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. 2021 Sep 10;12(9):e00400. doi: 10.14309/ctg.0000000000000400

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© 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology

This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Figure 2. — Effect of HSD17B13 rs72613567 (dominant genetic model) on risk of steatohepatitis and fibrosis. Adjusted risk at strata of moderators' cutoffs. Results based on ordered logistic regression. (a) Risk of steatohepatitis (0–2). (b) Risk of fibrosis (0–4). BMI, body mass index, NASH, nonalcoholic steatohepatitis. Analysis adjusted for nonheavy alcohol intake and those covariates not tested as moderators. The reference for all comparative analyses was the HSD17B13 rs72613567 (−/−) genotype.