Zobair M Younossi1, Maria Stepanova2, Janus Ong3, Yusuf Yilmaz4, Ajay Duseja5, Yuichiro Eguchi6, Mohamed El Kassas7, Marlen Castellanos-Fernandez8, Jacob George9, Ira M Jacobson10, Elisabetta Bugianesi11, Vincent Wai-Sun Wong12, Marco Arrese13, Victor de Ledinghen14, Manuel Romero-Gomez15, Nahum Mendez-Sanchez16, Aijaz Ahmed17, Robert Wong18, Georgios Papatheodoridis19, Lawrence Serfaty20, Issah Younossi2, Fatema Nader2, Mariam Ziayee2, Arian Afendy2. 1. Betty and Guy Beatty Center for Integrated Research, Inova Health System, Falls Church, Virginia; Department of Medicine, Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, Virginia. Electronic address: zobair.younossi@inova.org. 2. Center for Outcomes Research in Liver Diseases, Washington, DC. 3. College of Medicine, University of the Philippines, Manila, the Philippines. 4. Department of Gastroenterology, Marmara University, School of Medicine, Istanbul, Turkey. 5. Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. 6. Liver Center, Saga University Hospital, Saga, Japan. 7. Endemic Medicine Department, Faculty of Medicine, Helwan University, Cairo, Egypt. 8. Department of Research, National Institute of Gastroenterology, Havana, Cuba. 9. Storr Liver Centre, Westmead Institute for Medical Research, Westmead Hospital and University of Sydney, Sydney, Australia. 10. Division of Gastroenterology and Hepatology, New York University Medical Center, New York, New York. 11. Division of Gastroenterology, University of Torino, Torino, Italy. 12. Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, China. 13. Departamento de Gastroenterología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile. 14. Hepatology Unit, Bordeaux University Hospital, Bordeaux, France. 15. Digestive Diseases Department, Virgen del Rocío University Hospital, University of Seville, Seville, Spain. 16. Liver Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico. 17. Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California. 18. Division of Gastroenterology and Hepatology, Alameda Health System, Highland Hospital, Oakland, California. 19. Medical School of National and Kapodistrian University of Athens, Athens, Greece. 20. Hepatogastroenterology Service, Hôpital Hautepierre, Strasbourg, France.
Abstract
BACKGROUND & AIMS: Non-alcoholic and alcohol-related fatty liver disease are overlapping diseases in which metabolic syndrome and alcohol consumption each contribute to progressive liver disease. We aimed to assess the effects of alcohol consumption and metabolic syndrome on mortality in individuals with fatty liver. METHODS: We searched the National Health and Nutrition and Examination Survey III for adults (20-74 years old) with hepatic steatosis, detected by ultrasound, for whom mortality and follow-up data were available. We collected data from the alcohol use questionnaire (self-reported number of days a participant drank alcohol; the number of drinks [10 g alcohol] per day on a drinking day; the number of days the participant had 5 or more drinks) and calculated the average amount of alcohol consumption in drinks/day for each participant during the year preceding enrollment. Excessive alcohol consumption for men was >3 drinks/day and for women was >1.5 drinks/day. We also collected clinical data, and mortality data were obtained from the National Death Index. Demographic and clinical parameters were compared among consumption groups using the χ2 test for independence or survey regression models. We used Cox proportional hazard models to identify independent predictors of all-cause and cause-specific mortality. RESULTS: The study cohort included 4264 individuals with hepatic steatosis (mean age, 45.9 years; 51% male; 76% white; 46% with metabolic syndrome; 6.2% with excessive alcohol use). There was no significant difference in mean age between individuals with vs without excessive alcohol consumption (P=.65). However, overall mortality was significantly higher among participants with excessive alcohol consumption (32.2%) vs participants with non-excessive alcohol use (22.2%) after mean 20 years of follow up (P=.003), as well as after 5 years of follow up. In multivariate analysis, the presence of metabolic syndrome (adjusted hazard ratio [aHR], 1.43; 95% CI, 1.12-1.83) and excessive alcohol consumption (aHR, 1.79; 95% CI, 1.21-2.66) were independently associated with an increased risk of death in individuals with hepatic steatosis; any lower average amount of alcohol consumption was not associated with mortality (all P>.60). In a subgroup analysis, the association of excessive alcohol use with mortality was significant in individuals with metabolic syndrome (aHR, 2.46; 95% CI, 1.40-4.32) but not without it (P=.74). CONCLUSION: In review of data from the National Health and Nutrition and Examination Survey III, we associated alcohol consumption with increased mortality in participants with fatty liver and metabolic syndrome. These findings indicate an overlap between non-alcoholic and alcohol-related fatty liver disease.
BACKGROUND & AIMS: Non-alcoholic and alcohol-related fatty liver disease are overlapping diseases in which metabolic syndrome and alcohol consumption each contribute to progressive liver disease. We aimed to assess the effects of alcohol consumption and metabolic syndrome on mortality in individuals with fatty liver. METHODS: We searched the National Health and Nutrition and Examination Survey III for adults (20-74 years old) with hepatic steatosis, detected by ultrasound, for whom mortality and follow-up data were available. We collected data from the alcohol use questionnaire (self-reported number of days a participant drank alcohol; the number of drinks [10 g alcohol] per day on a drinking day; the number of days the participant had 5 or more drinks) and calculated the average amount of alcohol consumption in drinks/day for each participant during the year preceding enrollment. Excessive alcohol consumption for men was >3 drinks/day and for women was >1.5 drinks/day. We also collected clinical data, and mortality data were obtained from the National Death Index. Demographic and clinical parameters were compared among consumption groups using the χ2 test for independence or survey regression models. We used Cox proportional hazard models to identify independent predictors of all-cause and cause-specific mortality. RESULTS: The study cohort included 4264 individuals with hepatic steatosis (mean age, 45.9 years; 51% male; 76% white; 46% with metabolic syndrome; 6.2% with excessive alcohol use). There was no significant difference in mean age between individuals with vs without excessive alcohol consumption (P=.65). However, overall mortality was significantly higher among participants with excessive alcohol consumption (32.2%) vs participants with non-excessive alcohol use (22.2%) after mean 20 years of follow up (P=.003), as well as after 5 years of follow up. In multivariate analysis, the presence of metabolic syndrome (adjusted hazard ratio [aHR], 1.43; 95% CI, 1.12-1.83) and excessive alcohol consumption (aHR, 1.79; 95% CI, 1.21-2.66) were independently associated with an increased risk of death in individuals with hepatic steatosis; any lower average amount of alcohol consumption was not associated with mortality (all P>.60). In a subgroup analysis, the association of excessive alcohol use with mortality was significant in individuals with metabolic syndrome (aHR, 2.46; 95% CI, 1.40-4.32) but not without it (P=.74). CONCLUSION: In review of data from the National Health and Nutrition and Examination Survey III, we associated alcohol consumption with increased mortality in participants with fatty liver and metabolic syndrome. These findings indicate an overlap between non-alcoholic and alcohol-related fatty liver disease.
Authors: P V AshaRani; Mohamed Zakir Karuvetil; Tan Yeow Wee Brian; Pratika Satghare; Kumarasan Roystonn; Wang Peizhi; Laxman Cetty; Noor Azizah Zainuldin; Mythily Subramaniam Journal: Int J Ment Health Addict Date: 2022-01-23 Impact factor: 11.555
Authors: Helen Jarvis; Hannah O'Keefe; Dawn Craig; Daniel Stow; Barbara Hanratty; Quentin M Anstee Journal: BMJ Open Date: 2022-01-04 Impact factor: 2.692