Lonardo A. Alanine aminotransferase predicts incident steatotic liver disease of metabolic etiology: Long life to the old biomarker! World J Gastroenterol 2024; 30(24): 3016-3021 [PMID: 38983954 DOI: 10.3748/wjg.v30.i24.3016]
Corresponding Author of This Article
Amedeo Lonardo, MD, Academic Research, Doctor, Professor, Senior Lecturer, Department of Internal Medicine, Azienda Ospedaliero-Universitaria of Modena (2023), Ospedale Civile di Baggiovara, Modena 41126, Italy. a.lonardo@libero.it
Research Domain of This Article
Medicine, General & Internal
Article-Type of This Article
Editorial
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jun 28, 2024; 30(24): 3016-3021 Published online Jun 28, 2024. doi: 10.3748/wjg.v30.i24.3016
Alanine aminotransferase predicts incident steatotic liver disease of metabolic etiology: Long life to the old biomarker!
Amedeo Lonardo
Amedeo Lonardo, Department of Internal Medicine, Azienda Ospedaliero-Universitaria of Modena (2023), Modena 41126, Italy
Author contributions: Lonardo A was responsible for all steps of this editorial, from ideation to editing.
Conflict-of-interest statement: The author declares having no conflicts of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Noncommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Amedeo Lonardo, MD, Academic Research, Doctor, Professor, Senior Lecturer, Department of Internal Medicine, Azienda Ospedaliero-Universitaria of Modena (2023), Ospedale Civile di Baggiovara, Modena 41126, Italy. a.lonardo@libero.it
Received: March 3, 2024 Revised: May 7, 2024 Accepted: May 28, 2024 Published online: June 28, 2024 Processing time: 113 Days and 20.5 Hours
Abstract
Alanine aminotransferase (ALT) serum levels increase because of hepatocellular damage. Metabolic dysfunction-associated fatty liver disease (MAFLD), which identifies steatotic liver disease (SLD) associated with ≥ 2 metabolic abnormalities, has prominent sexual differences. The Metabolic Syndrome defines a cluster comprising abdominal obesity, altered glucose metabolism, dyslipidemia, and hypertension. Male sex, body mass index, glucose, lipids, ferritin, hypertension, and age independently predict ALT levels among blood donors. Over the last few decades, the reference range of ALT levels has been animatedly debated owing to attempts to update sex-specific reference ranges. With this backset, Chen et al have recently published a study which has two main findings. First, > 80% of individuals with MAFLD had normal ALT levels. Second, there was a linear increasing trend in the association between cumulative excess high-normal ALT levels and the rate of incident MAFLD. This study has biologically credible findings. However, it inaccurately considered sex differences in the MAFLD arena. Therefore, future studies on SLD owing to metabolic dysfunction should adopt locally determined and prospectively validated reference ranges of ALT and carefully consider sex differences in liver enzymes and MAFLD pathobiology.
Core Tip: The recent paper published by Chen et al has two main findings. First, > 80% of individuals with metabolic dysfunction-associated fatty liver disease (MAFLD) had normal alanine aminotransferase (ALT) levels. Second, there was a linear increasing trend in the association between cumulative excess high-normal ALT levels and the rate of incident MAFLD. Future studies on steatotic liver disease owing to metabolic dysfunction should adopt locally determined and prospectively validated reference ranges of ALT and carefully consider sex differences in liver enzymes and the pathobiology of MAFLD.
