Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 6th World Congress on Hepatitis & Liver Diseases Dublin, Ireland.

Day 1 :

Keynote Forum

Hani Oweira

Hirslanden Hospital Group, Switzerland

Keynote: Surgery of the Liver and intraoperative interventional Therapies What is possible today?

Time : TBD

Hepatitis 2018 International Conference Keynote Speaker Hani Oweira photo

Dr. med. Hani Oweira, is a visceral Surgeon working in the Hirslanden Hospital Group in Zurich and Cham in Switzerland. He was trained in Charite Berlin and the University Hospital in Heidelberg in Germany. His Research focused on the predictive markers for liver dysfunction after liver surgery and transplantation.


Liver resections are performed to manage Benign and Malignant focal lesions in the liver, and the post-operative outcome was improved over time due to improvement of surgical techniques which get benefit from understanding the liver anatomy and segmentation with improvement of hemostasis techniques. .Anatomy wise liver is divided to 2 lobes (Right and left) ant into 8 segments classified by Couinaud based on vascular inflow and outflow. There are many techniques for liver parenchymal transection started with clamp –crush technique and developed to ultrasonic vibration (harmonic shear), Cavitron Ultrasound Surgical Aspirator CUSA), hydro jet, radiofrequency dissector and recently staplers. There are numerous types of resection could be divided to major (>2 segments) and minor (<2 segments) and could be divided into anatomical (right and left hepatectomy, right anterior and posterior sectionectomy and left lateral sectionectomy), non-anatomical resection and individual segmentectomy. There are many other interventional procedures can be done during surgery for hepatic focal lesions rather than surgery as radiofrequency ablation (RFA), cryoablation or  irreversible electroporation (IRE) which usually kept as combined intervention with surgery in deep parenchymal lesions which difficult to be removed without injuring or scarifying a major hepatic structure. Also one of the elegant technique in management of hepatic focal lesions especially Malignant one is adjuvant or pre operatiove angio-embolization or chemo/ radio embolization which deprive the lesion from its blood supply and supplying it with chemo or radiotherapy which may decrease the size of lesion and make it easier and accessible to be removed. In addition to that, systemic chemotherapy could have benefit in malignant lesions as it may decrease the size of the lesions and minimize the liver parenchyma needed to be resected to remove the whole lesion, and sometimes it changes non resectable liver lesions to resectable one.

Keynote Forum

Samson Michel

Univ Rennes, France

Keynote: Protective role of RIPK1 in hepatitis

Time : TBD

Hepatitis 2018 International Conference Keynote Speaker Samson Michel photo

Michel Samson has got his PhD in 1993 at University of Paris XI (France). He studied as postdoctoral scientist at Université Libre de Bruxelles (Brussels, Belgium) supported by prestigious fellowships (EMBO, European Community, etc..). He passed two years as visiting scientist at Genentech (California, USA). He is now team leader and director of research of Inserm at University of Rennes (France) in UMR 1085 Inserm, vice-director of Institut de Recherche en Santé, Environnement et Travail. He studies the inflammation, cell death and fibrosis in liver pathologies.  He has published more than 90 papers in reputed journals (Nature, Cell, J Exp Med, Hepatology, J Hepatol., etc...), with already more than 8400 citations and H-index 37.


Hepatocyte death is a starting point of liver disease progression by promoting inflammatory and regenerative processes. The death of hepatocytes can be induced by the large variety of immune, infectious and toxic agents. When the hepatocyte death becomes chronic, a development of fibrosis, cirrhosis or hepatocellular carcinoma occur. The molecular mechanisms regulating these cell death pathways are poorly documented. Innate and acquired immune cells play key roles in the induction or amplification of hepatolysis, mainly mediated by expression and release of death ligands belonging to the TNF-superfamily including TNF-α, FasL and TRAIL.  In this study, we investigated the role of RIPK1, a protein known to regulate cell fate decisions, in the death of hepatocytes using different in vivo models of hepatitis. Hepatitis was induced in mice by Concanavalin A (ConA), lipopolysaccharide (LPS), DNA-CpG, recombinant IFN-γ and TRAIL co-administration, FASL, Poly I:C, Murine-Hepatitis virus type 3, and high fat diet. Using specific conditional mice deficient in RIPK1 only in liver parenchymal cells (LPC) (Ripk1LPC-KO), we reveal its necessary function in the protection of hepatocyte during hepatitis. Administration of lipsome-encapsulated Cl2MBP served to investigate the role of Kupffer cells in the establishment of the disease. Moreover, Etanercept, a TNF-decoy receptor, was used to study the contribution of TNF-α during liver injury. All together, these works demonstrate that deletion of RIPK1 sensitizes hepatocytes to TNF-α-induced apoptosis. Thus RIPK1 plays a key role in the protection of hepatocytes during acute and chronic hepatitis.

Keynote Forum

Ken Sato

Gunma University Graduate School of Medicine, Japan

Keynote: The next stage strategy for Direct-acting antiviral failure in patients with chronic hepatitis C

Time : TBD

Hepatitis 2018 International Conference Keynote Speaker Ken Sato  photo

Ken Sato is a Japanese, physician, hepatologist and gastroentelorogist, clinical and basic researcher in Gunma University Graduate School of Medicine in Japan; working for more than 20 years in this area. He started working as a physician at Gunma University and its affiliated hospitals in 1990. Some of Dr. Sato’s achievements in the field include researching tumors in the liver with non-alcoholic steatohepatitis. His research had lead in indentifying Werner Syndrome as a possible cause of the steatohepatitis. Additionally, Dr. Sato has researched carcinomas and hepatitis, especially pertaining to the liver.


Hepatitis B virus (HBV) infection is a major risk factor for developing hepatocellular carcinoma (HCC), although HCV infection and chronic alcoholism are also recognized risk factors. HBV-associated HCC in humans generally unfolds over many years of chronic infection with HBV; however, the reasons for the large time gap between HBV infection and onset of HCC and the exact molecular mechanisms by which HBV triggers hepatocarcinogenesis are largely unknown. Mutations of critical cellular genes (due to insertion of viral DNA in the host genome), the presence of viral protein HBx with transforming activities, acute inflammation, and aberrant epigenetic alterations in the host cellular genome have been proposed as possible mechanisms resulting in the development and progression of HCC associated with HBV infection. Because epigenetic mechanisms (including DNA methylation) are common cellular defense mechanisms known to silence invading foreign DNA and viral genomes, recent studies attempted to test whether HBV DNA is also methylated by host cellular defense mechanism. In addition, previous studies have exploited conceptual and technological advances in epigenetics and epigenomics to investigate the role of epigenetic events induced by HBV infection in liver tumors and non-tumor precancerous lesions. Our recent studies have identified a large number of genes and pathways that are targeted by epigenetic deregulation (changes in DNA methylation, histone modifications and long non-coding RNAs) during the development and progression of liver cancer. Our results provide evidence that HBV virus may abrogate cellular defense systems, induce silencing of host genes and promote liver cancer development via an "epigenetic strategy".


  • Hepatitis C

André-Jean REMY is Head of Hepatology and Gastroenterology Unit & Social Medicine, Unit of Perpignan Hospital and he is one of 41 viral hepatitis experts unit in France. Social medicine include jailhouse medical unit, retention center medical and primary care access unit. He is also Medical coordinator of Mobile Hepatitis Team, a new concept of HCV/HBV patients care from diagnosis to treatment. He is a Member of French hepatitis B and C guidelines follow-up national staff, General Secretary of ANGH, Administrator of AFEF (French Liver Diseases Association) and a specialist of viral hepatitis in drug users, inmates and precarious populations. He has published more than 150 scientific articles.


Background: Prevalence of viral hepatitis C is higher in prison environment than in the general population and is estimated of 4,8% in France. Systematic HCV screening on all inmates has been recommended in France since 1999. The impact in prison environment is little-known as based only on local studies. Inmate health care falls under USMP (Prison Setting Medical Unit), hospital specific units as by 1994 law. Access to antiviral C treatment for inmates has always been difficult in France, would it be for interferon and ribavirin or use of protease inhibitors, with less than 20% of treated patients. Arrival of DAA is an opportunity to propose treatment and the patient to accept it. In 2014, French guidelines recommended HCV carriers in prison should systematically be treated independently of stage of fibrosis; AAD treatment was permitted in 2015 without additional costs for hospitals. For prisoners, short treatment could be better to be treated in prison. Objectives: 1/ Evaluate completion rate of an 8-week antiviral C treatment by ledipasvir/sofosbuvir association in non-

cirrhotic genotype 1 patients in deprivation of liberty and achieve sustained virological response (SVR) 2/ Measure effectiveness of 8-week treatment (by protocol analysis).

Methodology: prospective non-interventional multicenter trial among inmates with chronic hepatitis C genotype 1 with fibrosis score F0 to F2 and who will receive a daily combination of sofosbuvir / ledipasvir during 8 weeks.

Results: for 100 first included patients: 91% men, mean age 37 years, contamination mode : drug injection 72%, nasal drug 9%, unknown 19%; genotype 1a  90%, initial liver fibroscan score: F0 66% F1 24% F2 10%; 95% have finished their antiviral treatment; only 5% stopped before end of 8 weekend and 5% have been responder/relapse; 91% have sustained virological response at time of these abstract.

Conclusion: It was first study of 8 weeks HCV treatment in prison; Almost all included patients have completed their treatment and are cured. Five percent of patients stopped the treatment because of cell promiscuity giving


Yuming Wang  M.D. Professor and Chief Physician   Institute for Infectious Diseases,  Southwest Hospital, Army Medical University, Chongqing. Currently serves as the vice president in Infectious Diseases Branch of Capacity Building and Continuing Education Center, National Health and Family Planning Commission. Current research fields include severe hepatitis/liver failure, pathogenesis and treatment of viral hepatitis. Chief editor of 23 monographs, associated editor for 31 monographs. He has  published more than 400 papers, including Gastroenterology, Hepatology and CGH, etc



40 kD PEG IFN α-2a and 12kD PEG IFN α-2b have demonstrated effective immune control and resulted in better response in HBeAg positive CHB patients compared to nucleos(t)ide drugs (NUCs), e.g. HBeAg seroconversion and HBsAg loss. [1,2]However, efficacy of another PEG IFN α, i.e. 40kD PEG IFN α-2b, has not been reported yet.


This study aimed to compare efficacy among three PEG IFNα monotherapies in antiviral treatment-naïve HBeAg-positive CHB patients.

Material and Methods

Total 117 antiviral treatment-naïve HBeAg-positive CHB patients were enrolled. Subjects were randomly to receive 24 weeks of 40kD PEG IFN-α-2a (180 μg/week, Group A, n=41), 12kD PEG IFN α-2b (80μg/week, Group B, n=41), or 40kD PEG IFN-α-2b (180 μg/week, Group C, n=52) monotherapy. Primary endpoint was defined as satisfactory response (virological and biochemical response, plus anti-HBe seroconversion) at week 24. Secondary endpoints included ideal response (HBsAg loss) and HBsAg decline at week 24. All patients were further followed up during treatment.


   There were no signi´Čücant differences in sex, age, HBV genotype and ALT level among three monotherapy groups (P>0.05). After treatment of 24 weeks, satisfactory response rate in 40kD PEG IFN-α-2b group (30.77%,16/52) was higher than Group A (17.07%, 7/41, P=0.1285) and Group B (12.20%,5/41, P=0.0634), although with no statistically significant difference (P>0.05). Ideal response rates in 40kD PEG IFN-α-2b group (17.31%,9/52) was slightly higher than Group A (7.32%,3/41, P=0.1536)and Group B (4.87%,2/41, P=0.0653) . Partial response rates as HBsAg level decline from baseline were a bit higher in 40kD PEG IFN-α-2b group compared to 40kD PEG IFN-α-2a group (P>0.05)(Table). 


Compared to 40kD PEG IFN-α-2a and 12kD PEG IFN α-2b monotherapies, 40kD PEG IFN-α-2b monotherapy showed trends for better efficacy for antiviral treatment-naïve HBeAg positive patients at week 24. Meanwhile, 40kD PEG IFN-α-2b is at a much cheaper price, which exerts a better cost effects.


Table.   Response after treatment of 12 weeks

HBsAg decline from baseline

Group A

40kD PEG IFN-α-2a


Group B

12kD PEG IFN α-2b


Group C

40kD PEG IFN-α-2b



1lg-2lg HBsAg decline from baseline





2lg-3lg HBsAg decline from baseline

12 (29.2%)




≥3lg HBsAg decline from baseline