Pietro Lampertico1, Federica Invernizzi1, Mauro Viganò2, Alessandro Loglio1, Giampaolo Mangia1, Floriana Facchetti1, Massimo Primignani1, Manol Jovani1, Massimo Iavarone1, Mirella Fraquelli3, Giovanni Casazza4, Roberto de Franchis5, Massimo Colombo6. 1. "A.M. and A. Migliavacca" Center for Liver Disease, Division of Gastroenterology and Hepatology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy. 2. Division of Hepatology, Ospedale San Giuseppe, Università degli Studi di Milano, Italy. 3. Division of Gastroenterology and Endoscopy, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy. 4. Department of Biomedical and Clinical Sciences, Ospedale Luigi Sacco, Università degli Studi di Milano, Milan, Italy. 5. Division of Gastroenterology, Ospedale Luigi Sacco, Università degli Studi di Milano, Milan, Italy. 6. "A.M. and A. Migliavacca" Center for Liver Disease, Division of Gastroenterology and Hepatology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy. Electronic address: massimo.colombo@unimi.it.
Abstract
BACKGROUND & AIMS: Esophageal varices (EV) are a marker of disease severity in compensated cirrhosis due to hepatitis B virus (HBV) which predicts also the risk of hepatocellular carcinoma (HCC), clinical decompensation and anticipated liver related death. The dynamics and prognostic significance of EV in patients under long-term HBV suppression by nucleos(t)ide analogs (NUC), are poorly known. METHODS: A standardized protocol (Baveno) including 414 upper gastrointestinal (GI) endoscopies was applied to 107 HBeAg-negative compensated cirrhotic patients (93% Child-Pugh A) during a median of 12 (range 2 to 17) years of NUC therapy. Patients who initially started on lamivudine (LMV) and then developed resistance (LMV-R), were rescued by early administration of adefovir, or were switched to tenofovir. Surveillance included serum HBV DNA every three months and abdominal ultrasound every six months. RESULTS: Twenty-seven patients had baseline F1 EV which regressed in 18, remained unchanged in eight and progressed in one patient; the 12-year cumulative incidence of EV regression was 83% (95% CI: 52-92%). De novo F1/F2 EV developed in 6/80 patients with a 12-year cumulative incidence of 10% (95% CI: 5-20%). Six of seven patients with de novo varices or progression of pre-existing varices had either a clinical breakthrough due to LMV-R and/or developed a HCC. No bleedings from ruptured EV occurred, 12 patients died (9 HCC) and 15 were transplanted (13 HCC): the 12-year cumulative incidence of HCC and overall survival was 33% (95% CI: 24-42%) and 76% (95% CI: 67-83%), respectively. CONCLUSIONS: Long-term pharmacological suppression of HBV in HBeAg-seronegative patients with compensated cirrhosis leads to a significant regression of pre-existing EV accompanied by a negligible risk of developing de novo EV.
BACKGROUND & AIMS: Esophageal varices (EV) are a marker of disease severity in compensated cirrhosis due to hepatitis B virus (HBV) which predicts also the risk of hepatocellular carcinoma (HCC), clinical decompensation and anticipated liver related death. The dynamics and prognostic significance of EV in patients under long-term HBV suppression by nucleos(t)ide analogs (NUC), are poorly known. METHODS: A standardized protocol (Baveno) including 414 upper gastrointestinal (GI) endoscopies was applied to 107 HBeAg-negative compensated cirrhotic patients (93% Child-Pugh A) during a median of 12 (range 2 to 17) years of NUC therapy. Patients who initially started on lamivudine (LMV) and then developed resistance (LMV-R), were rescued by early administration of adefovir, or were switched to tenofovir. Surveillance included serum HBV DNA every three months and abdominal ultrasound every six months. RESULTS: Twenty-seven patients had baseline F1 EV which regressed in 18, remained unchanged in eight and progressed in one patient; the 12-year cumulative incidence of EV regression was 83% (95% CI: 52-92%). De novo F1/F2 EV developed in 6/80 patients with a 12-year cumulative incidence of 10% (95% CI: 5-20%). Six of seven patients with de novo varices or progression of pre-existing varices had either a clinical breakthrough due to LMV-R and/or developed a HCC. No bleedings from ruptured EV occurred, 12 patients died (9 HCC) and 15 were transplanted (13 HCC): the 12-year cumulative incidence of HCC and overall survival was 33% (95% CI: 24-42%) and 76% (95% CI: 67-83%), respectively. CONCLUSIONS: Long-term pharmacological suppression of HBV in HBeAg-seronegative patients with compensated cirrhosis leads to a significant regression of pre-existing EV accompanied by a negligible risk of developing de novo EV.
Authors: Jonathan Chung-Fai Leung; Thomson Chi-Wang Loong; James Pang; Jeremy Lok Wei; Vincent Wai-Sun Wong Journal: Hepatol Int Date: 2017-03-30 Impact factor: 6.047
Authors: Young Eun Chon; Jun Yong Park; Sung-Min Myoung; Kyu Sik Jung; Beom Kyung Kim; Seung Up Kim; Do Young Kim; Sang Hoon Ahn; Kwang-Hyub Han Journal: Am J Gastroenterol Date: 2017-04-04 Impact factor: 10.864
Authors: Marina B Klein; Keri N Althoff; Yuezhou Jing; Bryan Lau; Mari Kitahata; Vincent Lo Re; Gregory D Kirk; Mark Hull; H Nina Kim; Giada Sebastiani; Erica E M Moodie; Michael J Silverberg; Timothy R Sterling; Jennifer E Thorne; Angela Cescon; Sonia Napravnik; Joe Eron; M John Gill; Amy Justice; Marion G Peters; James J Goedert; Angel Mayor; Chloe L Thio; Edward R Cachay; Richard Moore Journal: Clin Infect Dis Date: 2016-08-09 Impact factor: 9.079