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					                                          Evento: VEN-FOR10116

            XVIII SYMPOSIUM ASSOCIAZIONE ROBERTO FARINI & 4th ANNUAL
                     UNIVERSITY OF CALIFORNIA DAVIS SYMPOSIUM

     BENIGN AND MALIGNANT LIVER DISEASES: WHAT’S NEW AND EMERGING?
    PATOLOGIE EPATICHE BENIGNE E MALIGNE: COSA C’E’ DI NUOVO ED EMERGENTE?

                                    PADOVA – 26 e 27 Gennaio 2007



President Presidente Remo Naccarato, Padova
President Presidente Associazione Roberto Farini Giacomo Carlo Sturniolo, Padova


SCIENTIFIC SECRETARIAT SEGRETERIA SCIENTIFICA
Patrizia Burra, Tel +39 49 821 2892 - e-mail burra@unipd.it Fabio Farinati, Tel +39 049 821 1305 - e-mail
fabio.farinati@unipd.it Department of Surgical and Gastroenterological Sciences, Padua University Dipartimento
di Scienze Chirurgiche e Gastroenterologiche, Università di Padova
Lorenzo Rossaro, Tel +1 916 734 8693 - e-mail lorenzo.rossaro@ucdmc.ucdavis.edu Division of
Gastroenterology and Hepatology, University of California Davis Medical Center, Sacramento, California, USA

ORGANIZING SECRETARIAT SEGRETERIA ORGANIZZATIVA
KEY CONGRESS & COMMUNICATION Srl Via Makallè, 75 - 35138 Padova Tel +39 049 8729511; Fax +39 049 8729512; e-
mail: assfarini@keycongress.com and OFFICE OF CONTINUING MEDICAL EDUCATION UNIVERSITY OF CALIFORNIA
DAVIS HEALTH SYSTEM 3560 Business Drive, #130, Sacramento, California, USA Tel +1 916 734 1394; Fax +1 916 736
0188, e-mail: kimber.chavez@ucdmc.ucdavis.edu

Under the Patronage Con il Patrocinio di
Regione del Veneto (in richiesta) Comune di Padova Università di Padova (in richiesta) Facoltà di Medicina e
Chirurgia di Padova (in richiesta) Azienda Ospedaliera di Padova ULSS 16 di Padova Ordine dei Medici e dei
Chirurghi Odontoiatri di Padova University of California Davis Health System
S.I.G.E. Società Italiana di Gastroenterologia
A.I.G.O. Associazione Italiana Gastroenterologi Ospedalieri
A.I.S.F. Associazione Italiana per lo studio del Fegato
S.I.E.D. Società Italiana di Endoscopia Digestiva (in richiesta)


Relatori
STROFFOLINI Tommaso              Specialista in Gastroenterologia
IMPERIAL Joanne                  Hepatologist and Gastroenterologist
SMEDILE Antonina                 Specialista in Malattie dell’Apparato Digerente
BOWLUS Christopher               Associate Professor of Internal Medicine, University of California Davis
ANGELUCCI Emanuele               Specialista in Ematologia Generale – Oncologia Clinica – Medicina
                                 Interna - Professore Associato di Ematologia presso la Facoltà di
                                 Medicina dell’ Università degli Studi di Cagliari
MARTINES Diego                   Specializzazione in Medicina Interna - Ricercatore Confermato
                                 dell’Università di Padova presso Dipartimento di Scienze Chirurgiche e
                                 Gastroenterologiche
KEEFFEE Emmet                    Professor of Medicine, Stanford University School of Medicine –
                                 Chief of Hepatology and Co-Director, Liver Transplant Program,
                           Stanford University Medical Center
INVERNIZZI Pietro      Specialista in Gastronterologia
GERSHWIN Eric          Specialization in Internal Medicine – Professor of Medicine
BURROUGHS Andrew K.    Consultant Physician and Hepatologist at the Royal Free Hospital, Liver
                       Transplantation and Hepato-biliary Medicine Unit.
ROSSARO Lorenzo          Specialista in Gastronterologia ed Endoscopia Digestiva –
                         Associate Professor of Medicine, Department of Internal Medicine
                         University of California, Davis, School of Medicine Davis, California
POMEROY Claire           Diplomat, American Board of Internal Medicine, Subspecialty
                         Certification, Infectious Disease
FORBES Stuart          Chair of Transplantation and Regenerative Medicine at Edinburgh
                       University. - Consultant Hepatologist, Scottish Liver Transplant Unit,
                       Royal Infirmary of Edinburgh.
NESBITT Thomas         Family Phyisician - Advanced Cardiac Life Support - Advanced Trauma
                       Life Support
STURNIOLO Giacomo Carlo Professore Associato Confermato di Gastroenterologia presso
                       l’Università di Padova. Vincitore di direzione di modulo di Endoscopia
                       Digestiva dell’Azienda Ospedaliera di Padova.
PALU’ Giorgio          Diploma di Specializzazione in Oncologia e in Patologia Generale –
                       Professore in Virologia – Professore in Microbiologia – Università degli
                       Studi di Padova
FARINATI Fabio         Specializzato in Gastroenterologia ed Endoscopia Digestiva ed in
                       Oncologia - Professore Associato di Gastroenterologia dal 1.1.2005.
LEVRERO Massimo        Laboratory of Gene Expression, Fondazione A. Cesalpino, Università
                       “La Sapienza”, Roma
DELLE FAVE Gianfranco  Professore Ordinario di Gastroenterologia - Direttore Cattedra di
                       Gastroenterologia II Facoltà di Medicina e Chirurgia Università degli
                       Studi di Roma “La Sapienza” - Direttore Scuola di Specializzazione in
                       Gastroenterologia
MAZZAFERRO Vincenzo Specializzazione in Chirurgia Generale - Oncologia
BURRA Patrizia         SPECIALIZZAZIONE in Gastroenterologia ed Endoscopia Digestiva -
                       PROFESSORE A CONTRATTO insegnamento Scuola di Specialità
                       "Gastroenterologia ed Endoscopia Digestiva", Semeiotica Funzionale, II anno
CILLO Umberto          Professore Associato di Chirurgia Generale- Università degli Studi di
                       Padova, Specialista in Chirurgia d'Urgenza
VAN THIEL David H.     Professor of Medicine and Surgery at Loyola University’s Stritch School
                       of Medicine
NACCARATO Remo         Direttore del Dipartimento di Scienze Chirurgiche e Gastroenterologiche
                       dell’Università degli Studi di Padova



Quote Iscrizione

Corso Pre-meeting:
●Soci ASSOCIAZIONE FARINI gratuita
●Non Soci € 150,00 Iva incl.

XVIII Symposio Associazione Roberto Farini e 4° Simposio Università della California, Davis
●Soci ASSOCIAZIONE FARINI gratuita
●Non Soci € 180,00 VAT Iva incl.
Corso Pre-meeting e XVIII Symposio Associazione Roberto Farini e 4° Simposio
Università della California, Davis
●Soci ASSOCIAZIONE FARINI gratuita
●Non Soci € 260,00 VAT Iva incl.

Sponsors                 SI (ABBOTT Spa – ALFA WASSERMANN SpA – ALMIRALL – ALTANA PHARMA –
ASTELLAS – ASTRAZENECA SpA – AVENTIS SANOFI – BIOCURE Srl – BIOFUTURA PHARMA Spa –
BIOTEST Italia Srl – CaDi Group – Cassa di Risparmio Ag. Ospedale – CHIESI Farmaceutici Spa - CRINOS
Industria Farmacobiologica – ESAOTE – ETHICON J&J – EUROSPITAL – FERRING Spa – GILEAD – GLAXO
SMITH KLINE – GRIFOLS ITALIA SpA – H.S. HOSPITAL Service Spa/KERNA Italia Srl – HARDIS Srl - IBI
LORENZINI – INNOVAres – IPSEN Spa – JANSSEN-CILAG SpA – LABOREST – LORENZATTO M.G. SpA -
MALESCI SpA – MED Sas – MEDIMAR – MEDTRONIC Italia – MENARINI – MENFIS – NATHURA Srl –
NESTOR Spa – NOVARTIS Consumer Health Spa – NOVARTIS Farma Spa – NOVASOREL Srl OLYMPUS
Italia Srl – ORTHO Clinica Diagnostics – PHARMACIA Italia SpA – PROMEFARM Srl – RECORDATI – ROCHE
SpA – SCHERING-PLOUGH Spa – SIFFRA – SIGMA-TAU Spa – SOFAR Spa – SOLVAY / FURNIER –
TAKEDA Italia Farmaceutici SpA – THERABEL GiEnne PhARMA Spa – VALEAS Spa – WYETH LEDERLE -
XPHARMA

N. Partecipanti        150

Destinatari    Verrà fatta richiesta di accreditamento presso la Regione Veneto per le figure
professionali: medico chirurgo, specialità tutte, con priorità nelle iscrizioni a: Gastroenterologi,
Medicina Interna, Chirurghi (Oncologi – Chirurgia Generale, ecc.)



Metodo di verifica dell’apprendimento: Tramite Questionario a risposte multiple

Materiale Didattico consegnato:       CD contenente le relazioni presentate nel corso dell’evento

Tipo di supporto a distanza offerta:          Nessuno


Metodologia didattica:
Lezioni Magistrali                                  A1 ore       1    minuti   20
Lezioni Frontali standard                           A2 ore       7    minuti   00
Presentazione Problematiche (Didattica Interattiva) B2 ore       1    minuti   00
Discussione argomenti                               A2 ore       2    minuti   00
Compilazione Questionario e Scheda gradimento A2 ore             0    minuti   30
                                   Totale ore 11 minuti          50
           DESCRIZIONE DELL’INTERVENTO E DEGLI OBIETTIVI FORMATIVI

Le neoplasie epatiche sono lesioni a carattere neoproliferativo, sia primitive che
metastatiche, che interessano il fegato. Nei paesi socio-economicamnete più avanzati, i
tumori metastatici prevalgono rispetto ai tumori primitivi.
L’epatocarcinoma rappresenta il più frequente tumore maligno primitivo del fegato. Il tasso
di mortalità per epatocarcinoma varia notevolmente in base all’area geografica considerata.
Sono stati identificati precisi fattori di rischio per l’insorgenza di tale neoplasia come la
cirrosi HBV-correlata, HCV-correlata ed esotossica ed il sesso maschile. Il quadro clinico nel
paziente cirrotico è caratterizzato dalla comparsa di sintomi e segni che si sovrappongono a
quelli della sottostante malattia epatica. Se non trattato l’epatocarcinoma ha una prognosi
infausta con exitus del paziente che si verifica in media dopo 1-6 mesi in pazienti non
cirrotici, dopo 24 mesi dalla diagnosi nel paziente cirrotico.
I più frequenti tumori epatici benigni sono l’angioma, l’adenoma epatocellulare e l’iperplasia
nodulare focale. L’angioma è spesso asintomatico e viene diagnosticato occasionalmente nel
corso di un esame ecografico di controllo. Non necessita di terapia tranne nei casi di
emangiomi cavernosi giganti. Per quanto riguarda l’adenoma epatocellulare e l’iperplasia
nodulare focale, mentre per il primo è possibile l’evoluzione maligna e quindi la resezione
rappresenta il trattamento di scelta, questo non sembra verificarsi nell’iperplasia nodulare
focale.
Nell’ambito di tale argomento quindi l’obiettivo dei relatori sarà di definire i criteri per
diagnosticare precocemente le forme di neoplasia epatica maligna, di illustrare le opzioni
terapeutiche più adatte a seconda del tipo di neoplasia e della condizione clinica del
paziente e di identificare le terapie antivirali più attuali nella cura delle epatopatie da virus B
e C, fino alle più moderne terapie quali le cellule staminali ed il trapianto di fegato.
                                       PROGRAMMA
               FRIDAY, JANUARY 26TH 2007 VENERDÌ, 26 GENNAIO 2007
                        Morgagni Room, University Hospital, Padua
                     Aula Morgagni, Policlinico Universitario, Padova

President Presidente R. Naccarato, Padova
President Presidente Associazione Roberto Farini G.C. Sturniolo, Padova

08.00 Registration Registrazione
08.45 Welcome Announcement and Introductions
      Saluto delle Autorità e Apertura del Congresso
SESSION 1 SESSIONE 1
Benign liver diseases (I) Patologie epatiche benigne (I)
Dalle ore 09.00 Alle ore 10.40
Fare acquisire conoscenze teoriche e aggiornamenti in tema di Patologie epatiche benigne – parte I
Fare acquisire competenze per l’analisi e la risoluzione dei problemi nei vari contesti
Far migliorare le capacità relazionali e comunicative

Chairs   Moderatori Lajos Okolicsanyi, Treviso; Stefano Fagiuoli, Bergamo
09:00-09:20 Changing epidemiology of HBV in Italy
            Come sta cambiando l'epidemiologia dell'HBV in Italia
            Tommaso Stroffolini, Roma
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

09:20-09:40 Hepatitis C and liver cirrhosis: new approach
            Epatite C e cirrosi epatica: nuovi approcci
            Joanne Imperial, Palo Alto, California, USA
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

09:40-10:00 New antivirals for HBV infection before and after liver transplantation
            Nuovi farmaci antivirali per l’infezione da HBV prima e dopo trapianto di fegato
            Antonina Smedile, Torino
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                  Ore 0 minuti 20
                                                                  Lezione Frontale A2

10:00-10:20 Hemochromatosis: new developments       Emocromatosi: nuovi sviluppi
            Christopher Bowlus, Sacramento, California, USA
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                  Ore 0 minuti 20
                                                                  Lezione Frontale A2
10:20-10:40 Discussion Discussione
                     (Discussione sulle relazioni presentate)     Ore 0 minuti 20
                                                                  Lezione Frontale A2
10:40     Coffee break

SESSION 2 SESSIONE 2
Benign liver diseases (II) -     Patologie epatiche benigne (II)
Dalle ore 11.00 Alle ore 12.40
Fare acquisire conoscenze teoriche e aggiornamenti in tema di Patologie epatiche benigne – parte II
Fare acquisire competenze per l’analisi e la risoluzione dei problemi nei vari contesti
Far migliorare le capacità relazionali e comunicative

Chairs    Moderatori Antonio Gasbarrini, Roma; Giacomo Carlo Sturniolo, Padova
11:00-11:20 Hepatic involvement in haematological diseases
            Coinvolgimento epatico nelle malattie ematologiche
            Emanuele Angelucci, Cagliari
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                  Ore 0 minuti 20
                                                                  Lezione Frontale A2

11:20-11:40 Gut and the liver: a dangerous “liaison”? Intestino e fegato: una “liaison”
            pericolosa?
            Diego Martines, Padova
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

11:40-12:00 Discussion Discussione
             (Discussione sulle relazioni presentate)             Ore 0 minuti 20
                                                                  Lezione Frontale A2

12:00-12:40 State of the Art Lecture 1 - Stato dell’Arte Lettura 1
            Chronic Hepatitis B: updated treatment algorithm
            Epatite B cronica: algoritmo di trattamento
              Emmet Keeffe, Palo Alto, California, USA Gaetano Mastropaolo, Bassano del G. (VI)
             (Il relatore farà una lezione magistrale)
                                                                   Ore 0 minuti 40
                                                                  Lezione Magistrale A1

12:40         Lunch break

SESSION 2A SESSIONE 2A
Benign liver diseases - Patologie epatiche benigne
Dalle ore 14.20 Alle ore 15.20
Fare acquisire conoscenze teoriche e aggiornamenti in tema di Patologie epatiche benigne
Fare acquisire competenze per l’analisi e la risoluzione dei problemi nei vari contesti
Far migliorare le capacità relazionali e comunicative
14:20-15:20 Oral Communications     Comunicazioni Orali
Chairs      Moderatori        Angelo Gatta, Padova; Ermanno Ancona, Padova
             (Verranno lette e discusse le relazioni pervenute dai partecipanti)
                                                                          Ore 1 minuti 00
                                                                  Didattica Interattiva B2




SESSION 3 SESSIONE 3
Benign liver diseases (III) - Patologie epatiche benigne (III)
Dalle ore 15.30 Alle ore 16.50
Fare acquisire conoscenze teoriche e aggiornamenti in tema di Patologie epatiche benigne – parte III
Fare acquisire competenze per l’analisi e la risoluzione dei problemi nei vari contesti
Far migliorare le capacità relazionali e comunicative

Chairs    Moderatori Angelo Gatta, Padova; Ermanno Ancona, Padova
15:20     Introduction to the State of the Art Lecture 2
          Introduzione alla lettura - Stato dell’Arte 2
          Pietro Invernizzi, Milano


15:30-16:10 The State of the Art Lecture 2 - Stato dell’Arte Lettura 2
            The Immunological milieu of the liver Il sistema immunologico del fegato
            Eric Gershwin, California, USA
             (Il relatore farà una lezione magistrale)
                                                                   Ore 0 minuti 40
                                                                  Lezione Magistrale A1

16:10-16:30 Portal hypertension: band ligation and TIPS
            Ipertensione portale: legatura e TIPS
            Andrew K. Burroughs, London, UK
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

16:30-16:50 Palliative care and end stage liver disease
            Terapia palliativa e malattia epatica severa
            Lorenzo Rossaro, Sacramento, California, USA
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

16:50     Coffee break
SESSION 4 SESSIONE 4
Benign liver diseases (IV) -       Patologie epatiche benigne (IV)
Dalle ore 17.00 Alle ore 19.00
Fare acquisire conoscenze teoriche e aggiornamenti in tema di Patologie epatiche benigne – parte IV
Fare acquisire competenze per l’analisi e la risoluzione dei problemi nei vari contesti
Far migliorare le capacità relazionali e comunicative

Chairs Moderatori   Claire Pomeroy, Sacramento, California, USA; Lorenzo Rossaro, Sacramento,
                    California, USA
17:00-17:20 Stem cells, regenerative medicine and patient hopes
            Cellule staminali, medicina rigenerativa e aspettative dei pazienti
            Claire Pomeroy, Sacramento, California, USA
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

17:20-17:40 Stem cells and liver diseases Cellule staminali e malattie epatiche
            Stuart Forbes, Edinburgh, UK
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

17:40-18:00 Telemedicine and e-Health: bringing expertise to the point of need
            Medicina e salute per via telematica: raggruppare gli esperti
            Thomas Nesbitt, Sacramento, California, USA
             (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                  Lezione Frontale A2

18:00-18:20 Discussion Discussione
             (Discussione sulle relazioni presentate)             Ore 0 minuti 20
                                                                  Lezione Frontale A2

18:20-19:00 Closing of the day Chiusura dei lavori del giorno
            Giacomo Carlo Sturniolo, Padova
             (Il relatore leggerà una conclusione sui lavori della giornata)
                                                                     Ore 0 minuti 40
                                                                    Lezione Frontale A2
              SATURDAY, JANUARY 27TH 2007 SABATO, 27 GENNAIO 2007
                         Morgagni Room, University Hospital, Padua
                      Aula Morgagni, Policlinico Universitario, Padova

SESSION 5 SESSIONE 5 Benign and malignant liver tumors (I)
Tumori epatici benigni e maligni (I)
Dalle ore 08.40 Alle ore 10.00
Fare acquisire conoscenze teoriche e aggiornamenti in tema di Tumori epatici benigni e maligni –
parte I
Fare acquisire competenze per l’analisi e la risoluzione dei problemi nei vari contesti
Far migliorare le capacità relazionali e comunicative

Chairs   Moderatori Massimo Rugge, Padova; Alberto Amadori, Padova
08:40-09:00   Gene therapy and vaccines Terapia genica e vaccini
              Giorgio Palù, Padova
              (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                    Ore 0 minuti 20
                                                                   Lezione Frontale A2
09:00-09:20   Benign liver tumors: a new approach Tumori epatici benigni: un nuovo approccio
              Fabio Farinati, Padova
              (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                   Lezione Frontale A2
09:20-09:40   Genetic and epigenetic changes in hepatocellular carcinoma
              Mutazioni genetiche ed epigenetiche nel carcinoma epatocellulare
              Massimo Levrero, Roma
              (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                    Ore 0 minuti 20
                                                                   Lezione Frontale A2

09:40-10:00   Discussion Discussione
              (Discussione sulle relazioni presentate)             Ore 0 minuti 20
                                                                   Lezione Frontale A2
10:00    Coffee break

SESSION 6 SESSIONE 6
Benign and malignant liver tumors (II) - Tumori epatici benigni e maligni (II)
Chairs   Moderatori Gennaro Favia, Padova; Luigi Bolondi, Bologna
10:20-11:00   Liver endocrine tumors Tumori epatici endocrini
              Gianfranco Delle Fave, Roma
              (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                   Ore 0 minuti 20
                                                                   Lezione Frontale A2
10:40-11:00    Cholangiocarcinoma and downstaging therapies
               Colangiocarcinoma e terapie di downstaging
               Vincenzo Mazzaferro, Milano
               (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                    Ore 0 minuti 20
                                                                    Lezione Frontale A2

11:00-11:20    Discussione Discussion
               (Discussione sulle relazioni presentate)             Ore 0 minuti 20
                                                                    Lezione Frontale A2


SESSION 7 SESSIONE 7
Hepatocellular carcinoma and liver transplantation - Carcinoma epatocellulare e trapianto di fegato
Chairs  Moderatori Davide D’Amico, Padova; Antonio Francavilla, Bari
11:20-11:40 Hepatocellular carcinoma: priority in the waiting list for liver transplantation ?
          Carcinoma epatocellulare: priorità in lista d’attesa per trapianto di fegato?
          Patrizia Burra, Padova
               (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                     Ore 0 minuti 20
                                                                    Lezione Frontale A2

11:40-12:00 Liver transplantation for hepatocellular carcinoma: pros and cons of extended criteria
          Trapianto di fegato per carcinoma epatocellulare: pro e contro rispetto ai criteri di estensione
          Umberto Cillo, Padova
               (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                     Ore 0 minuti 20
                                                                    Lezione Frontale A2

12:00-12:20    Discussione Discussion
               (Discussione sulle relazioni presentate)             Ore 0 minuti 20
                                                                    Lezione Frontale A2


SESSION 8 SESSIONE 8
Summary of the Meeting    Riassunto del congresso
Chair   Moderatore Remo Naccarato, Padova
12:20     What did we learn? Cosa abbiamo imparato?
          David H. Van Thiel, Chicago, Illinois, USA
               (Il relatore leggerà una relazione sul tema che verrà discussa con i partecipanti)
                                                                     Ore 0 minuti 20
                                                                    Lezione Frontale A2

12.40–13.10    Compilazione questionario di verifica apprendimento e scheda di valutazione evento
                                                                    Ore 0 minuti 30
                                                                    Lezione Frontale A2
13:15     Awards Consegna dei Premi
          Avv. Francesco Farini, Padova
          Closing remarks   Conclusioni
          Remo Naccarato, Padova




SATURDAY, JANUARY 27TH 2007 SABATO, 27 GENNAIO 2007 Congress Centre Papa Luciani
Centro Congressi Papa Luciani
From 15:00 to 18:00 hrs Dalle ore 15:00 alle ore 18:00

A Health Service for care Per una Sanità che curi.
How to “live your life” Proposte per “vivere la vita” anche
through the disease durante la malattia

Hosted by Conduce Dr. Paolo Barnard – Rai Educational
The Representatives of the following Non-Profit Associations, will attend the Meeting
Saranno presenti in Aula i rappresentanti delle Associazioni di Volontariato

AMICI Associazione Italiana Celiachia Associazione Nazionale di Volontariato "CONTINUANDO A
VIVERE" Associazione Trapianti d’Organo Veneto Schola Medica Studi Padoani AVO Fondazione
Marina Minnaja per la ricerca e la cura nel trapianto di fegato

Followed by Seguirà
From 18:00 to 20:00 Dalle ore 18:00 alle ore 20:00

Charity performance Spettacolo a scopo di beneficenza




                                        ABSTRACTS

THE CHANGING PATTERN OF HEPATITIS B VIRUS INFECTION OVER TIME IN ITALY
Tommaso Stroffolini - Dipartimento di Gastroenetrologia, Ospedale San Giacomo, Roma, Italia

   By the end of 1970s, Italy was a country at medium endemic level of hepatitis B virus infection,
with wide geographical differences; intrafamily transmission was the major mode by which infection
spread; hepatitis B e antigen positivity and hepatitis Delta positivity were frequently detected in
hepatitis B surface antigen chronic carriers; a high proportion of subjecs with chronic liver diseases
resulted as hepatitis B surface antigen positive. Three decades apart, the picture was completely
changed, as documented by several surveys. Nowadays, Italy is a country at very low endemic level of
hepatitis B, without geographical differences; the infection is mostly sexually transmitted; hepatitis B e
antigen positivity and hepatitis Delta positivity are rarely detected in hepatitis B surfaces antigen
chronic carriers; a low proportion of subjects with chronic liver disease result hepatitis B surface
antigen positive. These important changes my be due to both non-specific (i.e. improvement in socio-
demographic features) and specific (i.e. comprehensive vaccination program against hepatitis B)
prevention measures.


Hemochromatosis: New Developments
BOWLUS
Topics to be discussed:

1. Normal and pathologic iron metaoblism
2. Genetics of hemochromatosis and other iron overload syndromes
3. Diagnosis of hemochromatosis, particularly with chronic liver disease
4. The role of hemochromatosis as a risk factor for other diseases
5. Questions still to be answered


Scaletta dell’intervento Dr. Angelucci
 In my review I will try to address the following items related to hepatic involvement in haematological
diseases and related therapies

Hemopoietic stem cell transplant and intensive chemotherapy
     Venous occlusive disease
     Acute and chronic hepatic graft versus host disease
     Hepatic failure
     HBV reactivation

Direct liver involvement in acute Leukemia and Lymphomas
        Leukemia
        Spleen lymphoma

Liver involvement in Chronic haematological diseases
        Iron overload
        HCV and HBV infection
        Iron and viral infection interaction


Gut and the liver: a dangerous “liaison”?
D. Martines

The small intestine epithelium besides playing a key role in the absorption, digestion and secretion
processes, represents a relatively impermeable barrier between the external environment, the
intestinal lumen and the bloodstream.
The integrity of this barrier is crucial for the protection of the human body from toxic agents,
carcinogens and gut-derived bacterial products and depends on the intercellular tight junctions within
the paracellular space. Thus, it is not difficult to envisage that patients with gastrointestinal diseases or
disruption of the intestinal barrier can develop hepatic disorders. Despite the association between
inflammatory bowel diseases (ulcerative colitis, Crohn’s disease) and liver disorders is well
recognized, only recent data have shown the association between celiac disease and hepatic
disease. Moreover, current evidence support the association between the disruption of the intestinal
barrier and alcohol and non alcohol-induced liver injury.
The lecture will focus on:
          1. the hepatic and biliary abnormalities commonly observed during intestinal diseases and
          the potential clinical and therapeutical implications
          2. the potential mechanisms involved in the hepatic disease, in particular the role of
          endotoxins on the development of liver injury.



Chronic Hepatitis B: Updated Treatment Algorithm
Emmet B. Keeffe, MD, MACP
Abstract
      Chronic hepatitis B is diagnosed in patients with elevated alanine aminotransferase (ALT) levels,
       detectable serum HBV DNA, and necroinflammation on liver biopsy.
      The natural history of HBV infection can be divided into 3 phases: immune tolerant, immune active (or
       chronic hepatitis B), and inactive carrier.
      Treatment is currently recommended only for patients in the immune active phase--those with chronic
       hepatitis B (defined by the presence of elevated ALT and HBV DNA levels and necroinflammatory
       findings, with or without fibrosis, on liver biopsy).
      ALT criteria used for determining the indications for therapy should be the revised upper limits of
       normal, i.e., 19 U/L in women and 30 U/L in men.
      The primary goal of therapy for chronic hepatitis B is long-term suppression of serum HBV DNA,
       which will likely reduce progression to cirrhosis and hepatic decompensation as well as decrease the risk
       of HCC.
      The FDA-approved therapies for chronic hepatitis B include interferon alfa-2b (1992), lamivudine
       (1998), adefovir (2002), entecavir (2005), and peginterferon alfa-2a (2005).
      The currently preferred treatments include adefovir, entecavir, and peginterferon alfa-2a; standard
       interferon alfa-2b has been replaced by peginterferon alfa-2a, and lamivudine is not a preferred first-line
       drug due to high rates of resistance.
      HBeAg-positive chronic hepatitis B patients should receive treatment when serum HBV DNA levels are
        20,000 IU/mL and ALT levels are elevated, particularly 2-fold.
      HBeAg-negative chronic hepatitis B patients should receive treatment when serum HBV DNA levels are
        2,000 IU/mL and ALT levels are elevated.
      Patients considering peginterferon alfa-2a therapy should be tested for HBV genotype; genotype A
       responds much better than genotype D (both common Caucasians), and genotype B responds somewhat
       better than genotype C (both common in Asians).
      All patients with chronic hepatitis B and cirrhosis with HBV DNA levels  2,000 IU/mL should be
       treated. There is increasing evidence supporting the use of combination nucleoside/nucleotide agents in
       these patients, and therapy should probably be long-term for both HBeAg-positive and HBeAg-negative
       patients.
       The rates of resistance with long-term therapy are high with lamivudine (70% at 4 years), intermediate
        with adefovir (29% at 5 years of therapy), and low with entecavir (not identified in treatment-naïve
        patients after 2 years of therapy). Resistance does not occur with interferon or peginterferon therapy.
       Potential future therapies for chronic hepatitis B include peginterferon alfa-2b and other nucleoside
        analogues, including tenofovir and telbivudine that are in late-stage study. Clevudine and pradefovir are
        in earlier phases of study.


PRIMARY BILIARY CIRRHOSIS
M. Eric Gershwin, M.D. - Division of Rheumatology, Allergy and Clinical Immunology, University of
California at Davis School of Medicine, 451 E. Health Sciences Drive, Suite 6510, Davis, CA 95616
Primary biliary cirrhosis (PBC) is an autoimmune disease of unknown etiology, often associated with other
autoimmune conditions. Controlled studies have so far provided conflicting data on risk factors and comorbidity
rates in PBC. We enrolled patients with PBC (n = 1032) from 23 tertiary referral centers for liver diseases in the
United States and random digit dialed controls (n = 1041) matched for sex, age, race, and geographical location.
Patients and controls were administered a modified version of the US National Health and Nutrition
Examination Study (NHANES III) questionnaire by trained personnel to evaluate associations between PBC and
social, demographic, personal and family medical histories, lifestyle, and reproductive factors and the rates of
comorbidity in affected individuals. Data indicate that having a first-degree relative with PBC (adjusted odds
ratio [AOR] 10.736; 95% confidence interval 4.227-27.268), history of urinary tract infections (AOR 1.511, 95%
CI 1.192-1.915), past smoking (AOR 1.569, 95% CI 1.292-1.905), or use of hormone replacement therapies
(AOR 1.548, 95% CI 1.273-1.882) were significantly associated with increased risk of PBC. The frequent use of
nail polish slightly increased the risk of having PBC. Other autoimmune diseases were found in 32% of cases
and 13% of controls (P<0.0001). In conclusion, environmental factors, possibly including infectious agents
through urinary tract infections or chemicals contained in cigarette smoke, may induce PBC in genetically
susceptible individuals. Exogenous estrogens may also contribute to explain the female predominance of the
disease. These data should be contrasted with the concordance of PBC in identical twins.
There is growing evidence that the interplay of genetic susceptibility and environmental factors leads to primary
biliary cirrhosis (PBC). In particular, family members of an infected individual have up to a 100-fold higher risk
of developing PBC. Although concordant rates for identical twins in other autoimmune diseases range between
25% and 50%, there are no such data on PBC. Accordingly, we evaluated the concordance of PBC in a
genetically defined population of twin sets and evaluated the clinical characteristics between concordant
subjects. We identified 16 pairs of twins within a 1400-family cohort followed up y several centers worldwide,
evaluated the diagnosis of PBC in all individuals, and determined the zygosity of sets reported as identical by the
analysis of 2 highly variable HLA class II regions and 5 short tandem repeats. Eight of 16 sets of twins were
monozygotic. In 5 of 8 monozygotic twin sets, both individuals had PBC (pairwise concordance rate, 0.63).
Among the dizygotic twins (n=8), no set was found to be concordant for PBC. Interestingly, the age of onset of
disease was similar in 4 of 5 concordant sets of monozygotic pairs; however, there were differences in natural
history and disease severity. The concordance rate of PBC in identical twins is among the highest reported in
autoimmunity. However, discordant pairs were identified. The data show not only the role of genetics but also
emphasize that either epigenetic factors and/or environment play a critical role.



Palliative care and end stage liver disease
Terapia palliativa e malattia epatica severa
Lorenzo Rossaro and Valentina Medici - University of California Davis Medical Center
Sacramento, California, USA
Rapid and continuous improvements in health science have allowed a longer life expectancy of
patients with severe and often concomitant chronic diseases. This gain has come with its own burden,
which is the increased need for quality end of life (EOL) care in this growing patient population. End
stage liver disease (ESLD) accounted for 27,257 deaths in 2002 and it responsible of 9.5
deaths/100,000 populations annually in Unites States (1).

Traditionally, the primary goal of hospice care is the palliation of physical and mental sufferings of
terminally ill patients, whose life expectancy is predicted to be of six months or less. This service
includes nursing care, physician’s consultations, drugs, physical, psychosocial and spiritual support
(2).

Liver transplant (LT) and hospice candidacy have always been perceived as mutually exclusive.
Potential transplant recipients are treated aggressively with disease directed therapy or so-called
curative efforts in order to maximize their chances to receive a LT. Little attention is given to the need
for EOL care that many will face with the shortage of donor organs or with the possibility of not being a
candidate for LT. Only when the patient’s medical condition worsens and the hope for LT is lost in the
last weeks of life, patients are offered palliative care or hospice care. With this strategy, however, the
amount of time is insufficient for patients and family members to optimally benefit from the hospice
programs. The result is often a poor quality of life and poor quality of care at the patient’s end of life.

The introduction of the MELD score has improved the ability to predict the prognosis of ESLD and has
been adopted by the United Network for Organ Sharing (UNOS) to determine priorities in allocating
organs (3,4). Therefore, the MELD score could be used as an indicator of concurrent hepatic
transplantation prioritization and hospice referral(5).

In order to (1) study the value of the MELD score in guiding the referral for hospice care, (2) to
evaluate the possibility of a new integrated model between hospice/palliative care and liver
transplantation, and (3) to delineate the demographic and clinical features of patients with ESLD
admitted at our combined hospice/liver service, we retrospectively reviewed the medical records of
patients with end stage liver disease admitted to the UCDHS hospice service between October 2001
and December 2005.

The data collected include: demographic (age, gender), main diagnosis: hepatitis C (HCV), hepatitis B
(HBV), alcoholic liver disease (ETOH), hepatocellular carcinoma (HCC), complications while under the
care of the hospice team (bleeding, hepatic encephalopathy, ascites), and MELD score at the time of
hospice admission.

169 ESLD patients were admitted to the combined hospice/ liver service. 49 cases (29%) were also
evaluated for LT. The mean age was 58 years (31-87). In 41 cases (24%), the chronic liver disease
was complicated by hepatocellular carcinoma. The mean hospice length of stay (LOS) was 37  51.9
days.

Liver-related diagnosis at hospice admission were: HCV 33 %, HBV 10 %, HCC 52 %. Liver related
complications while enrolled in the hospice program included: Tense ascites + dyspnea 75%, GI
bleeding 10 %, Hepatic encephalopathy 66%.

At the time of hospice admission the mean MELD score of the whole group was 21 ± 8.3. Five patients
were offered a liver graft while on the combined hospice/liver program; they revoked hospice and
received LT. The mean time elapsed between the hospice admission and LT was 96.7 days (60-153).
Four patients survived with a follow up of 7-45 months. One patient died after LT because of
progressive heart and kidney failure.
A significant correlation was observed between length of hospice stay and MELD score at hospice
admission (p= 0.004). A MELD > 28 is an absolute indication for hospice referral as virtually no patient
survived for more than 17 days. In patients with MELD between 15 and 27 there were both early
deaths (LOS less than 2 weeks) as well as some patients who survived up to 3 months.

Our study support the need for a clinical pathways between Liver and Hospice Services in order to
improve the management of ESLD. A combined Liver/Hospice specific skills are needed to manage
ESLD complications. Early referral to hospice/palliative care is improved by using the MELD score:
referring patients with a defined MELD to the hospice can optimize both the quality of life and care for
patients and families.

We suggest hospice care as a possible simultaneous strategy to improve the management of ESLD
selected patients waiting for Liver Transplantation.

References
1.     Centers for disease Control and Prevention. Monthly vital statistics report. Available at
       http://www.cdc.gov/nchswww/fastats.htm.

2.     Christakis NA, Escarce JJ. Survival of Medicare patients after enrollment in hospice programs. N Engl
       J Med. 1996;335:172-178.

3.     Freeman RB Jr, Wiesner RH, Harper A, et al. The new liver allocation system; moving toward evidence-
       based transplantation policy. Liver Transpl. 2002;8:851-858.

4.     Freeman RB Jr, Wiesner RH, Edwards E, et al. Results of the first year of the liver allocation plan. Liver
       Transpl. 2004;10:7-15

5.     Rossaro L, Troppman C, McVicar JP, Sturges M, Fisher K, Meyers FJ. A strategy for the simultaneous
       provision of pre-operative palliative care for patients awaiting liver tranplantation. Transpl Int.
       2004;17:473-475.


STEM CELLS IN LIVER REGENERATION AND FIBROSIS
FORBES

The hepatic parenchyma is made up of hepatocytes and cholangiocytes. Unlike other organs such as
the gut, liver cell mass is restored primarily through division of the majority of mature hepatocytes and
not via a dedicated stem cell population. After a regenerative stimulus, such as hepatic resection,
hepatocytes rapidly enter the cell cycle and undergo mitosis. At times of severe or chronic liver
damage regeneration occurs via a second cell compartment. This compartment remains poorly
defined and seems to arise from the terminal branches of the biliary tree- the canals of Hering. In
rodents these cells are called “oval cells” but in humans they are named hepatic progenitor cells
(HPCs). Recently it was suggested that the bone marrow (BM) was an additional source of
hepatocytes and oval cells within the liver. The implication was that stem cells could cross
conventionally-demarcated lineage boundaries through a process termed transdifferentiation or stem
cell plasticity. We have systematically studied the intra and extra-hepatic sources of liver cell
replacement in mouse models of chronic liver injury. Our results indicate that parenchymal
regeneration occurs principally through hepatocyte replication. The BM very rarely contributed to
hepatocyte regeneration and, when seen this was largely due to cell fusion between indigenous
hepatocytes and donor BM. However, BM cells largely contribute to non-parenchymal cells and the
fibrotic cell populations within the liver. This has been investigated further in two ways: (1) by studying
patients who had received sex-mismatched liver and BM transplants. This has indicated that the BM is
a significant source of fibrosis in patients who have liver disease of diverse aetiology. (2) by studying
mouse models of liver fibrosis in BM-transplanted mice. Here the BM contributed significantly to
hepatic stellate cell and myofibroblast populations (scar forming cells). These BM-derived cells are
active for collagen type 1 transcription and can influence the fibrotic response to organ injury. These
BM-derived myofibroblasts originate largely from the BM’s mesenchymal stem cells and is therefore a
potential therapeutic target in liver fibrosis. The BM also supplies “scar associated macrophages” that
populate the areas of liver fibrosis. These macrophages are of interest as they help stimulate liver
fibrosis during damage but can also help the resolution of scar tissue during the resolution of liver
fibrosis.
Various fractions of BM have been used for “BM stem cell therapy” in rodent models of liver injury,
including endothelial progenitor cells (EPCs) and these seem to be effective at provoking a reduction
in liver fibrosis and stimulating liver regeneration. To date there are only a handful of clinical trials
which have looked at the effect of autologous “BM stem cell therapy” for liver disease, all of which are
small-scale, uncontrolled feasibility studies. These studies have looked at a variety of scenarios. In
patients undergoing hepatectomy for cancer, accelerated hepatic regeneration was seen in patients
after the infusion of autologous CD133+ BM cells. Other studies have examined stem cell therapy for
liver cirrhosis. Although uncontrolled, preliminary results from these studies are encouraging.



GENE THERAPY AND VACCINES
Luisa Barzon, Giorgio Palù - Dipartimento di Istologia, Microbiologia e Biotecnologie Mediche
Università degli Studi di Padova

Gene therapy and immunotherapy approaches against hepatocellular carcinoma (HCC) using a
variety of strategies are currently in development, some of which are entering clinical trials. Most gene
therapy strategies focus on the genetic manipulation of accessory cells involved in the immune
reaction against cancer cells, or on the direct transduction of tumor cells with transgenes able to
"suicide" cancer cells. The identification of the role of miRNA on the pathogenesis of cancer and in the
control of viral replication (including HCV replication) could offer new therapeutic tools fot HCC



Benign Liver Tumors: a new approach
F. Farinati, A. Baldan, C.Tieppo, A. Sergio, C.Cristofori
Gastroenterology, Dept. Surgical and Gastroenterological Sciences, Padua University

Benign hepatic tumours include a broad spectrum of regenerative and true neoplastic processes. A liver tumour
is occasionally found by coincidence during upper abdominal imaging and the diagnostic and therapeutic
strategies for incidental liver tumours are often debatable. Generally speaking, the “a priori” chance of certain
diagnoses depends on the presence or absence of risk factors. Using simple imaging techniques, liver lesions can
be categorized as single or multiple and as cystic or solid. Cystic lesions are usually benign, either congenital or
parasitic, while solid lesions can be benign or malignant. The most common benign lesions are haemangioma,
focal nodular hyperplasia, hepatocellular adenoma and dysplastic lesions (precursor lesions of hepatocellular
carcinoma).
Due to advances in imaging procedures like MRI, CT-scan and ultrasound, either regular or contrast-enhanced,
as well as to progress in immuno-histochemistry, the appropriate diagnosis is made in a high percentage of
patients without laparotomy and resection.
In the majority of cases of benign hepatic tumors, patients are asymptomatic, and no treatment is indicated. The
main indication for treatment is the presence of significant clinical symptoms or suspicion of malignancy or fear
of malignant transformation.
Most important in clinical practice and for the hepatologist is the diagnostic and therapeutic algorithm in Focal
Nodular Hyperplasia (FNH), Hepatic adenoma (HA) and Macroregenerative and Displastic nodules (MRN -
DN).
FNH is the second most common benign solid tumor of the liver and makes up approximately 8% of all primary
hepatic tumors. It’s non neoplastic, being considered an hyperplastic response to a congenital vascular
malformation. FNH is encountered in as many as 3% of general population, predominantly in childbearing-aged
women with a female to-male ratio of 6 to 8:1. Oral contraceptive use may be associated with FNH, but its
association is not clear. Although FNH may grow to more that 10 cm in diameter, patients are rarely
symptomatic. Spontaneous rupture leading to hemorrhage is extremely rare. Most patients have normal liver
function test. Malignant transformation of FNH has not been clearly described. The central fibrous scar is the
most characteristic finding in imaging studies. US is often the initial imaging modality that indicates a focal
hepatic lesion, but FNH is not well demonstrated by simple sonographic technique. On multiphasic CT and
enhanced MRI, typical features of FNH are very characteristic: in CT at late arterial phase, FNH typically
presents with a bright homogeneous enhancement and a hypodense central scar, while on MRI, FNH is slightly
hypointense on T1-weighted images and slightly hyperintense on T2-weighted images. In asymptomatic patients
with FNH, treatment generally includes clinical follow-up to observe for the development of symptoms and
radiologic follow-up with US to detect enlarging tumors. Most of resected cases are due to the undetermined
nature of the tumor, the presence of symptoms, or suspicion of metastasis in patients previously operated for
malignant diseases.
HA is a rare hepatic tumor that is pathologically characterized by the benign proliferation of hepatocytes. As
seen with FNH, HA also occurs predominantly in young women. The pathogenesis of HA remains disputed, but
a strong association with oral contraceptive use has been documented. In addition to oral contraceptives,
anabolic androgen-containing steroid medications also may increase the incidence, number, and size of HA.
Another risk group for HA includes patients with glycogen storage disease. Most patients with no more than a
few small adenomas are asymptomatic. HA is of clinical importance because of its tendency to spontaneous
rupture, hemorrhage. Therefore, acute abdominal pain and catastrophic intraperitoneal hemorrhage are not
uncommon presentation of HA. Rare cases of malignant transformation have also been reported, particularly in
multifocal cases. On US, hepatic adenomas have variable and nonspecific appearances depending on the
character of the tumor. On multiphasic CT and MRI, HA may show more specific findings. Unlike FNH, HA is
frequently heterogeneous due to intratumoral hemorrhage, necrosis, and fat components on CT. MRI findings
can also be very characteristic. On T1-weighted images, adenomas have been described variously as
hyperintense, isointense, or hypointense due to the presence of hemorrhage, necrosis, or fat components.
Because of the risk of spontaneous rupture and malignant transformation, HA must be identified and treated
promptly. After the diagnosis of HA, the most common recommended treatment is a surgical resection due to the
above complications.
MRN were previously classified as adenomatous hyperplasia and on their precancerous meaning the debate is
still open, even though neoplastic transformation has been described in as high as 20% of the cases. Low- or
high-grade DN (>1 cm) and occurs mainly on the background of the cirrhotic liver, their clinical importance
laying on their malignant transformation to HCC, although it is not clear in what percentage they progress to
malignancy, an event described as quite frequent (>60% of the cases in 48 moths of follow-up). Patients have no
specific symptoms since DN are usually discovered by imaging studies in patients with cirrhosis or advanced
fibrosis for evaluation of HCC and are usually detected on screening by US. On CT, the presence of DN can be
suggested by nodular hepatic contour, and nodules are iso-attenuating to surrounding liver during arterial and
portal phases. On MNR, lesions show variable signal intensities on T1-weighted images and typically hypo-
intensity on T2-weighted images with no clear-cut enhancement on arterial enhanced phase. These are
distinguishable features from HCC, which typically are hyper-intense on T2-weighted images with strong
enhancement during the arterial phase. Imaging findings are often not characteristic and biopsy remain the
diagnostic gold standard. Because of its malignant potential, surgical resection of DN is sometimes advocated,
especially in those with high grade dysplasia, but percutaneous loco-regional treatments may represent a more
reasonable approach. In any case, optimal management of DN and MRN remains unknown pending ongoing
investigation.
Recently, a new entity has been described, identified as teleangectatic focal nodular hyperplasia (TFNH).
TFNHs are monoclonal lesions frequently subject to bleeding that are similar to adenomas not carrying
HNF1alpha ( a transcription factors that control liver regeneration) mutations and require a similar type of
treatment. However, morphologic and molecular data support the hypothesis that TFNH is a separate entity.
Again recently, a subgroup of hepatocellular adenomas, carrying an activation of the beta-catenin Wnt pathway
and characterized by high risk of neoplastic evolution has also been described and further investigations on the
molecular characterization of these lesions, which we hopefully lead to a better management, are ongoing.

References
   De Rave S, Hussain SM. A liver tumour as an incidental finding: differential diagnosis and treatment.
    Scand J Gastroenterol Suppl. 2002;(236):81-6.
   Choi BY, Nguyen MH. The diagnosis and management of benign hepatic tumors. J Clin Gastroenterol 2005;39:401–
    412
   Libbrecht L, Desmet V, Roskams T. Preneoplastic lesions in human hepatocarcinogenesis. Liver Int. 2005
    Feb;25(1):16-27.
   Federle MP, Brancatelli G. Imaging of benign hepatic masses. Semin Liver Dis. 2001;21:237-249
   Kehagias D, Moulopoulos L, Antoniou A, et al. Focal nodular hyperplasia: imaging findings. Eur Radiol. 2001;11:202-
    212
   Kim J, Ahmad SA, Lowy AM, et al. An algorithm for the accurate identification of benign liver lesions. Am J Surg.
    2004;187:274-279.
   Borzio M, Fargion S, Borzio F, Fracanzani AL, Croce AM, Stroffolini T, Oldani S, Cotichini R, Roncalli M. Impact of
    large regenerative, low grade and high grade dysplastic nodules in hepatocellular carcinoma development. J Hepatol.
    2003 Aug;39(2):208-14.




Experience with treatment of CCC (cholangiocarcinoma) at the Istituto
Nazionale Tumori of Milan
M. Nicolosi, V. Orvieni, A. Russo, V. Mazzaferro

Background
Cholangiocarcinoma is the second malignant tumor of the liver and represents 10% of all hepatobiliary
malignancies. Surgery with or without preoperative management (i.e. biliary drainage or chemotherapy) is the
best approach with chances of cure.
Liver resection is often refused because of lymph nodes metastases or local and peritoneal invasion;
consequently many patients are managed by palliative therapies.
Univariate and multivariate analyses have by now shown that significant prognostic factors for survival are clear
surgical margin, lymph nodal status and associated vascular resection. R0 resection and early diagnosis remains
the cornerstone for possible long-term survival.
The combination of chemotherapy, brachitherapy, radiotherapy with surgery (including orthotopic liver
transplantation) contributed to prolongation of disease-free survival.
Methods
From March 1995 to July 2006, 120 patients underwent potentially curative surgery for cholangiocarcinoma at
the National Cancer Institute of Milan. 30 patients presented with hilar cholangiocarcinoma, 70 patients with
intrahepatic cholangiocarcinoma (ICC) and 20 patients with gallbladder cholangiocarcinoma. Most patients
underwent major hepatobiliary resection and 3 underwent liver transplantation. Pre- and post-operative
chemo/radiation therapies were performed when judged appropriate.
Results
84 patients (70%) underwent R0 resection and 36 (30%) ended up with an uncurative procedure (R1-R2). Most
of the latter patient category received chemotherapy and/or radiotherapy (brachitherapy, or classical
radiotherapy) after surgical procedures. The overall 5-years survival rate after surgery for mass-forming
intrahepatic CCC was 56% (36% recurrence-free-survival) while hilar cholangiocarcinoma was 50% (47%
recurrence-free-survival) and for gallbladder cholangiocarcinoma was 18% (15% recurrence-free-survival).
Overall survival was significantly higher in patients with R0 resection, negative lymph nodes and single tumor.
Conclusions
High surgical morbidity and mortality rates have been reported undergoing liver resection for CCC. Aggressive
resection with extensive lymhadenectomy has been proven beneficial in our experience. The role of adjuvant
therapy is not well defined and benefits of palliative chemotherapy and/or radiotherapy in patients with
unresectable disease is questionable.
The role of liver transplantation in the management of biliary cancer is probably very important within precise
selection criteria and using pre-transplant downstaging procedures.



CARCINOMA EPATOCELLUALRE: PRIORITÀ IN LISTA D’ATTESA PER TRAPIANTO DI FEGATO?
Dott.ssa P. Burra

Il MELD score, utilizzato per sviluppare un sistema di priorità al trapianto di fegato in pazienti con alto
rischio di mortalità a breve-termine, presenta scarsa potenza predittiva in pazienti con patologie
epatiche colestatiche e non predice accuratamente il rischio di mortalità in pazienti concarcinoma
epatocellulare. Ai pazienti con epatocarcinoma in lista d’attesa per trapianto di fegato fu così
inizialmente aggiunto al MELD preesesitente un punteggio extra di 24 punti per nodulo singolo <2cm e
di 29 punti per nodulo singolo di 2-5 cm oppure 3 noduli ciascuno <3cm. Tale strategia però risultava
in un ecessivo aumento nella priorità dei pazienti con malattia epatica neoplastica a discapito dei
pazienti in lista d’attesa per altra eziologia. Il punteggio venne quindi ridotto dapprima a 20 e 29 punti
per le due categorie sopra descritte, poi a 0 e 24 ed infine a 0 e 22. In aggiunta, fu dato un aumento
del 10% del punteggio ogni tre mesi in lista d’attesa.
La maggior difficoltà nel creare una politica di prioritizzazione giusta ed equa consiste nella mancanza
di dati predittivi per identificare i pazienti ad elevato rischio di progressione di malattia e quindi di
esclusione dalla lista d’attesa. In aggiunta, un ruolo significativo nel valutare la priorità al trapianto,
giocano i trattamenti locoregionali dell HCC prima del trapianto di fegato. Molti gruppi utilizzano la
chemioembolizzazone trans-arteriosa come metodica ponte al trapianto di fegato poichà riduce le
dimensioni del tumore e ritarda la progressione dello stesso. Tuttavia in pazienti con malattia epatica
decompensata tale trattamento potrebbe portare ald insufficienza epaticae a decesso del paziente.
Pazienti invece con neoplasie epatiche di piccole dimensioni possono usufruire di metodiche come
l’alcolizzazione percutanea o la radiofrequenza qualora il tempo d’attesa prevsito sia superiore ai 6
mesi.


Trapianto di fegato pre carcinoma epatocellulare: pro e contro rispetto ai criteri di
estensione
Prof. U. Cillo

Il carcinoma epatocellulare è un tumore che insorge nella maggiorparte dei pazienti affetti da
epatopatia cronica e da cirrosi. La diagnosi avviene spesso tardivamente e questo a causa
dell’assenza di sintomi specifici. Molti pazienti quindi arrivano alla diagnosi già con una malattia non
trattabile e questo si traduce in una sopravvivenza media di 6-20 mesi dalla diagnosi. La resezione
epatica ed il trapianto di fegato sono considerate attualmente terapie potenzialmente curative. A
causa però delle dimensioni del tumore, della sua posizione o della severità della malattia epatica di
base, molti pazienti non sono eleggibili per un intervento di resezione epatica. In questi pazienti quindi
il trapianto di fegato sembra essere la terapia migliore per poter garantire loro una sopravvivenza
maggiore. Inizialmente non avveniva alcuna selezione tra i candidati al trapianto di fegato per HCC ed
i risultati erano sconfortanti, con una sopravvivenza media a 5 anni del 30-40%. Nel 1996 sono stati
proposti i criteri di Milano (lesione singola <= a 5 cm o fino a 3 lesioni, nessuna delle quali >3 cm,
senza evidenza di invasione neoplastica dei vasi principali e senza localizzazione metastatica a livello
locale o a distanza). Recenti studi hanno dimostrato che, utilizzando tali criteri di selezione, i pazienti
trapiantati per epatocarcinoma hanno raggiunto una sopravvivenza post-trapianto confrontabile con i
pazienti sottoposti a trapianto di fegato per altre eziologie. D’altra parte, l’applicazione di tali criteri ha
portato alla controindicazione del trapianto di fegato per una larga percentuale di pazienti affetti da
epatocarcinoma. È nata così una controversia riguardo l’opportunità o meno di espandere i criteri di
selezione di Milano poiché recenti studi hanno dimostrato come l’estensione di tali criteri non influenzi
negativamente i risultati del trapianto in termini di sopravvivenza, ma provochi un aumento dei casi di
recidiva di malattia neoplastica post-trapianto. Il confronto della sopravvivenza post-trapianto di fegato
tra pazienti sottoposti a trapianto per patologia epatica neoplastica con pazienti trapiantati per altra
eziologia, i potenziali fattori prognostici ed infine l’utilità di metodiche “ponte” potrebbero essere punti
cruciali nella discussione dell’espansione dei criteri di selezione dei candidati a trapianto di fegato per
carcinoma epatocellulare.




SCIENTIFIC INFORMATION INFORMAZIONI SCIENTIFICHE
USA Continuing Medical Education
Sponsored by University of California, Davis, Medical Center, Health System, Office of Continuing Medical Education, Division of
Gastroenterology and Hepatology, Department of Internal Medicine
NEEDS ASSESSMENT
International meeting with the University of California, Davis, Medical Center, and University of Padua, Italy, that is focusing on
gastrointestinal pathophysiology and benign and malignant liver diseases. The target audience includes internists,
gastroenterologists and hepatologists as well as experts in the area of transplantation, palliative care, telemedicine, stem cell
research and new advances in the diagnosis and management of gastrointestinal and liver diseases.
COURSE OBJECTIVES
After attending this course, participants will be able to:
- discuss benign and malignant liver diseases
- list the mechanisms of disease of gastrointestinal disorders
- discuss emergent technologies and therapy for gastrointestinal and liver diseases

ACCREDITATION
The University of California, Davis, Medical Center, Health System is accredited by the Accreditation Council for Continuing Medical
Education (ACCME) to provide continuing medical education for physicians. Physician Credit: The Office of Continuing Medical
Education of the University of California, Davis, Health System (School of Medicine, Medical Center and Medical Group) designates
this educational activity for a maximum of 11 AMA PRA Category 1 Credits™ of the Physician’s Recognition Award of the American
Medical Association and the Certification Program of the California Medical Association. Physicians should only claim credit
commensurate with the extent of their participation in the activity.
UC DAVIS HEALTH SYSTEM CME MISSION
The Office of Continuing Medical Education at the University of California, Davis, Health System (School of Medicine, Medical
Center and Medical Group) offers physicians and other health care professionals educational opportunities that foster excellence in
patient care. In concert with the overall mission of the UC Davis Health System, our endeavor is supported by the Office of
Continuing Medical Education Advisory Committee to ensure that activities comply with the Essentials and Standards of the
Accreditation Council for Continuing Medical Education. We support the concept of continuous undergraduate, graduate and post-
graduate medical education throughout the lifetime of the healthcare professional. To achieve our mission, we support the expansion
of both traditional and innovative modes of learning.

DISCLOSURE
As a sponsor accredited by the Accreditation Council for Continuing Medical Education, the UC Davis, Medical Center, Health
System, Office of Continuing Medical Education must insure balance, independence, objectivity and scientific rigor in all
individually or jointly sponsored educational activities. Speakers, moderators, panel members and planning committee members
participating in a sponsored activity are expected to disclose to the audience any significant financial interests or other
relationships with manufacturers of commercial products and/or providers of commercial services that will be discussed in their
presentations. The intent of this disclosure is not to prevent speakers with significant financial or other relationships from making
presentations. Rather, disclosure allows listeners to determine if content is evidence based and free of commercial bias, and it
demonstrates how speakers will resolve conflict when it exists. All presenters must agree to provide verbal disclosure prior to
presentations. A complete disclosure statement and acknowledgment of commercial support for this program will be included in
the syllabus provided at the activity.
FOR FURTHER USA INFORMATION UC Davis Health System Office of Continuing Medical Education 3560 Business
Drive, Suite 130 Sacramento, California, USA 95820-2161 1-866-CME4EDU (263-4338) (916) 734-5390 Fax (916) 453-
9429 http://cme.ucdavis.edu


CREDITI ECM
XVIII Simposio Associazione Roberto Farini e 4° Simposio UC, Davis “Patologie epatiche benigne e maligne: cosa c’è di
nuovo ed emergente?”
Ogni partecipante potrà conseguire i crediti assegnati all’evento, in base ai seguenti criteri:
1. schede dei dati personali complete;
2. valutazione del questionario pre-test e post-test completi;
3. schede di valutazione/gradimento dell’evento complete.
La mancata compilazione o consegna delle schede e del questionario, non darà diritto ai Crediti
ECM, ma solamente all’attestato di partecipazione.

CERTIFICATE OF ATTENDANCE
A certificate of attendance will be provided to participants upon request at the end of the Congress.

ATTESTATO DI PARTECIPAZIONE
Un attestato di partecipazione al Corso e al Simposio verrà rilasciato al termine della manifestazione a tutti i partecipanti
che ne faranno richiesta alla Segreteria Organizzativa.

PARTICIPATION GRANTS
Roberto Farini Association will provide five Participation Grants for young physicians and biologists to cover their Registration fee
to the Symposium and Hotel accommodation for a maximum 3 nights. Roberto Farini Association will provide further five
Participation Grants for young physicians and biologists from Undeveloped Countries to cover their Registration fee to the
Symposium and Hotel accommodation for a maximum 3 nights.

Applications shall be made and send to Organizing Secretariat, Key Congress, not later than December 10th 2006, by fax or
e-mail with a letter of recommendation from the Head of Department/Institution.

BORSE DI STUDIO PER LA PARTECIPAZIONE
L’Associazione Roberto Farini per la Ricerca Gastroenterologica, mette a disposizione:
  .n. 5 borse di studio per medici o biologi iscritti a Scuole di Specialità, Dottorati di Ricerca, Assegnisti di Ricerca, con diritto a
iscrizione al Simposio e sistemazione alberghiera per max. 3 notti.
  .n. 5 borse di studio per medici o biologi iscritti a Scuole di Specialità, Dottorati di Ricerca, Assegnisti di Ricerca, provenienti da
Paesi in via di sviluppo, con diritto a iscrizione al Simposio e sistemazione alberghiera per max. 3 notti.

La richiesta di assegnazione dovrà essere inoltrata alla Segreteria Organizzativa entro il 10 dicembre 2006, a mezzo e-mail o
fax, accompagnata dalla dichiarazione del Direttore della struttura di appartenenza.
CALL FOR ABSTRACT
Participants are requested to submit an abstract for oral communication (presentation 7 minutes, discussion 3 minutes) or poster no
later than December 10th , 2006 Abstract should be submitted by e-mail to assfarini@keycongress.com ABSTRACTS SUBMITTED
BY FAX WILL NOT BE ACCEPTED. NO PROOF READING WILL BE DONE

GUIDELINES FOR SUBMISSION
1. Title
2. I° Author [Name, Family Name]
3. Other Author [Name, Family Name]
4. Affiliation or Institute
5. Town and Country
6. Abstract should contain approximately 300 words The Best Oral Communication and the best Poster will be awarded at the end of
the Meeting.

CONTRIBUTI SCIENTIFICI
E’ possibile inviare un abstract entro il 10 dicembre 2006, a mezzo e-mail, con file di testo in
formato word, in allegato a assfarini@keycongress.com, secondo le seguenti caratteristiche:
TITOLO
I° AUTORE [Nome,Cognome]
ALTRI AUTORI [Nome,Cognome]
ISTITUZIONE DI APPARTENENZA e CITTA’
Altri autori come sopra
TESTO (massimo 300 parole)


Gli abstracts verranno selezionati come comunicazioni orali (tempo a disposizione 7 minuti per la
presentazione e 3 minuti per la discussione) o come posters.

La migliore comunicazione orale e il miglior poster (selezionati dal Comitato Direttivo dell’Associazione Farini) verranno
premiati al termine dei lavori.


GENERAL INFORMATION                                      INFORMAZIONI GENERALI
DATE AND CONGRESS VENUES
The Meeting is developed in three parts that will take place in different venues:
DATE E SEDI
Il Convegno è articolato in più parti che si svolgeranno in sedi diverse:
                 th
JANUARY, 25 2007 PRE-MEETING COURSE:
“GASTROINTESTINAL PATHOPHYSIOLOGY: PRACTICAL
APPROACH” 25 GENNAIO, 2007 CORSO PRE-MEETING: “LA
FISIOPATOLOGIA DIGESTIVA IN PRATICA”
Palafellin Palafellin, University Hospital, Padua Policlinico Universitario Via Giustiniani, 2 - Padova
                 th                                                                    th
JANUARY, 26 2007 XVIII SYMPOSIUM ASSOCIAZIONE R. FARINI 4 ANNUAL UNIVERSITY OF
CALIFORNIA, DAVIS SYMPOSIUM BENIGN AND MALIGNANT LIVER DISEASES: WHAT’S NEW AND
EMERGING?
26 GENNAIO, 2007 XVIII SIMPOSIO ASSOCIAZIONE R. FARINI 4° SIMPOSIO UNIVERSITÀ DELLA
CALIFORNIA, DAVIS PATOLOGIE EPATICHE BENIGNE E MALIGNE: COSA C’È DI NUOVO ED
EMERGENTE?
Morgagni Room Aula Morgagni, Policlinico Universitario University Hospital, Padua Via Giustiniani, 2 - Padova
                 th
JANUARY, 27 2007 27 GENNAIO, 2007 MEETING WITH THE PUBLIC INCONTRO CON IL PUBBLICO
Congress Centre Papa Luciani     Centro Congressi Papa Luciani Via Forcellini, 107 – Padova


ISCRIZIONI

QUOTE D’ISCRIZIONE
Corso Pre-meeting:
●Soci   ASSOCIAZIONE FARINI gratuita
●Non    Soci € 150,00 Iva incl.

XVIII Symposio Associazione Roberto Farini e 4° Simposio Università della California, Davis
●Soci   ASSOCIAZIONE FARINI gratuita
●Non    Soci € 180,00 VAT Iva incl.

Corso Pre-meeting e XVIII Symposio Associazione Roberto Farini e 4° Simposio Università della California, Davis
●Soci   ASSOCIAZIONE FARINI gratuita
●Non    Soci € 260,00 VAT Iva incl.

Le quote sopraindicate comprendono:
Accesso ai lavori scientifici, materiale congressuale, libro degli atti, attestato di partecipazione, coffee breaks.


Associazione Roberto Farini
L’iscrizione all’Associazione si potrà effettuare richiedendo l’apposito modulo ed eventuali informazioni alla Segreteria Organizzativa
KEY CONGRESS & COMMUNICATION Srl per poter usufruire delle quote gratuite bisogna risultare di essere soci in regola con le
quote e almeno iscritti da un anno.

				
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