# Metabolic-associated steatotic liver disease in children and adolescents: a scoping review and narrative synthesis of epidemiology, risk factors, and screening approaches with emerging implications for sub-Saharan Africa

**Authors:** Bruno Basil, Peace Ngozi Okoro

PMC · DOI: 10.3389/fendo.2026.1784970 · Frontiers in Endocrinology · 2026-03-13

## TL;DR

This paper reviews how metabolic liver disease in children is rising globally, with a focus on unique challenges in Sub-Saharan Africa due to a mix of malnutrition and obesity.

## Contribution

The study highlights the 'African Paradox' and proposes new screening approaches tailored to Sub-Saharan Africa's distinct metabolic and diagnostic landscape.

## Key findings

- Global pediatric MASLD prevalence ranges from 7.6% to 14%, with 41% in obese children.
- In Sub-Saharan Africa, MASLD prevalence among overweight children is 31.1%, but detection is hindered by outdated screening methods.
- The region shows a lower frequency of the PNPLA3 genetic risk variant, complicating diagnosis and suggesting a unique metabolic profile.

## Abstract

Metabolic-Associated Steatotic Liver Disease (MASLD) is recognized as one of the most common chronic liver diseases in children globally, rising in tandem with the childhood obesity pandemic. Although high-income countries focus on advanced phenotyping, Sub-Saharan Africa (SSA) faces a distinct “two-speed” epidemic characterized by rapid urbanization and a unique “double burden” of malnutrition and obesity. This review examines the global and regional epidemiology of paediatric MASLD, contrasting established Western practices with the unique genetic, environmental, and diagnostic challenges of SSA.

A scoping review was conducted following the PRISMA-ScR guidelines and using the JBI methodological framework. PubMed/MEDLINE, Embase, and African Journals Online (AJOL) were searched for literature published between 2010 and 2025 focusing on epidemiology, risk factors, and diagnostic performance in children aged 0–19 years. Evidence was synthesized to compare global prevalence patterns with emerging African data and to evaluate the validity of conventional screening approaches in resource-limited settings.

A total of 68 studies were included. Global evidence estimates paediatric MASLD prevalence between 7.6% and 14% in the general population and as high as 41% among children with obesity. In SSA, data remain sparse but alarming, with pooled prevalence among overweight children reaching 31.1%, a figure derived mostly from studies in the NAFLD-era utilizing ultrasound or ALT proxies, which may not align perfectly with newer MASLD criteria. The region exhibits a distinct “African Paradox” with a lower frequency of the PNPLA3 genetic risk variant (13.7%), which contributes to lower hepatic steatosis on imaging despite pronounced insulin resistance. As a result, reliance on alanine aminotransferase (ALT) and ultrasonography for screening risks under-detection, obscuring the metabolically high-risk yet hepatically lean phenotype common in SSA. Furthermore, environmental drivers such as high-fructose diets and endocrine-disrupting chemicals may be overriding genetic protection.

Paediatric MASLD in SSA reflects a multifactorial pathology likely driven by environmental stressors, epigenetic “thrifty phenotype” programming, and rapid nutritional transition rather than simple caloric excess. Western-calibrated diagnostic algorithms are poorly suited to the African metabolic phenotype. To mitigate a future surge in advanced liver disease, public health strategy must prioritize low-cost innovations, including validating scalable markers such as Waist-to-Height Ratio (WHtR) and integrating task-shifting approaches within existing HIV and diabetes care platforms.

Infographic illustrating the African Paradox in paediatric MASLD in Sub-Saharan Africa, comparing global and regional prevalence, genetic factors, diagnostic challenges, dietary influences, and proposing cost-effective local screening and integration with HIV and diabetes care systems.

## Linked entities

- **Genes:** PNPLA3 (patatin like domain 3, 1-acylglycerol-3-phosphate O-acyltransferase) [NCBI Gene 80339]
- **Chemicals:** alanine aminotransferase (PubChem CID 251717)
- **Diseases:** obesity (MONDO:0011122), diabetes (MONDO:0005015)

## Full-text entities

- **Genes:** GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, PNPLA3 (patatin like domain 3, 1-acylglycerol-3-phosphate O-acyltransferase) [NCBI Gene 80339] {aka ADPN, C22orf20, iPLA(2)epsilon}
- **Diseases:** diabetes (MESH:D003920), malnutrition (MESH:D044342), obesity (MESH:D009765), NAFLD (MESH:D065626), insulin resistance (MESH:D007333), hepatic steatosis (MESH:D005234), MASLD (MESH:D008107), overweight (MESH:D050177)
- **Chemicals:** fructose (MESH:D005632)
- **Species:** Human immunodeficiency virus 1 (no rank) [taxon 11676]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13021469/full.md

## References

68 references — full list in the complete paper: https://tomesphere.com/paper/PMC13021469/full.md

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Source: https://tomesphere.com/paper/PMC13021469