Sabela Lens1, Diego Rincón2, Montserrat García-Retortillo3, Agustín Albillos4, Jose Luis Calleja5, Rafael Bañares2, Juan González Abraldes6, Jaume Bosch7, Jose Maria Sanchez-Tapias1, Xavier Forns1, Juan Carlos García-Pagán8. 1. Liver Unit, Hospital Clínic, Institut d'Investigacions Biomèdiques August-Pi-Sunyer, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivass, Spain. 2. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivass, Spain; Liver Unit, Hospital Gregorio Marañón, Madrid, Spain. 3. Liver Unit, Hospital Clínic, Institut d'Investigacions Biomèdiques August-Pi-Sunyer, Barcelona, Spain. 4. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivass, Spain; Liver Unit, Hospital Ramón y Cajal, Madrid, Spain. 5. Liver Unit, Hospital Puerta del Hierro, IDIPHIM, Madrid, Spain. 6. Liver Unit, Hospital Clínic, Institut d'Investigacions Biomèdiques August-Pi-Sunyer, Barcelona, Spain; Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Barcelona, Spain. 7. Liver Unit, Hospital Clínic, Institut d'Investigacions Biomèdiques August-Pi-Sunyer, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivass, Spain; Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Barcelona, Spain. 8. Liver Unit, Hospital Clínic, Institut d'Investigacions Biomèdiques August-Pi-Sunyer, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivass, Spain; Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Barcelona, Spain. Electronic address: jcgarcia@clinic.ub.es.
Abstract
BACKGROUND & AIMS: Hepatic venous pressure gradient (HVPG) is associated with a risk of liver events in patients with chronic hepatitis C. Antiviral therapies that lead to a sustained virologic response (SVR) reduce portal pressure and prevent liver disease progression. However, it is not clear to what extent the progression of hepatitis C is modified once patients develop cirrhosis with severe portal hypertension (CSPH) (HVPG ≥ 10 mm Hg). We assessed the effects of HVPG and SVR on the risk of liver decompensation, hepatocellular carcinoma, and/or death in patients with hepatitis C-related cirrhosis. METHODS: We collected data from 100 patients with hepatitis C and compensated cirrhosis who underwent HVPG measurement 3 months or less before (baseline) and 24 weeks after therapy with pegylated interferon alfa-2a and ribavirin at 4 hospitals in Spain, from 2001 through 2009. SVR was defined as undetectable serum HCV RNA level 24 weeks after treatment ended. Clinical data were collected until death, liver transplantation, or December 2012 (median, 5 y; interquartile range, 1.4-7 y). RESULTS: Seventy-four patients had CSPH at baseline and 35% of patients achieved an SVR. During the follow-up period, 19 patients developed liver decompensation (ascites, variceal bleeding, or encephalopathy). The actuarial probability values for liver decompensation at 1, 5, and 7 years were 3%, 19% and 22%, respectively. The baseline level of HVPG, but not SVR, was associated independently with the risk of liver decompensation. CONCLUSIONS: Patients with CSPH, regardless of an SVR to therapy for hepatitis C, remain at risk for liver decompensation within the first 5 years after treatment; they should be monitored closely.
BACKGROUND & AIMS: Hepatic venous pressure gradient (HVPG) is associated with a risk of liver events in patients with chronic hepatitis C. Antiviral therapies that lead to a sustained virologic response (SVR) reduce portal pressure and prevent liver disease progression. However, it is not clear to what extent the progression of hepatitis C is modified once patients develop cirrhosis with severe portal hypertension (CSPH) (HVPG ≥ 10 mm Hg). We assessed the effects of HVPG and SVR on the risk of liver decompensation, hepatocellular carcinoma, and/or death in patients with hepatitis C-related cirrhosis. METHODS: We collected data from 100 patients with hepatitis C and compensated cirrhosis who underwent HVPG measurement 3 months or less before (baseline) and 24 weeks after therapy with pegylated interferon alfa-2a and ribavirin at 4 hospitals in Spain, from 2001 through 2009. SVR was defined as undetectable serum HCV RNA level 24 weeks after treatment ended. Clinical data were collected until death, liver transplantation, or December 2012 (median, 5 y; interquartile range, 1.4-7 y). RESULTS: Seventy-four patients had CSPH at baseline and 35% of patients achieved an SVR. During the follow-up period, 19 patients developed liver decompensation (ascites, variceal bleeding, or encephalopathy). The actuarial probability values for liver decompensation at 1, 5, and 7 years were 3%, 19% and 22%, respectively. The baseline level of HVPG, but not SVR, was associated independently with the risk of liver decompensation. CONCLUSIONS:Patients with CSPH, regardless of an SVR to therapy for hepatitis C, remain at risk for liver decompensation within the first 5 years after treatment; they should be monitored closely.
Authors: Lukas Haider; Mattias Mandorfer; Zeynep Güngören; Thomas Reiberger; Nina Bastati; Jacqueline C Hodge; David Chromy; Michael Trauner; Christian Herold; Markus Peck-Radosavljevic; Ahmed Ba-Ssalamah Journal: Contrast Media Mol Imaging Date: 2018-07-12 Impact factor: 3.161
Authors: Mattias Mandorfer; Karin Kozbial; Philipp Schwabl; David Chromy; Georg Semmler; Albert F Stättermayer; Matthias Pinter; Virginia Hernández-Gea; Monika Fritzer-Szekeres; Petra Steindl-Munda; Michael Trauner; Markus Peck-Radosavljevic; Juan C García-Pagán; Peter Ferenci; Thomas Reiberger Journal: Hepatology Date: 2019-10-14 Impact factor: 17.425