Macarena Simón-Talero1, Davide Roccarina2, Javier Martínez3, Katharina Lampichler4, Anna Baiges5, Gavin Low6, Elba Llop7, Michael Praktiknjo8, Martin H Maurer9, Alexander Zipprich10, Michela Triolo11, Guillaume Vangrinsven12, Rita Garcia-Martinez13, Annette Dam14, Avik Majumdar2, Carmen Picón15, Daniel Toth4, Anna Darnell16, Juan G Abraldes17, Marta Lopez7, Guido Kukuk18, Aleksander Krag14, Rafael Bañares19, Wim Laleman12, Vincenzo La Mura20, Cristina Ripoll10, Annalisa Berzigotti21, Jonel Trebicka22, Jose Luis Calleja7, Puneeta Tandon17, Virginia Hernandez-Gea5, Thomas Reiberger23, Agustín Albillos3, Emmanuel A Tsochatzis2, Salvador Augustin24, Joan Genescà25. 1. Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain. 2. Sheila Sherlock Liver Unit and University College London Institute for Liver and Digestive Health, Royal Free Hospital and University College London, London, UK. 3. Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Madrid, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain. 4. Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria. 5. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain; Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Universitat de Barcelona, Barcelona, Spain. 6. Department of Radiology, University of Alberta, Edmonton, Alberta, Canada. 7. Liver Unit, Hospital U. Puerta de Hierro, Universidad Autónoma de Madrid, Madrid, Spain. 8. Department of Internal Medicine I, University of Bonn, Bonn, Germany. 9. Department of Radiology, Inselspital, University of Bern, Bern, Switzerland. 10. First Department of Internal Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany. 11. Internal Medicine, IRCCS San Donato, Department of Biomedical Sciences for Health, University of Milan, San Donato Milanese, Milan, Italy. 12. Department of Gastroenterology and Hepatology, University Hospitals Leuven, Leuven, Belgium. 13. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain; Liver Unit, Hospital General Universitario Gregorio Marañón, Universidad Complutense, Madrid, Spain; Instituto de Investigacion Sanitaria Gregorio Marañon, Madrid, Spain. 14. Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark. 15. Department of Radiology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria, Universidad de Alcalá, Spain. 16. Department of Radiology, Hospital Clinic, Universitat de Barcelona, Barcelona, Spain. 17. Cirrhosis Care Clinic, Division of Gastroenterology (Liver Unit), Centre of Excellence for Gastrointestinal Inflammation and Immunity Research, University of Alberta, Edmonton, Canada. 18. Department of Radiology, University of Bonn, Bonn, Germany. 19. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain; Liver Unit, Hospital General Universitario Gregorio Marañón, Universidad Complutense, Madrid, Spain. 20. Internal Medicine, IRCCS San Donato, Department of Biomedical Sciences for Health, University of Milan, San Donato Milanese, Milan, Italy; Centro di Ricerca Coordinata "A. M. e A. Migliavacca per lo Studio e la Cura delle Malattie del Fegato," Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy. 21. Hepatology, Inselspital, University of Bern, Bern, Switzerland. 22. Department of Internal Medicine I, University of Bonn, Bonn, Germany; European Foundation for Study of Chronic Liver Failure, Barcelona, Spain. 23. Division of Gastroenterology and Hepatology, Vienna Hepatic Hemodynamic Lab, Medical University of Vienna, Vienna, Austria. 24. Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain. Electronic address: salva.augustin@gmail.com. 25. Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain. Electronic address: jgenesca@vhebron.net.
Abstract
BACKGROUND & AIMS: Spontaneous portosystemic shunts (SPSS) have been associated with hepatic encephalopathy (HE). Little is known about their prevalence among patients with cirrhosis or clinical effects. We investigated the prevalence and characteristics of SPSS in patients with cirrhosis and their outcomes. METHODS: We performed a retrospective study of 1729 patients with cirrhosis who underwent abdominal computed tomography or magnetic resonance imaging analysis from 2010 through 2015 at 14 centers in Canada and Europe. We collected data on demographic features, etiology of liver disease, comorbidities, complications, treatments, laboratory and clinical parameters, Model for End-Stage Liver Disease (MELD) score, and endoscopy findings. Abdominal images were reviewed by a radiologist (or a hepatologist trained by a radiologist) and searched for the presence of SPSS, defined as spontaneous communications between the portal venous system or splanchnic veins and the systemic venous system, excluding gastroesophageal varices. Patients were assigned to groups with large SPSS (L-SPSS, ≥8 mm), small SPSS (S-SPSS, <8 mm), or without SPSS (W-SPSS). The main outcomes were the incidence of complications of cirrhosis and mortality according to the presence of SPSS. Secondary measurements were the prevalence of SPSS in patients with cirrhosis and their radiologic features. RESULTS: L-SPSS were identified in 488 (28%) patients, S-SPSS in 548 (32%) patients, and no shunt (W-SPSS) in 693 (40%) patients. The most common L-SPSS was splenorenal (46% of L-SPSS). The presence and size of SPSS increased with liver dysfunction: among patients with MELD scores of 6-9, 14% had L-SPSS and 28% had S-SPSS; among patients with MELD scores of 10-13, 30% had L-SPSS and 34% had S-SPSS; among patients with MELD scores of 14 or higher, 40% had L-SPSS and 32% had S-SPSS (P < .001 for multiple comparison among MELD groups). HE was reported in 48% of patients with L-SPSS, 34% of patients with S-SPSS, and 20% of patients W-SPSS (P < .001 for multiple comparison among SPSS groups). Recurrent or persistent HE was reported in 52% of patients with L-SPSS, 44% of patients with S-SPSS, and 37% of patients W-SPSS (P = .007 for multiple comparison among SPSS groups). Patients with SPSS also had a larger number of portal hypertension-related complications (bleeding or ascites) than those W-SPSS. Quality of life and transplantation-free survival were lower in patients with SPSS vs without. SPSS were an independent factor associated with death or liver transplantation (hazard ratio, 1.26; 95% confidence interval, 1.06-1.49) (P = .008) in multivariate analysis. When patients were stratified by MELD score, SPSS were associated with HE independently of liver function: among patients with MELD scores of 6-9, HE was reported in 23% with L-SPSS, 12% with S-SPSS, and 5% with W-SPSS (P < .001 for multiple comparison among SPSS groups); among those with MELD scores of 10-13, HE was reported in 48% with L-SPSS, 33% with S-SPSS, and 23% with W-SPSS (P < .001 for multiple comparison among SPSS groups); among patients with MELD scores of 14 or more, HE was reported in 59% with L-SPSS, 57% with S-SPSS, and 48% with W-SPSS (P = .043 for multiple comparison among SPSS groups). Patients with SPSS and MELD scores of 6-9 were at higher risk for ascites (40.5% vs 23%; P < .001) and bleeding (15% vs 9%; P = .038) than patients W-SPSS and had lower odds of transplant-free survival (hazard ratio 1.71; 95% confidence interval, 1.16-2.51) (P = .006). CONCLUSIONS: In a retrospective analysis of almost 2000 patients, we found 60% to have SPSS; prevalence increases with deterioration of liver function. SPSS increase risk for HE and with a chronic course. In patients with preserved liver function, SPSS increase risk for complications and death. ClinicalTrials.gov ID NCT02692430.
BACKGROUND & AIMS: Spontaneous portosystemic shunts (SPSS) have been associated with hepatic encephalopathy (HE). Little is known about their prevalence among patients with cirrhosis or clinical effects. We investigated the prevalence and characteristics of SPSS in patients with cirrhosis and their outcomes. METHODS: We performed a retrospective study of 1729 patients with cirrhosis who underwent abdominal computed tomography or magnetic resonance imaging analysis from 2010 through 2015 at 14 centers in Canada and Europe. We collected data on demographic features, etiology of liver disease, comorbidities, complications, treatments, laboratory and clinical parameters, Model for End-Stage Liver Disease (MELD) score, and endoscopy findings. Abdominal images were reviewed by a radiologist (or a hepatologist trained by a radiologist) and searched for the presence of SPSS, defined as spontaneous communications between the portal venous system or splanchnic veins and the systemic venous system, excluding gastroesophageal varices. Patients were assigned to groups with large SPSS (L-SPSS, ≥8 mm), small SPSS (S-SPSS, <8 mm), or without SPSS (W-SPSS). The main outcomes were the incidence of complications of cirrhosis and mortality according to the presence of SPSS. Secondary measurements were the prevalence of SPSS in patients with cirrhosis and their radiologic features. RESULTS:L-SPSS were identified in 488 (28%) patients, S-SPSS in 548 (32%) patients, and no shunt (W-SPSS) in 693 (40%) patients. The most common L-SPSS was splenorenal (46% of L-SPSS). The presence and size of SPSS increased with liver dysfunction: among patients with MELD scores of 6-9, 14% had L-SPSS and 28% had S-SPSS; among patients with MELD scores of 10-13, 30% had L-SPSS and 34% had S-SPSS; among patients with MELD scores of 14 or higher, 40% had L-SPSS and 32% had S-SPSS (P < .001 for multiple comparison among MELD groups). HE was reported in 48% of patients with L-SPSS, 34% of patients with S-SPSS, and 20% of patientsW-SPSS (P < .001 for multiple comparison among SPSS groups). Recurrent or persistent HE was reported in 52% of patients with L-SPSS, 44% of patients with S-SPSS, and 37% of patientsW-SPSS (P = .007 for multiple comparison among SPSS groups). Patients with SPSS also had a larger number of portal hypertension-related complications (bleeding or ascites) than those W-SPSS. Quality of life and transplantation-free survival were lower in patients with SPSS vs without. SPSS were an independent factor associated with death or liver transplantation (hazard ratio, 1.26; 95% confidence interval, 1.06-1.49) (P = .008) in multivariate analysis. When patients were stratified by MELD score, SPSS were associated with HE independently of liver function: among patients with MELD scores of 6-9, HE was reported in 23% with L-SPSS, 12% with S-SPSS, and 5% with W-SPSS (P < .001 for multiple comparison among SPSS groups); among those with MELD scores of 10-13, HE was reported in 48% with L-SPSS, 33% with S-SPSS, and 23% with W-SPSS (P < .001 for multiple comparison among SPSS groups); among patients with MELD scores of 14 or more, HE was reported in 59% with L-SPSS, 57% with S-SPSS, and 48% with W-SPSS (P = .043 for multiple comparison among SPSS groups). Patients with SPSS and MELD scores of 6-9 were at higher risk for ascites (40.5% vs 23%; P < .001) and bleeding (15% vs 9%; P = .038) than patientsW-SPSS and had lower odds of transplant-free survival (hazard ratio 1.71; 95% confidence interval, 1.16-2.51) (P = .006). CONCLUSIONS: In a retrospective analysis of almost 2000 patients, we found 60% to have SPSS; prevalence increases with deterioration of liver function. SPSS increase risk for HE and with a chronic course. In patients with preserved liver function, SPSS increase risk for complications and death. ClinicalTrials.gov ID NCT02692430.
Authors: Noelle H Ebel; Kristen Carlin; Michele L Shaffer; Giri Shivaram; Matthew Hawkins; Erin R Lane; Kara Cooper; Will S Lindquester; Gaurav Gadodia; Karen F Murray Journal: J Pediatr Gastroenterol Nutr Date: 2019-06 Impact factor: 2.839
Authors: Justin R Boike; Bartley G Thornburg; Sumeet K Asrani; Michael B Fallon; Brett E Fortune; Manhal J Izzy; Elizabeth C Verna; Juan G Abraldes; Andrew S Allegretti; Jasmohan S Bajaj; Scott W Biggins; Michael D Darcy; Maryjane A Farr; Khashayar Farsad; Guadalupe Garcia-Tsao; Shelley A Hall; Caroline C Jadlowiec; Michael J Krowka; Jeanne Laberge; Edward W Lee; David C Mulligan; Mitra K Nadim; Patrick G Northup; Riad Salem; Joseph J Shatzel; Cathryn J Shaw; Douglas A Simonetto; Jonathan Susman; K Pallav Kolli; Lisa B VanWagner Journal: Clin Gastroenterol Hepatol Date: 2021-07-15 Impact factor: 13.576