Diagnostic challenges of clinically significant portal hypertension in geriatric metabolic dysfunction-associated fatty liver disease: A case report

BACKGROUND Metabolic dysfunction-associated fatty liver disease (MAFLD) may progress to cirrhosis and lead to serious complications. Lipid accumulation, hepatocellular ballooning, and sinusoidal endothelial dysfunction increase intrahepatic vascular resistance, resulting in early clinically significant portal hypertension (CSPH). Although hepatic venous pressure gradient (HVPG) remains the gold standard, decompensated cirrhosis may yield deceptively low values. Transient elastography and platelet count provide supportive diagnostic evidence, yet obesity can overestimate disease severity. This report highlights the diagnostic challenge of CSPH, especially MAFLD in geriatric patients. CASE SUMMARY A 78-year-old woman with class I obesity, type 2 diabetes mellitus, and dyslipidemia presented with hematemesis and melena for a three-day period. A prior computed tomography scan revealed moderate diffuse hepatic steatosis, splenic vein dilatation, and splenomegaly. On admission, she presented with pallor, epigastric tenderness, splenomegaly, and mild ascites. Laboratory findings showed anemia, thrombocytopenia, hypoalbuminemia, and hyperglycemia. Abdominal ultrasound confirmed chronic liver disease with splenomegaly. Esophagogastroduodenoscopy demonstrated grade II-III esophageal varices and portal hypertensive gastropathy. Noninvasive fibrosis assessments (non-alcoholic fatty liver disease fibrosis score, aspartate transaminase-to-platelet ratio index, fibrosis-4 index, and FibroScan: E = 28 kPa, controlled attenuation parameter = 191 dB/m) indicated advanced hepatic fibrosis. HVPG measurement was not performed, however due to the Baveno VII criteria (transient elastography ≥ 25 kPa and platelet count < 150 × 109/L), confirmed the diagnosis of CSPH. The patient received endoscopic variceal ligation, a nonselective beta-blocker, a proton pump inhibitor, insulin, a sodium-glucose cotransporter 2 inhibitor, and lifestyle modification, resulting in clinical improvement. CONCLUSION Early and precise evaluation of CSPH in geriatric MAFLD requires an integrated clinical assessment to optimize diagnosis, management, and improve outcomes.