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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Hepatol. Oct 27, 2026; 18(10): 125487
Published online Oct 27, 2026. doi: 10.4254/wjh.125487
Treatment response in pediatric metabolic dysfunction-associated steatotic liver disease: Noninvasive endpoints and body composition
Toshifumi Yodoshi
Toshifumi Yodoshi, Division of Gastroenterology, Hepatology, Pancreatology and Nutrition, University of Iowa Stead Family Children’s Hospital, Iowa City, IA 52242, United States
Author contributions: Yodoshi T conceptualized and designed the review, conducted the literature search, analyzed and interpreted the literature, and drafted and critically revised the manuscript; the author read and approved the final version.
AI contribution statement: AI was not used to generate or analyze study data.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
Corresponding author: Toshifumi Yodoshi, MD, PhD, Clinical Assistant Professor, Division of Gastroenterology, Hepatology, Pancreatology and Nutrition, Stead Family Children’s Hospital, 200 Hawkins Drive, Iowa City, IA 52242, United States. toshifumi-yodoshi@uiowa.edu
Received: July 8, 2026
Revised: August 9, 2026
Accepted: September 18, 2026
Published online: October 27, 2026
Processing time: 105 Days and 10.2 Hours
Abstract

Metabolic dysfunction-associated steatotic liver disease is the most common chronic liver disease in youth, yet treatment response remains difficult to define as lifestyle therapy, anti-obesity pharmacotherapy, and metabolic and bariatric surgery produce changes across different biological domains. This narrative review examines histology, alanine aminotransferase, magnetic resonance imaging proton density fat fraction, elastography, serum biomarkers, body composition, cardiometabolic health, and patient-centered outcomes as candidate response endpoints. Diagnostic accuracy, cross-sectional severity, prognostic validity, longitudinal responsiveness, association with histological response, and validated thresholds for meaningful change are considered separately. Pediatric evidence remains strongest for repeated aminotransferases, growth-adjusted adiposity measures, and selected imaging approaches, but no single test defines response and normal aminotransferases do not exclude persistent steatohepatitis or fibrosis. Adult magnetic resonance imaging and drug-trial thresholds are informative but cannot be adopted uncritically in children. Loss of lean mass should also not be equated with sarcopenia without evidence of low muscle quantity and impaired strength or function. A practical three-tier framework is proposed: Minimum clinical assessment, specialist-center assessment, and research endpoints. The proposed tiers and reassessment intervals are pragmatic author guidance, not validated pediatric standards, and require prospective validation. Until pediatric longitudinal thresholds are validated, response assessment should be multidimensional, treatment-specific, growth-aware, patient-centered, and adapted to feasibility and equity.

Keywords: Metabolic dysfunction-associated steatotic liver disease; Pediatric; Treatment response; Alanine aminotransferase; Magnetic resonance imaging proton density fat fraction; Elastography; Body composition; Sarcopenic obesity; Bariatric surgery; Glucagon-like peptide-1 receptor agonist

Core Tip: Treatment response in pediatric metabolic dysfunction-associated steatotic liver disease cannot currently be defined by a single biomarker. Alanine aminotransferase, liver fat, liver stiffness, histology, cardiometabolic health, growth, body composition, and patient-reported outcomes capture complementary domains and may change at different rates. Diagnostic or prognostic performance does not by itself establish longitudinal responsiveness. This review separates those measurement properties, qualifies adult-derived thresholds, and proposes a three-tier, treatment-aware framework that distinguishes hepatic improvement with preserved muscle and normal growth from weight loss alone.

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