S2627 Metabolic Liver Disease in HCC: Underdiagnosis and Advanced Portal Hypertension in Patients With a MASH-Consistent Phenotype in a Diverse Southwestern Cohort

Introduction: Metabolic dysfunction–associated steatohepatitis (MASH) is a growing driver of hepatocellular carcinoma (HCC), yet it remains underdiagnosed, especially in underserved populations. We evaluated the prevalence, clinical profile, and diagnostic workup of patients with a metabolic phenotype suggestive of MASH in a diverse cohort from the American Southwest. Methods: We retrospectively analyzed clinical data from 260 patients with confirmed HCC diagnosed between 2015 and 2023 at the University of New Mexico Comprehensive Cancer Center. A metabolic phenotype consistent with MASH was defined as the presence of ≥2 of the following: obesity (BMI ≥30), type 2 diabetes, and dyslipidemia. We compared tumor and hepatic biomarkers—including AFP, Fib-4, albumin, platelet counts, and portal vein thrombosis (PVT)—between patients with and without this phenotype. We also assessed use of fibrosis assessment tools (biopsy, Fibroscan). Results: Eighty-five patients (34.1%) met criteria for a MASH-consistent phenotype. Among them, only 6% underwent liver biopsy, and just one received Fibroscan evaluation. Use of GLP-1 receptor agonists or SGLT2 inhibitors was negligible. Patients with a MASH-consistent phenotype had significantly higher rates of PVT (P = 0.035), a marker of advanced portal hypertension. Mean platelet count were numerically lower in the MASH group (132.5 × 10³/µL) compared to the non-MASH group (145.0 × 10³/µL), (P = 0.27). No significant differences were observed in AFP (P = 0.20), Fib-4 score (P = 0.97), albumin (P = 0.24), or ECOG (P = 0.64). Native American patients had the highest prevalence of this phenotype (56%) but the lowest rates of fibrosis staging (biopsy 3%, Fibroscan 0%). Conclusion: Over one-third of HCC patients in this Southwestern cohort had a metabolic phenotype consistent with MASH, yet formal fibrosis assessment and therapeutic intervention were rare. These patients demonstrated higher rates of portal vein thrombosis and numerically lower platelet counts, suggesting later-stage disease at presentation. Improved recognition of metabolic liver disease and earlier non-invasive staging are critical for optimizing care in this growing HCC population.