Pediatric Research Update: Consensus Statement on Metabolic Dysfunction–Associated Steatotic Liver Disease (MASLD) in Children and Adolescents

Each month, the OMA Pediatric Committee reviews a pediatric-focused obesity research update to help keep you up to date about the latest findings. This month’s article highlights a new expert consensus on pediatric metabolic dysfunction–associated steatotic liver disease (MASLD), outlining current recommendations for screening, diagnosis, and management in children and adolescents with obesity.

Article Summary

Pediatric MASLD is rapidly rising alongside childhood obesity. This expert consensus outlines current evidence on epidemiology, diagnosis, and management, highlighting screening strategies and emerging therapies to guide early identification and care.

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Article Review

Overview

Metabolic dysfunction–associated steatotic liver disease (MASLD), previously termed nonalcoholic fatty liver disease (NAFLD), is now the most common chronic liver disease in children and adolescents. This joint consensus statement from the Taiwan Association for the Study of the Liver (TASL) and the Taiwan Society of Pediatric Gastroenterology, Hepatology, and Nutrition (TSPGHAN) provides a comprehensive synthesis of pediatric MASLD, emphasizing epidemiology, pathophysiology, diagnosis, and management within Asian populations while offering globally relevant clinical insights.

Epidemiology

The estimated prevalence of MASLD is approximately 7.4% among the general pediatric population, rising above 50% in children with obesity. Prevalence increases with higher body mass index (BMI) and is greater in males. Regional Asian surveys demonstrate a wide prevalence range, from 16% to 63% depending on obesity severity and local cohorts. The authors highlight that inconsistent diagnostic criteria and lack of systematic screening practices likely contribute to substantial underdiagnosis worldwide.

Pathophysiology

MASLD results from excessive hepatic fat accumulation in the presence of metabolic dysfunction, including obesity, insulin resistance, type 2 diabetes, and dyslipidemia. The currently accepted “multi-hit” hypothesis describes disease progression through overlapping metabolic, oxidative, inflammatory, and lipotoxic insults to the liver. Pediatric MASLD may begin early in life—risk is increased with maternal obesity, gestational diabetes, preterm birth, and suboptimal early nutrition—while breastfeeding for at least six months appears protective. Environmental exposures such as dietary fructose intake and emerging concerns over microplastic exposure may further contribute to hepatic metabolic stress.

Histopathology

MASLD spans simple steatosis (metabolic dysfunction–associated fatty liver, MAFL) to metabolic dysfunction–associated steatohepatitis (MASH) characterized by inflammation and fibrosis. Pediatric histologic patterns differ from adults. Children more often demonstrate zone 1 periportal or panacinar steatosis rather than adult zone 3 patterns. Schwimmer’s pediatric “type 2” pattern—more common in boys—and the NASH Clinical Research Network “zone 1 borderline pattern” are noted pediatric variants. Progression to cirrhosis and liver failure can occur but remains less frequent than in adult populations.

Clinical Presentation

Most children with MASLD are asymptomatic. When present, symptoms are nonspecific and include fatigue, abdominal discomfort, or hepatomegaly. Laboratory abnormalities are often discovered incidentally, most commonly elevated alanine aminotransferase (ALT) or aspartate aminotransferase (AST). Clinical correlates of insulin resistance such as acanthosis nigricans and dyslipidemia are frequently observed. The consensus emphasizes careful tracking of BMI and waist circumference, noting that waist circumference correlates more closely with cardiometabolic risk and hepatic fat accumulation than BMI alone.

Gut Microbiota and Intestinal Barrier

The gut–liver axis appears increasingly important in pediatric MASLD pathogenesis. Altered microbiota profiles include increased Escherichia, Prevotella, and Streptococcus, with reductions in beneficial species such as Faecalibacterium, Ruminococcus, and Coprococcus. Probiotic trials have produced modest reductions in ALT, though effects on steatosis remain inconsistent. Novel therapeutic approaches—including engineered probiotics, prebiotics, postbiotics, fecal microbiota transplantation, and bacteriophage therapy—are currently investigational. Increased intestinal permeability, elevated serum zonulin, and impaired tight junction integrity correlate with obesity and disease severity. Vitamin D repletion may support restoration of barrier function and represents a low-risk adjunct therapeutic strategy.

Genetic Risk

Several gene variants modify MASLD susceptibility and progression. PNPLA3 I148M and TM6SF2 E167K variants increase risks of steatosis and fibrosis, while MBOAT7 and GCKR further enhance lipid accumulation. The HSD17B13 variant appears protective, whereas SAMM50 may influence mitochondrial integrity and insulin sensitivity. Despite growing genetic insights, current pediatric guidelines do not advocate routine genetic screening. Risk stratification using polygenic profiles remains limited to research and specialized clinical contexts.

Screening and Diagnosis

Screening guidance varies internationally. NASPGHAN recommends ALT screening in children with obesity between ages 9–11 using cutoffs of ≥50 U/L for boys and ≥44 U/L for girls. The American Academy of Pediatrics recommends screening obese children beginning at age 10 and overweight children with additional risk factors. ESPGHAN supports ultrasound as a screening tool, while AASLD does not endorse universal screening. ALT and ultrasound remain first-line diagnostic tools but have limited sensitivity and specificity. Advanced modalities such as vibration-controlled transient elastography (VCTE), MRI–proton density fat fraction (MRI-PDFF), and magnetic resonance elastography offer improved quantification of steatosis and fibrosis, although access and pediatric normative ranges remain barriers.

Noninvasive Biomarkers

Most children with MASLD are asymptomatic. When symptoms occur, they are nonspecific and include fatigue, right upper quadrant discomfort, or hepatomegaly. Elevated ALT or AST levels typically lead to diagnosis. Common metabolic associations include insulin resistance markers such as acanthosis nigricans and dyslipidemia. The statement highlights the importance of regular BMI and waist circumference measurements, with waist circumference correlating more closely than BMI to metabolic risk and hepatic fat deposition.

Management and Treatment

Lifestyle intervention remains the cornerstone of MASLD management. A BMI z-score reduction of >0.25 or total weight loss of 7–10% is associated with improvements in steatosis and liver enzymes. Multidisciplinary approaches integrating nutrition counseling, physical activity promotion, and behavioral therapy achieve the most consistent results.

Pharmacologic options remain limited. Vitamin E has shown benefit for biopsy-confirmed pediatric MASH, though long-term safety remains uncertain. Vitamin D supplementation may improve hepatic steatosis in children with deficiency. Metformin, omega-3 fatty acids, losartan, and cysteamine demonstrate inconsistent or limited benefit. GLP-1 receptor agonists, including liraglutide and semaglutide, are effective for pediatric obesity treatment but lack definitive evidence for MASLD resolution. Resmetirom, approved in 2024 for adult MASH, has not yet been studied in pediatric populations. Metabolic bariatric surgery can improve liver histology in adolescents with severe obesity, but it is not indicated solely for MASLD treatment.

Future Directions and Conclusion

Research priorities include validation of pediatric imaging thresholds and biomarkers, longitudinal studies across ethnic groups, microbiome-targeted therapies, and pediatric pharmacologic trials. Integrating MASLD management into multidisciplinary obesity treatment frameworks remains critical.

Pediatric MASLD represents an expanding metabolic challenge driven largely by childhood obesity. Early detection, standardized screening, and effective lifestyle interventions remain the most impactful strategies for disease reversal and long-term complication prevention.