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

Background 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. Methods 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. Results 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. Conclusion 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.