Sabela Lens1, Edilmar Alvarado-Tapias2, Zoe Mariño1, María-Carlota Londoño1, Elba LLop3, Javier Martinez4, Jose Ignacio Fortea5, Luís Ibañez6, Xavier Ariza1, Anna Baiges1, Adolfo Gallego2, Rafael Bañares6, Angela Puente5, Agustín Albillos4, Jose Luís Calleja3, Xavier Torras2, Virginia Hernández-Gea1, Jaume Bosch7, Cándid Villanueva2, Xavier Forns8, Juan Carlos García-Pagán9. 1. Liver Unit, Hospital Clinic de Barcelona, Universidad de Barcelona, IDIBAPS, Barcelona, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. 2. Department of Gastroenterology, Hospital Santa Creu i Sant Pau, Barcelona, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. 3. Liver Unit, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. 4. Department of Gastroenterology and Hepatology, Hospital Ramon y Cajal, Universidad de Alcalá, Madrid, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. 5. Department of Digestive Diseases, Marqués de Valdecilla University Hospital, IDIVAL, Santander, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. 6. Liver Unit, Hospital Gregorio Marañón, Facultad de Medicina, Universidad Complutense Madrid, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. 7. Liver Unit, Hospital Clinic de Barcelona, Universidad de Barcelona, IDIBAPS, Barcelona, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain; Swiss Liver Centre, Inselspital, Bern University, Bern, Switzerland. 8. Liver Unit, Hospital Clinic de Barcelona, Universidad de Barcelona, IDIBAPS, Barcelona, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. Electronic address: xforns@clinic.cat. 9. Liver Unit, Hospital Clinic de Barcelona, Universidad de Barcelona, IDIBAPS, Barcelona, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain. Electronic address: jcgarcia@clinic.cat.
Abstract
BACKGROUND & AIMS: Patients with hepatitis C virus-associated cirrhosis and clinical significant portal hypertension (CSPH, hepatic venous pressure gradient [HVPG] 10 mmHg or greater), despite achieving sustained virological response (SVR) to therapy, remain at risk of liver decompensation. We investigated hemodynamic changes following SVR in patients with CSPH and whether liver stiffness measurements (LSMs) can rule out the presence of CSPH. METHODS: We performed a multicenter prospective study of 226 patients with hepatitis C virus-associated cirrhosis and CSPH who had SVR to interferon-free therapy at 6 Liver Units in Spain. The portal pressure gradient was determined based on HVPG at baseline and 24 weeks after therapy; patients also underwent right-heart catheterization and LSM at these time points. Primary outcomes were effects of SVR on the hepatic, pulmonary, and systemic hemodynamics; factors related to HVPG ≥10% reduction and to CSPH persistence; and whether LSMs can rule out the presence of CSPH after SVR. RESULTS: Most patients (75%) had esophageal varices, 21% were Child-B, and 29% had at least 1 previous episode of liver decompensation. Overall, HVPG decreased from 15 (IQR: 12-18) before treatment to 13 (10-16) mmHg after SVR (reduction of 2.1 ± 3.2 mmHg; P < .01). However, CSPH persisted in 78% of patients. HVPG decreased by 10% or more from baseline in 140 patients (62%). Baseline level of albumin below 3.5 g/dL was the only negative factor associated with an HVPG reduction of 10% or more. LSM decreased from 27 (20-37) kPa before treatment to 18 (14-28) kPa after SVR (P < .05). One third of patients with a reduction in LSM to below 13.6 kPa after SVR still had CSPH. A higher baseline HVPG and a lower decrease in LSM after treatment were associated with persistence of CSPH after SVR. Systemic hemodynamics improved after SVR. Interestingly, pulmonary hypertension was present in 13 patients at baseline and 25 after SVR, although only 3 patients had increased pulmonary resistance. CONCLUSIONS: In a multicenter prospective study of patients with hepatitis C virus-associated cirrhosis, an SVR to all-oral therapy significantly reduced HVPG, compared with before treatment. Nevertheless, CSPH persists in most patients despite SVR, indicating persistent risk of decompensation. In this population, changes in LSM do not correlate with HVPG and cut-off values are not reliable in ruling out CSPH after SVR.
BACKGROUND & AIMS:Patients with hepatitis C virus-associated cirrhosis and clinical significant portal hypertension (CSPH, hepatic venous pressure gradient [HVPG] 10 mmHg or greater), despite achieving sustained virological response (SVR) to therapy, remain at risk of liver decompensation. We investigated hemodynamic changes following SVR in patients with CSPH and whether liver stiffness measurements (LSMs) can rule out the presence of CSPH. METHODS: We performed a multicenter prospective study of 226 patients with hepatitis C virus-associated cirrhosis and CSPH who had SVR to interferon-free therapy at 6 Liver Units in Spain. The portal pressure gradient was determined based on HVPG at baseline and 24 weeks after therapy; patients also underwent right-heart catheterization and LSM at these time points. Primary outcomes were effects of SVR on the hepatic, pulmonary, and systemic hemodynamics; factors related to HVPG ≥10% reduction and to CSPH persistence; and whether LSMs can rule out the presence of CSPH after SVR. RESULTS: Most patients (75%) had esophageal varices, 21% were Child-B, and 29% had at least 1 previous episode of liver decompensation. Overall, HVPG decreased from 15 (IQR: 12-18) before treatment to 13 (10-16) mmHg after SVR (reduction of 2.1 ± 3.2 mmHg; P < .01). However, CSPH persisted in 78% of patients. HVPG decreased by 10% or more from baseline in 140 patients (62%). Baseline level of albumin below 3.5 g/dL was the only negative factor associated with an HVPG reduction of 10% or more. LSM decreased from 27 (20-37) kPa before treatment to 18 (14-28) kPa after SVR (P < .05). One third of patients with a reduction in LSM to below 13.6 kPa after SVR still had CSPH. A higher baseline HVPG and a lower decrease in LSM after treatment were associated with persistence of CSPH after SVR. Systemic hemodynamics improved after SVR. Interestingly, pulmonary hypertension was present in 13 patients at baseline and 25 after SVR, although only 3 patients had increased pulmonary resistance. CONCLUSIONS: In a multicenter prospective study of patients with hepatitis C virus-associated cirrhosis, an SVR to all-oral therapy significantly reduced HVPG, compared with before treatment. Nevertheless, CSPH persists in most patients despite SVR, indicating persistent risk of decompensation. In this population, changes in LSM do not correlate with HVPG and cut-off values are not reliable in ruling out CSPH after SVR.
Authors: Andrew M Moon; Pamela K Green; Don C Rockey; Kristin Berry; George N Ioannou Journal: Aliment Pharmacol Ther Date: 2019-11-27 Impact factor: 8.171
Authors: Amit G Singal; Nicole E Rich; Neil Mehta; Andrea D Branch; Anjana Pillai; Maarouf Hoteit; Michael Volk; Mobolaji Odewole; Steven Scaglione; Jennifer Guy; Adnan Said; Jordan J Feld; Binu V John; Catherine Frenette; Parvez Mantry; Amol S Rangnekar; Omobonike Oloruntoba; Michael Leise; Janice H Jou; Kalyan Ram Bhamidimarri; Laura Kulik; George N Ioannou; Annsa Huang; Tram Tran; Hrishikesh Samant; Renumathy Dhanasekaran; Andres Duarte-Rojo; Reena Salgia; Sheila Eswaran; Prasun Jalal; Avegail Flores; Sanjaya K Satapathy; Sofia Kagan; Purva Gopal; Robert Wong; Neehar D Parikh; Caitlin C Murphy Journal: Gastroenterology Date: 2019-07-30 Impact factor: 22.682