Heidi S Ahmed1,2, Natalie Pedersen3, Manju Bengaluru Jayanna3,4, Patrick Ten Eyck5, Antonio Sanchez3, Arvind R Murali3,6. 1. Department of Internal Medicine, University of Iowa Hospitals and Clinics, Iowa City, IA, USA. heidi.s.ahmed@gmail.com. 2. Division of Gastroenterology and Hepatology, Boston University Medical Center, 85 E. Concord Street, Boston, MA, 02118, USA. heidi.s.ahmed@gmail.com. 3. Department of Internal Medicine, University of Iowa Hospitals and Clinics, Iowa City, IA, USA. 4. Lankenau Institute for Medical Research, Wynnewood, PA, USA. 5. Biostatistics and Research Design, Institute of Clinical and Translational Science, University of Iowa, Iowa City, IA, USA. 6. Division of Gastroenterology and Hepatology, The University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA, 52240, USA.
Abstract
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of cirrhosis in the USA. OBJECTIVES: We aimed to determine the time to develop hepatic events in patients with NAFLD and develop a simple model to identify patients at risk for hepatic decompensation. DESIGN: Retrospective cohort study. PATIENTS: Seven hundred patients with NAFLD met inclusion criteria for the study. Patients were divided into model construction (n = 450) and validation (n = 250) cohorts. MAIN MEASURES: Demographic, clinical, and laboratory variables were gathered at the time of diagnosis of NAFLD. Kaplan-Meier analysis determined the time to development of hepatic events from initial diagnosis. A time-to-event prediction model was established in the model construction cohort using the multivariate Cox proportional hazards model and was then internally validated. KEY RESULTS: Forty-nine (7%) patients developed hepatic events at a mean duration of 6.2 ± 4.2 years from initial diagnosis. Kaplan-Meier probability of developing a hepatic event at 5-, 10-, and 12-year intervals was 4.8%, 10.6%, and 11.3%, respectively. Age, presence of diabetes, and platelet count were identified as significant variables to predict hepatic events. NAFLD decompensation risk score was developed as "age × 0.06335 + presence of diabetes (yes = 1, no = 0) × 0.92221 - platelet count × 0.01522" to predict the probability of hepatic decompensation. Risk score model had an area under the curve of 0.89 (95% CI = 0.92, 0.86) and it performed well in both the validation (0.91, 0.87-0.94) and the overall cohort (0.89, 0.87-0.91). CONCLUSIONS: A significant proportion of patients with NAFLD developed hepatic decompensation. We have provided a simple, objective model to help identify "at-risk" patients.
BACKGROUND:Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of cirrhosis in the USA. OBJECTIVES: We aimed to determine the time to develop hepatic events in patients with NAFLD and develop a simple model to identify patients at risk for hepatic decompensation. DESIGN: Retrospective cohort study. PATIENTS: Seven hundred patients with NAFLD met inclusion criteria for the study. Patients were divided into model construction (n = 450) and validation (n = 250) cohorts. MAIN MEASURES: Demographic, clinical, and laboratory variables were gathered at the time of diagnosis of NAFLD. Kaplan-Meier analysis determined the time to development of hepatic events from initial diagnosis. A time-to-event prediction model was established in the model construction cohort using the multivariate Cox proportional hazards model and was then internally validated. KEY RESULTS: Forty-nine (7%) patients developed hepatic events at a mean duration of 6.2 ± 4.2 years from initial diagnosis. Kaplan-Meier probability of developing a hepatic event at 5-, 10-, and 12-year intervals was 4.8%, 10.6%, and 11.3%, respectively. Age, presence of diabetes, and platelet count were identified as significant variables to predict hepatic events. NAFLD decompensation risk score was developed as "age × 0.06335 + presence of diabetes (yes = 1, no = 0) × 0.92221 - platelet count × 0.01522" to predict the probability of hepatic decompensation. Risk score model had an area under the curve of 0.89 (95% CI = 0.92, 0.86) and it performed well in both the validation (0.91, 0.87-0.94) and the overall cohort (0.89, 0.87-0.91). CONCLUSIONS: A significant proportion of patients with NAFLD developed hepatic decompensation. We have provided a simple, objective model to help identify "at-risk" patients.
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