Loading
Life sciences · Journal article
Jpgn Reports · October 23, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Abstract Metabolic dysfunction‐associated steatotic liver disease (MASLD) is a common comorbidity of pediatric obesity that predisposes patients to hepatocellular adenomas (HCAs). HCAs however are nonspecific to MASLD and warrant further evaluation. We present a case of a 16‐year‐old male with severe obesity, and persistently elevated liver enzymes, initially evaluated for MASLD. Imaging revealed multiple hepatic lesions consistent with HCAs, prompting further genetic evaluation. Trio exome sequencing identified biallelic variants in the glucose‐6‐phophatase gene, confirming a diagnosis of glycogen storage disease type Ia (GSD Ia). This case highlights the diagnostic challenge posed by overlapping features of MASLD and GSD Ia, particularly hepatic steatosis, HCAs, and metabolic syndrome. Initial management of MASLD with glucagon‐like peptide‐1 therapy was discontinued given risk for hypoglycemia, and the patient continues glucose monitoring and cornstarch therapy. This case emphasizes the importance of including inborn errors of metabolism in the differential diagnosis for multifocal HCAs and concerns with obesity treatments.