Su1720 Differentiation of Alcoholic Liver Disease From Nonalcoholic Fatty Liver Disease Using a Logistic Regression Model Based on Clinical Parameters

2013 ◽  
Vol 144 (5) ◽  
pp. S-1006
Author(s):  
Nobuyuki Toshikuni ◽  
Nobuhiko Hayashi ◽  
Atsushi Fukumura ◽  
Yasuhiro Matsue ◽  
Takahiro Minato ◽  
...  
2019 ◽  
Vol 105 (3) ◽  
pp. e791-e804
Author(s):  
Xu Wang ◽  
Jiewen Xie ◽  
Juan Pang ◽  
Hanyue Zhang ◽  
Xu Chen ◽  
...  

Abstract Context SHBG, a homodimeric glycoprotein produced by hepatocytes has been shown to be associated with metabolic disorders. Whether circulating SHBG levels are predictive of later risk of nonalcoholic fatty liver disease (NAFLD) remains unknown. In this study, we prospectively investigated the association between SHBG and NAFLD progression through a community-based cohort comprising 3389 Chinese adults. Methods NAFLD was diagnosed using abdominal ultrasonography. Serum SHBG levels were measured by chemiluminescent enzyme immunometric assay, and their relationship with NAFLD development and regression was investigated after a mean follow-up of 3.09 years using multivariable logistic regression. Results Basal SHBG was negatively associated with NAFLD development, with a fully adjusted odds ratio (OR) and its 95% confidence interval (CI) of 0.22 (0.12-0.40) (P < .001). In contrast, basal SHBG was positively associated with NAFLD regression, with a fully adjusted OR of 4.83 (2.38-9.81) (P < .001). Multiple-stepwise logistic regression analysis showed that SHBG concentration was an independent predictor of NAFLD development (OR, 0.28 [0.18-0.45]; P < .001) and regression (OR, 3.89 [2.43-6.22]; P < .001). In addition, the area under the receiver operating characteristic curves were 0.764 (95% CI, 0.740-0.787) and 0.762 (95% CI, 0.738-0.785) for the prediction models of NAFLD development and regression, respectively. Conclusions Serum SHBG concentration is associated with the development and regression of NAFLD; moreover, it can be a potential biomarker for predicting NAFLD progression, and also a novel preventive and therapeutic target for NAFLD.


2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Emma Purón-González ◽  
Arnulfo González-Cantú ◽  
Edgar Ulises Coronado-Alejandro ◽  
Oswaldo Enrique Sánchez-Dávila ◽  
Héctor Cobos-Aguilar ◽  
...  

2007 ◽  
Vol 132 (5) ◽  
pp. 2076-2077
Author(s):  
Roberto J. Carvalho Filho ◽  
André N. Milani ◽  
Juliana P. Sampaio ◽  
Leonardo L. Schiavon ◽  
Janaína N. Schiavon ◽  
...  

2020 ◽  
Vol 40 (02) ◽  
pp. 154-162 ◽  
Author(s):  
Fredrik Åberg ◽  
Martti Färkkilä

AbstractAlcohol and obesity are the main risk factors for alcoholic liver disease and nonalcoholic fatty liver disease (NAFLD), respectively, and they frequently coexist. There are considerable synergistic interaction effects between hazardous alcohol use and obesity-associated metabolic abnormalities in the development and progression of fatty liver disease. Intermittent binge-drinking has been shown to promote steatohepatitis from obesity-related steatosis, and binge-drinking is associated with progression to cirrhosis even when average alcohol intake is within the currently used criteria for a NAFLD diagnosis. Recent longitudinal studies in NAFLD have shown that light-to-moderate alcohol use is associated with fibrosis progression and incident clinical liver disease, suggesting that there is no liver-safe limit of alcohol intake in the presence of NAFLD; a J-shaped association between alcohol and all-cause mortality remains controversial. The interaction effects between alcohol and obesity make the present strict dichotomization of liver disease into alcoholic and NAFLD inappropriate, and require attention in future research, public health policy, individual counseling, and risk stratification.


HPB ◽  
2017 ◽  
Vol 19 (12) ◽  
pp. 1074-1081 ◽  
Author(s):  
Stephen O'Neill ◽  
Sara Napetti ◽  
Sorina Cornateanu ◽  
Andrew I. Sutherland ◽  
Stephen Wigmore ◽  
...  

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