Prediction of non-alcoholic fatty liver disease and liver fat using metabolic and genetic factors.

By A. Kotronen, Markku Peltonen, A. Hakkarainen, Ksenia Sevastianova, R. Bergholm, Lina M. Johansson, N. Lundbom, A. Rissanen, M. Ridderstråle, Leif Groop and 2 more. Gastroenterology, 2009

789 citations recorded by the source corpus.

BACKGROUND & AIMS Our aims were to develop a method to accurately predict non-alcoholic fatty liver disease (NAFLD) and liver fat content based on routinely available clinical and laboratory data and to test whether knowledge of the recently discovered genetic variant in the PNPLA3 gene (rs738409) increases accuracy of the prediction. METHODS Liver fat content was measured using proton magnetic resonance spectroscopy in 470 subjects, who were randomly divided into estimation (two thirds of the subjects, n = 313) and validation (one third of the subjects, n = 157) groups. Multivariate logistic and linear regression analyses were used to create an NAFLD liver fat score to diagnose NAFLD and liver fat equation to estimate liver fat percentage in each individual. RESULTS The presence of the metabolic syndrome and type 2 diabetes, fasting serum (fS) insulin, fS-aspartate aminotransferase (AST), and the AST/alanine aminotransferase ratio were independent predictors of NAFLD. The score had an area under the receiver operating characteristic curve of 0.87 in the estimation and 0.86 in the validation group. The optimal cut-off point of -0.640 predicted increased liver fat content with sensitivity of 86% and specificity of 71%. Addition of the genetic information to the score improved the accuracy of the prediction by only <1%. Using the same variables, we developed a liver fat equation from which liver fat percentage of each individual could be estimated. CONCLUSIONS The NAFLD liver fat score and liver fat equation provide simple and noninvasive tools to predict NAFLD and liver fat content.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3ec7a174bce357c8f2fe0f24c9baab99be8c09b3

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In Endocrinology, Diabetes and Metabolism

1. C. Day
2. S. Bellentani
3. E. Bugianesi

In Epidemiology

1. C. Day
2. S. Bellentani
3. V. Ratziu
4. Giulio Marchesini
5. H. Cortez‐Pinto
6. E. Bugianesi

Citations in the corpus

• A position statement on NAFLD/NASH based on the EASL 2009 special conference. (2010, background): “Liver fat reduces insulin clearance resulting in hyperinsulinemia, a feature of pre-diabetes [82].”
• Homozygosity for the patatin‐like phospholipase‐3/adiponutrin I148M polymorphism influences liver fibrosis in patients with nonalcoholic fatty liver disease (2010, result): “These results confirm that the frequency of the 148M variant is significantly higher in patients with NAFLD compared to controls with normal liver enzymes and metabolic parameters.(32) The risk of NAFLD was about 3.”
• EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. (2016, neutral): “79 NA NA NA NA - Population-based from NHANES III; predicts CV risk & DM [14, 15] Kotronen 2009 [16] NAFLD liver fat score MS, DM, AST, ALT 470 -0.”