P4758 - Weight Loss is the Boss: Hepatic Adenomas

Christopher J. Cieker, MD¹, Eugenia Tsai, MD², Lisa Pedicone, PhD², Andres Gomez-Aldana, MD², Jan Petrasek, MD, PhD², Carmen Landaverde, MD³, Eric J. Lawitz, MD⁴, Fred Poordad, MD², Fabian Rodas, MD^2
1University of Texas Health San Antonio, San Antonio, TX; ²Texas Liver Institute, San Antonio, TX; ³Texas Liver Institute, Austin, TX; ⁴The Texas Liver Institute, University of Texas Health, San Antonio, TX

Introduction: A hepatocellular adenoma (HCA) is a benign liver tumor with incidence of 1 case per million people.¹ HCAs have a prevalence of 10-30 per million women on oral contraceptives (OCPs).¹ We present a case where HCAs were managed indirectly by weight loss with semaglutide, a glucagon-like peptide-1 (GLP-1A) receptor agonist.

Case Description/Methods: A 36-year-old obese female (body mass index of 53) with 10 years of OCP use was seen due to elevated liver enzymes from hepatic steatosis (HS) versus metabolic dysfunction-associated steatohepatitis (MASH). She started semaglutide for obesity and was referred for MRI. Findings showed moderate to severe HS (fat fraction of 20.7-22.8%) and at least 7 T2 bright liver masses reaching up to 3.4 cm (figure 1A shows a 2.76 cm lesion). Her OCP was stopped.



A liver biopsy showed findings consistent with HCA (benign hepatocytes without portal tracts), stage 1 fibrosis, mild lobular hepatitis-type changes, and background HS. This was consistent with a diagnosis of MASH with HCAs. Conservative treatment was chosen through imaging surveillance. Improvement was seen on 3-month follow-up MRI (figure 1B). Over 10 months, the patient lost 18.5% of her body weight (60 lbs) and had resolution of the HCAs and HS on MRI (figure 1C).

Discussion: HCAs are monoclonal proliferations of hepatocytes that lack normal hepatic structure and have large stores of fat or glycogen.^1,2,3 HS is also due to fat accumulation from dysregulation of lipid metabolism. HCAs are affected by OCPs, metabolic syndrome, and androgen use.^1,2,3 HCAs can cause life-threatening bleeds from ruptured lesions or turn into hepatocellular carcinoma.^1,2,3 High risk lesions >5 cm are managed by surgical resection or embolization.⁴ Low risk lesions can be managed by stopping OCPs and weight loss.⁴



GLP-1A mediated weight loss is a potential treatment option for HCAs. Our case shows that stopping OCPs and weight loss can lead to resolution of HCAs.



References:

1. Grazioli L, et al. Primary benign liver lesions. Eur J Radiol. 2017 Oct; 95:378-98.

2. Torbenson M. Hepatic Adenomas: Classification, Controversies, and Consensus. Surg Pathol Clin. 2018 Jun; 11(2):351-66.

3. Reizine E, et al. Focal Benign Liver Lesions and Their Diagnostic Pitfalls. Radiol Clin North Am. 2022 Sep; 60(5):755-73.

4. Marrero JA, et al. ACG Clinical Guidelines: The Diagnosis and Management of Focal Liver Lesions. American Journal of Gastroenterology. 2014 Sep; 109(9):1328-47.





Disclosures:


Christopher J. Cieker, MD¹, Eugenia Tsai, MD², Lisa Pedicone, PhD², Andres Gomez-Aldana, MD², Jan Petrasek, MD, PhD², Carmen Landaverde, MD³, Eric J. Lawitz, MD⁴, Fred Poordad, MD², Fabian Rodas, MD². P4758 - Weight Loss is the Boss: Hepatic Adenomas, ACG 2024 Annual Scientific Meeting Abstracts. Philadelphia, PA: American College of Gastroenterology.