Salvatore Petta1, Giada Sebastiani2, Mauro Viganò3, Javier Ampuero4, Vincent Wai-Sun Wong5, Jerome Boursier6, Annalisa Berzigotti7, Elisabetta Bugianesi8, Anna Ludovica Fracanzani9, Calogero Cammà10, Marco Enea11, Marraud des Grottes12, Vito Di Marco10, Ramy Younes8, Aline Keyrouz2, Sergio Mazzola13, Yuly Mendoza7, Grazia Pennisi10, Manuel Romero-Gomez4, Antonio Craxì10, Victor de Ledinghen12. 1. Sezione di Gastroenterologia e Epatologia, Mother and Child Care, Internal Medicine and Medical Specialties, Università di Palermo, Palermo, Italy. Electronic address: salvatore.petta@unipa.it. 2. Division of Gastroenterology and Hepatology, McGill University Health Centre, Montreal, Quebec, Canada. 3. Hepatology Unit, Ospedale San Giuseppe, University of Milan, Milan, Italy. 4. Digestive Diseases Unit, Hospital Universitario Virgen del Rocío, Biomedical Research Networking Center in Hepatic and Digestive Diseases, Instituto de Biomedicina de Sevilla, University of Seville, Seville, Spain. 5. Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong. 6. Hepato-Gastroenterology Department, Angers University Hospital, Angers, France. 7. Hepatology Group, University Clinic for Visceral Surgery and Medicine, Inselspital, Department for Biomedical Research, University of Bern, Bern, Switzerland. 8. Division of Gastroenterology, Department of Medical Sciences, University of Torino, Turin, Italy. 9. Department of Pathophysiology and Transplantation, Ca' Granda IRCCS Foundation, Policlinico Hospital, University of Milan, Milan, Italy. 10. Sezione di Gastroenterologia e Epatologia, Mother and Child Care, Internal Medicine and Medical Specialties, Università di Palermo, Palermo, Italy. 11. Dipartimento di Scienze Economiche, Aziendali e Statistiche, University of Palermo, Palermo, Italy. 12. Centre d'Investigation de la Fibrose Hépatique, INSERM U1053, Hôpital Haut-Lévêque, Bordeaux University Hospital, Pessac, France. 13. Clinical Epidemiology and Cancer Registry Operative Unit, University Hospital Policlinico "Paolo Giaccone," Palermo, Italy.
Abstract
BACKGROUND & AIMS: Patients with advanced fibrosis related to nonalcoholic fatty liver disease (NAFLD) are at risk of developing hepatic and extrahepatic complications. We investigated whether, in a large cohort of patients with NAFLD and compensated advanced chronic liver disease, baseline liver stiffness measurements (LSMs) and their changes can be used to identify patients at risk for liver-related and extrahepatic events. METHODS: We performed a retrospective analysis of consecutive patients with NAFLD (n = 1039) with a histologic diagnosis of F3-F4 fibrosis and/or LSMs>10 kPa, followed for at least 6 months, from medical centers in 6 countries. LSMs were made by FibroScan using the M or XL probe and recorded at baseline and within 1 year from the last follow-up examination. Differences between follow up and baseline LSMs were categorized as: improvement (reduction of more than 20%), stable (reduction of 20% to an increase of 20%), impairment (an increase of 20% or more). We recorded hepatic events (such as liver decompensation, ascites, encephalopathy, variceal bleeding, jaundice, or hepatocellular carcinoma [HCC]) and overall and liver-related mortality during a median follow-up time of 35 months (interquartile range, 19-63 months). RESULTS: Based on Cox regression analysis, baseline LSM was independently associated with occurrence of hepatic decompensation (hazard ratio [HR], 1.03; 95% CI, 1.02-1.04; P < .001), HCC (HR, 1.03; 95% CI, 1.00-1.04; P = .003), and liver-related death (HR, 1.02; 95% CI, 1.02-1.03; P = .005). In 533 patients with available LSMs during the follow-up period, change in LSM was independently associated with hepatic decompensation (HR, 1.56; 95% CI, 1.05-2.51; P = .04), HCC (HR, 1.72; 95% CI, 1.01-3.02; P = .04), overall mortality (HR, 1.73; 95% CI, 1.11-2.69; P = .01), and liver-related mortality (HR, 1.96; 95% CI, 1.10-3.38; P = .02). CONCLUSIONS: In patients with NAFLD and compensated advanced chronic liver disease, baseline LSM and change in LSM are associated with risk of liver-related events and mortality.
BACKGROUND & AIMS:Patients with advanced fibrosis related to nonalcoholic fatty liver disease (NAFLD) are at risk of developing hepatic and extrahepatic complications. We investigated whether, in a large cohort of patients with NAFLD and compensated advanced chronic liver disease, baseline liver stiffness measurements (LSMs) and their changes can be used to identify patients at risk for liver-related and extrahepatic events. METHODS: We performed a retrospective analysis of consecutive patients with NAFLD (n = 1039) with a histologic diagnosis of F3-F4 fibrosis and/or LSMs>10 kPa, followed for at least 6 months, from medical centers in 6 countries. LSMs were made by FibroScan using the M or XL probe and recorded at baseline and within 1 year from the last follow-up examination. Differences between follow up and baseline LSMs were categorized as: improvement (reduction of more than 20%), stable (reduction of 20% to an increase of 20%), impairment (an increase of 20% or more). We recorded hepatic events (such as liver decompensation, ascites, encephalopathy, variceal bleeding, jaundice, or hepatocellular carcinoma [HCC]) and overall and liver-related mortality during a median follow-up time of 35 months (interquartile range, 19-63 months). RESULTS: Based on Cox regression analysis, baseline LSM was independently associated with occurrence of hepatic decompensation (hazard ratio [HR], 1.03; 95% CI, 1.02-1.04; P < .001), HCC (HR, 1.03; 95% CI, 1.00-1.04; P = .003), and liver-related death (HR, 1.02; 95% CI, 1.02-1.03; P = .005). In 533 patients with available LSMs during the follow-up period, change in LSM was independently associated with hepatic decompensation (HR, 1.56; 95% CI, 1.05-2.51; P = .04), HCC (HR, 1.72; 95% CI, 1.01-3.02; P = .04), overall mortality (HR, 1.73; 95% CI, 1.11-2.69; P = .01), and liver-related mortality (HR, 1.96; 95% CI, 1.10-3.38; P = .02). CONCLUSIONS: In patients with NAFLD and compensated advanced chronic liver disease, baseline LSM and change in LSM are associated with risk of liver-related events and mortality.
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