HEPATITIS C VIRUS GENOTYPE 1 (S. Zeuzem, Germany)
Question 1: What will be the concern of using ritonavir outside clinical trials?
Answer 1: Minor concern with some drug-drug interactions
11 April 2014
SPEAKER: Lisa Vanwagner
Presentation
"EARLY CARDIOVASCULAR DISEASE MORTALITY AFTER LIVER TRANSPLANTATION - IS NONALCOHOLIC STEATOHEPATITIS (NASH) TO BLAME? (L.B. VanWagner, United States)"
Question 1: Did you identify any individual factors that segregate those at higher risk?
Answer 1: We are continuing to perform additional stratified analyses to determine what combination of risk factors is able to best predict outcomes in the early perioperative period after liver transplantation for NASH.
Question 2: Would you avoid transplant listing by CVS risk factors alone based on your data?
Answer 2: No, we would not restrict liver transplant based on this information alone. It is possible that intervention prior to transplant may actually mitigate some of the observed risk and further studies are needed in order to determine what types of testing, and potential interventions, such as early statin therapy or more aggressive hypertension management postoperatively, is warranted in this population.
Question 3: Will pretreatment with statin angiotensin 2 receptor block and aspirin decrease early death?
Answer 3: This is an excellent question. Unfortunately one of the limitations of the Organ Procurement and Transplantation Network (OPTN) database is that granular data, such as cardiovascular medication use, is not available for review on a national level in the United States. We are looking at our center-specific data to answer some of these questions, but you raise an excellent point that further trials are needed in order to ascertain if these medications in particular may be of benefit in this high risk population.
Question 4: What is your protocol to evaluate the cardiovascular risk pre-transplant?
Answer 4: At our center, we have historically followed the 2005 AASLD practice guidelines for evaluation of the patient for liver transplantation, which include an opinion-based recommendation that “chronic smokers, patients over the age of 50, and those with a clinical or family history of heart disease or diabetes should undergo evaluation for CAD.” Based on cohort or case-control analytic studies, the guidelines also state that “Dobutamine stress echocardiogram appears to be an effective screening test in this setting; however, positive test results should be confirmed with cardiac catheterization.” For flow-limiting coronary artery disease (stenosis > 70%), percutaneous coronary intervention (PCI) is often performed, preferably with a bare metal stent. In early years, we attempted coronary artery bypass grafting (CABG) in Child’s A and B cirrhosis, however, outcomes were overwhelmingly poor and this practice has since been abandoned at our center. Importantly, all candidates at our center undergo 2d echocardiography with Doppler imaging and bubble study to assess for valvular disease, pulmonary hypertension, and subclinical heart failure. All candidates also undergo ECG testing to evaluate for potential underlying arrhythmia. All cardiac evaluations are performed by a group of cardiologists at our center who are dedicated to risk stratification in this complex population.
SPEAKER: Stanislas Pol
Presentation
SUCCESSFUL RETREATMENT WITH SOFOSBUVIR OF HCV GENOTYPE-1 INFECTED PATIENTS WHO FAILED PRIOR THERAPY WITH PEGINTERFERON + RIBAVIRIN PLUS 1 OR 2 ADDITIONAL DIRECT-ACTING ANTIVIRAL AGENTS (S. Pol, France)
Question 1: Were RAVs more significant in single treatment NS3 exposed pts?
Answer 1: What do you mean by significant? RAVs, whatever the drug class, did not impact SVR12
Question 2: Any difference in baseline characteristics in the subset of patients analysed for SVR12
Answer 2: No
Question 3: Was there a difference in SVR12 in cirrhotics v non-cirrhotics?
Answer 3: Patients were all non cirrhotic
Question 4: The relapse rates for 8 vs 12 wks (11 vs 3) are significantly different (p=0.03). Doesn't that suggest 12 wks is needed to minimize failure?
Answer 4: All patients were given a 12 weeks-course of SOF +PR
Question 5: Was resistance to LDV a reason for relapse?
Answer 5: Not clearly
SPEAKER: Christophe Hezode
Presentation
RESULTS FROM THE PHASE 2 PEARL-I STUDY: INTERFERON-FREE REGIMENS OF ABT-450/R + ABT-267 WITH OR WITHOUT RIBAVIRIN IN PATIENTS WITH HCV GENOTYPE 4 INFECTION (C. Hezode, France)
Question 1: Why did you choose to not use ABT 333 instead of resorting to RBV?
Answer 1: Because ABT-333 is not effective on HCV genotype 4.
SPEAKER: Jordan Feld
Presentation
SAPPHIRE I: PHASE 3 PLACEBO-CONTROLLED STUDY OF INTERFERON-FREE, 12-WEEK REGIMEN OF ABT-450/R/ABT-267, ABT-333, AND RIBAVIRIN IN 631 TREATMENT-NAÏVE ADULTS WITH HEPATITIS C VIRUS GENOTYPE 1 (J.J. Feld, Canada)
Question 1: Have the authors considered that Ritonavir has contributed to SAEs?
Answer 1: It's a good question but at the dose of ritonovir used (100 mg) it is extremely well tolerated. It is unlikely that it contributed significantly to any adverse events from the regimen but of course it is a possibility.
Question 2: Did the patients that achieved SVR12 have at baseline any of the resistance mutations seen in the relapsers or breakthrough?
Answer 2: Resistance testing was not done in all patients. For every patient who relapsed, 2 matched patients who achieved SVR were sequenced. The presence of baseline NS5A mutations did not seem to affect the chance of SVR but it is hard to be absolutely conclusive because not all patients had sequencing performed and there were very few failures. In the Phase 2 AVIATOR trial with the same regimen, there was no association between baseline resistance mutations and response and in that study all patients were sequenced.
Question 3: We're there any precautions for phototoxicity in the protocol?
Answer 3: None specifically beyond what is usually advised in patients taking ribavirin.
Question 4: May the UOL bilirrubin values be related to low levels of Hb (haemolitic anaemia)?
Answer 4: This is certainly a good point. The elevated bilirubin levels are a likely from a combination of increased bilirubin load from hemolysis due to ribavirin and reduced clearance due to inhibition of the OATBI transporters by ABT-450.
SPEAKER: Steve Bloom
Presentation
Hormones and obesity (S. Bloom, United Kingdom)
Question 1: protein preload has good effect on weight loss and satiety Do you think combining PYY and protein preload has strong effect on weight loss
Answer 1:High protein diets (eg Atkins diet) do cause weight loss, at least over the first six months, and this is likely to be additive to any effect of PYY on inhibition of appetite and thus cause further weight loss.  I don’t think it has been tested, however.
12 April 2014
SPEAKER: Paul Kwo
Presentation
RESULTS OF THE PHASE 2 STUDY M12-999: INTERFERON-FREE REGIMEN OF ABT-450/R/ABT-267+ABT-333+RIBAVIRIN IN LIVER TRANSPLANT RECIPIENTS WITH RECURRENT HCV GENOTYPE 1 INFECTION (P. Kwo, United States)
Question 1: Were there any episodes of acute cellular rejections associated with tac dose reductions
Answer 1: No there were no episodes of rejection
Question 2: Why was trough levels of cyclosporine used as against C2 levels?
Answer 2: C2 levels are not uniformly used by all centers, and the participating centers all were more comfortable using trough levels. Morover, the drug drug interaction studies did not examine change in C2
Question 3: Will the treatment be extended to patients with F3/4?
Answer 3: Yes to F#
Question 4: In the patient with tac levels of 15 did you skip the tac for two weeks at a stretch or what was the protocol followed in the case?
Answer 4: Yes, the interval went to q 2 weeks
Question 5: Were prograf dosing higher post treatment than pre?
Answer 5: No clear pattern, but in general, slightly higher though not significant
SPEAKER: Vincent Su
Presentation
COMBINATION THERAPY WITH PEGINTERFERON ALFA-2A AND A NUCLEOS(T)IDE ANALOGUE FOR HBEAG-POSITIVE CHRONIC HEPATITIS B PATIENTS: RESULTS OF A LARGE, RANDOMISED, MULTICENTRE, DOUBLE-BLIND, PLACEBO-CONTROLLED STUDY (W.W. Su, Taiwan)
Question 1: Did you measure sAg seroconversion?
Answer 1: Yes, sAg seroconversion measurement is included in the analysis and will be provided in the coming conference once this analysis is completed and available
Question 2: Did you look at eAg seroconversion and HBV DNA suppression at 24 weeks post treatment?
Answer 2: Yes, one year data will be available and presented in coming congress
Question 3: What was the HBsAg loss rate?
Answer 3: Data is still under analysis as I had answered in the conference. We hope that qHBsAg will be available at the end of this year 2014
Question 4: What percentage patients had surface antigen loss at the end of study
Answer 4: Data is still under analysis as I had answered in the conference. We hope that qHBsAg will be available at the end of this year 2014
Question 5: Which HBV genotype do you treat?
Answer 5: Genotype B and C are the major genotype for this study, but full data will be not be ready until 3Q 2014
SPEAKER: Juan Abraldes
Presentation
ADDITION OF SIMVASTATIN TO STANDARD TREATMENT IMPROVES SURVIVAL AFTER VARICEAL BLEEDING IN PATIENTS WITH CIRRHOSIS. A DOUBLE-BLIND RANDOMIZED TRIAL (NCT01095185) (J.G. Abraldes, Spain)
Question 1: Would there be survival benefit in non bleeders
Answer 1: This is an interesting question but still needs to be analized
Question 2: How many patient Had HCV related cirrosis?
Answer 2: 25% of the patients had HCV
Question 3: How did you dose the simvastatin?
Answer 3: It was started 20 mg OD for 15 days, and then increased to 40 mg OD
Question 4: Did you measure hs CRP inthis group
Answer 4: We did not measure hsCRP
Question 5: Was there any significant rise on transaminases seen
Answer 5: Only one patient had a significant increase in transaminases, that led to discontinuation of the medication
"
Question 6: 1. The survival benefit appeared late. How late was this, how many patients at risk, and what causes of death separated the two groups?
Answer 6: The survival benefit was observed throughout the observation period. Numbers at risk were 36/41 at 12 months, 23/20 at 18 months, and 13/8 at 24 months. The main differences in terms of causes of death were bleeding related death (5 events in placebo, 1 in simvastatin), and SBP related death (3 placebo, 0 simvastatin)
"
Question 7: Was the intensity of the accompanying therapy the same in the two groups?
Answer 7: This still needs detailed analysis
Question 8: Usually cirrotic patients have low level of cholesterol. Is there any concern about ?
Answer 8: The rate of side effects were similar between groups, and survival was better with simvastatin. Thus, there are no signals suggesting a potential harm with simvastatin, despite the low levels of cholesterol in these patients.
SPEAKER: Nezam Afdhal
Presentation
ALL ORAL FIXED-DOSE COMBINATION SOFOSBUVIR/LEDIPASVIR WITH OR WITHOUT RIBAVIRIN FOR 12 OR 24 WEEKS IN TREATMENT-EXPERIENCED GENOTYPE 1 HCV-INFECTED PATIENTS: THE PHASE 3 ION-2 STUDY (N. Afdhal, United States)
Question 1: What is the SVR rate in 1b patients with cirrhosis?
Question 2: What were grade 3 and 4 lab events?
Question 3: What resistance mutation was the commonest
Question 4: How rapidly did PI non-responders achieve HCV negativity on treatment ?
Question 5: how is moving from an 86 to 99 SVR in cirrhotics by extending to 24 weeks not considered to be a significant increase without RIBA?
Question 6: Did relapses have slower viral load decline
Question 7: Other than anemia, what were the other grade 3 and greater lab abnormalities?
Question 8: Did relapses have slower viral load decline.
Answers: Please see all detained in the published article: http://www.nejm.org/doi/full/10.1056/NEJMoa1316366
SPEAKER: Philip Johnson
Presentation
AN INTERNATIONAL COLLABORATIVE STUDY ASSESSING THE ROLE OF AETIOLOGY AND STAGE IN SURVIVAL IN HCC - IMPLICATIONS FOR SCREENING (P. Johnson, United Kingdom)
Question 1: How did demographics of screened pts difere from those diagnosed with symptoms?
Answer 1: In our initial analysis we did not focus on symptoms, as these are highly subjective, both in terms as being reported by the patients and recorded by the doctors. Perhaps reflecting this some of the centres had not attempted to record symptoms. However, in the light of some of the questions, such as yours, and those asked at the meeting, we are now assembling ""performance scores"" for patients in this study, which will be reported in the ensuing publication. It will not quite answer your question, but it will be close.
Question 2: Did you conduct any cost-effectiveness studies between Japan (high screening) to other regions?
Answer 2: No. This was not one of the aims of the study. However, it is clearly a crucial question and figures identifying the cost per HCC case detected in Japan would be of great interest. I have little doubt that the costs will be very high, but we should bear in mind that the costs of treating advanced disease are also likely to be very significant. I am writing to my colleagues in Japan with the suggestion that they undertake such an analysis.
Question 3: Please clarify why etiology ruled out as a contributing factor?
Answer 3: What we did in the statistical analysis was to put in all those factors that we knew influenced survival such as tumour size, AFP, liver function etc. When a model was built taking these factors into account aetiology (Hep B or C) dropped out. I agree that this seems a perverse conclusion since Hep B or C are presumably the initiating factors. Perhaps all our analysis is telling us is what those factors that are attributable to HBV and HCV are. We are undertaking detailed discussions with statistical colleagues to sort this matter out prior to publication.
Question 4: Did hbv prevalence change along time in Japan?
Answer 4: Good question - I don't know the answer. I now have the raw data and I shall put this information in the final publication.
SPEAKER: Greg Everson
Presentation
SAFETY AND EFFICACY OF TREATMENT WITH THE INTERFERON-FREE, RIBAVIRIN-FREE COMBINATION OF SOFOSBUVIR+GS-5816 FOR 12 WEEKS IN TREATMENT NAïVE PATIENTS WITH GENOTYPE 1-6 HCV INFECTION (G.T. Everson, United States)
Question 1: Why in all these HCV trials primary end point is SVR below LLQ not LLD ?
Answer 1: Too many false positives with LLD. LLQ has been shown to long-term freedom from HCV and cure.
Question 2: Does the rate of failure in pts with baseline RAVs (3/17) warrants the use of the higher GS-5816 dose in these patients ?
Answer 2: Increasing dose might not reliably overcome the RAV issue. If RAVs maintain clinical relevance, multi-DAA strategies would likely be more efficacious.
Question 3: 2 suicides in the small sample? Any concerns?
Answer 3: These were not treatment related.
Question 4: Can GS-5816 be co-formulated with SOF?
Answer 4: Yes, this is possible.
Question 5: Given the present exit of a suicide, was there any change I depression scores in the other patients on treatment?
Answer 5: We have not systematically analysed depression.
Question 6: Would you recommend the higher dose for g2/3 patients?
Answer 6: This is small study, but there may be greater virologic response with the higher dose.
Question 7: There were 8 weeks arms in GT 1-3 patients--do you have SVR12 data from these arms?
Answer 7: I do not have data on 8 weeks of treatment.
Question 8: What dose would you propose to use in future studies?
Answer 8: That is under discussion, but I would tend to favour the higher dose.
SPEAKER: Fred Poordad
Presentation
TURQUOISE-II: SVR12 RATES OF 92%-96% IN 380 HEPATITIS C VIRUS GENOTYPE 1-INFECTED ADULTS WITH COMPENSATED CIRRHOSIS TREATED WITH ABT-450/R/ABT-267 AND ABT-333 PLUS RIBAVIRIN (3D+RBV) (F. Poordad, United States)
Question 1: Do you have meld scores
Answer 1: We did not pre specify MELD scores in the study, but of course we do have the data and will be a doing a post hoc analysis of baseline MELD and post treatment follow up week 48 to see if they changed. That will be a presentation at a future meeting.
Question 2: If this combination is used first line, you won't be able separate out IF non-responders. Please reconcile with your dose duration.
Answer 2: The null 1a cirrhotics are suggested to be treated for 24 weeks. All others are 12 weeks
SPEAKER: Alessandra Mangia
Presentation
ALL ORAL FIXED-DOSE COMBINATION SOFOSBUVIR/LEDIPASVIR WITH OR WITHOUT RIBAVIRIN FOR 12 OR 24 WEEKS IN TREATMENT-NAIVE GENOTYPE 1 HCV-INFECTED PATIENTS: THE PHASE 3 ION-1 STUDY (A. Mangia, Italy)
Question 1: What about the Genoyypre sub analysis
Answer 1: Out of 865 patients treated, 67% were genotype 1a infected. SVR rates ranged from 97% to 100% in patients infected with genotype 1b and from 99% to 100% in patients infected with genotype 1a.
Question 2: How was cirrhosis defined in your study?
Answer 2: In this study, all the patients had non invasive evaluation by lab biomarkers. In addition, in more than 50% of cases liver biopsy and histological evaluation were performed. In 33% of cases, in addition to biomarkers, cirrhosis was diagnosed by Fibroscan. Finally, in 13% of cases it was only assessed by lab biomarkers.
SPEAKER: Eric Lawitz
Presentation
SIMEPREVIR PLUS SOFOSBUVIR WITH/WITHOUT RIBAVIRIN IN HCV GENOTYPE 1 PRIOR NULL-RESPONDER/TREATMENT-NAïVE PATIENTS (COSMOS STUDY): PRIMARY ENDPOINT (SVR12) RESULTS IN PATIENTS WITH METAVIR F3-4 (COHORT 2) (E. Lawitz, United States)
Question 1: When is the paper coming?
Answer 1: We are aiming at 3Q2014.
Question 2: Any meld over 12 treated
Answer 2: We did not collect nor calculated MELD scores, however based on looking at the data it is highly unlikely anyone with a MELD over 12 entered the trial
Question 3: Why exclud patient > 70 years ?
Answer 3: Although some trials have not excluded patients over 70 years of age, It is not unusual to exclude these patients in proof-of-concept studies, such as COSMOS
Question 4: Do you recommend 24wk w/o RBV or 12wk w/ RBV
Answer 4: Janssen is conducting 2 phase III trials evaluation the safety and efficacy of SMV + SOF for either 8 or 12 weeks in F0-F3 (treatment-naïve and treatment-experienced with no prior DAA exposure) patients and 12 weeks in F4 patients (treatment-naïve and treatment-experienced with no prior DAA exposure). None of the study arms include RBV.
SPEAKER: Omesh Goyal
Presentation
RIFAXIMIN VERSUS LACTULOSE IN THE TREATMENT OF MINIMAL HEPATIC ENCEPHALOPATHY IN PATIENTS WITH CIRRHOSIS: A PROSPECTIVE, RANDOMIZED, ACTIVE-COMPARATOR, NON-INFERIORITY TRIAL (O. Goyal, India)
Question 1: Which version of rifaximin - amorphous or polymorphous - was used in your study? Amorphous is better absorbed and may affect efficacy.
Answer 1: Polymorphous form of rifaximin was used as the other form is not available in India.
Question 2: Why was a non treatment or placebo group not included?
Answer 2: Lactulose is the current gold standard for treatment of MHE. Comparison of a new drug (rifaximin) with the existing gold standard is the best which can be done. Moreover, our group had already compared rifaximin with placebo in a previous trial (RIME TRIAL) and found it to be effective.
Question 3: Any data on bacterial resistance with rifaximin
Answer 3: Bacterial resistance was not studied.
Question 4: I couldn't see that recent antibiotics were excluded. Were they?
Answer 4: Patients with history of any antibiotic use within the past 6 weeks were exuded.

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