SAT-661 Hepatic and Cardiovascular Outcomes of Patients with Metabolic Dysfunction-Associated Steatotic-Liver Disease and Diabetes Mellitus Type 2 Treated with Glucagon-Like Peptide 1 Agonists

Abstract Disclosure: S. Al Ashi: None. R. Shah: None. N. Iftikhar: None. P. Phan: None. I. Lingvay: None. M. Kinaan: None. I. Mansi: None. Background: Metabolic Dysfunction-Associated Steatotic-Liver Disease (MASLD) is the most common cause of chronic liver disease in the United States. MASLD can progress to liver cirrhosis and is associated with increased risk of major acute cardiovascular events (MACE). Purpose: To examine the association of Glucagon-like peptide 1 receptor agonists (GLP1-RA) use with liver disease progression, cardiovascular events and all-cause mortality among patients with MASLD. Methods: This retrospective study used national data of the Department of Veteran Affairs. Patients with MASLD who initiated either GLP1-RA or dipeptidyl-peptidase-4 inhibitor (DPP4-i) between October 1, 2005, and September 30, 2021, were included. Patients with other chronic liver disease etiologies or decompensated cirrhosis at baseline were excluded. Primary outcomes were: 1) liver disease progression and 2) MACE or all-cause mortality. GLP1-RA users and DPP4-I users were propensity score matched on 73 baseline characteristics including demographics, liver function tests and scores, measures of diabetes control, cardiovascular risks, other comorbidities, use of other medications, and frailty score. Results: We matched 58,157 pairs of GLP1-RA and DPP4-I users. GLP1-RA users had less liver disease progression (6.1%) compared with DPP4-I users (7.0%), hazard ratio (HR): 0.86; 95% confidence interval (95% CI): 0.82- 0.90 and a lower risk of MACE or all-cause mortality (11.1%), compared with DPP4-i users (14.7%), (HR: 0.72; 95% CI: 0.70-0.75). Conclusions: Among patients with MASLD, GLP1-RA use was associated with a lower risk of liver disease progression, and a lower risk of MACE or all-cause mortality compared to DPP4-I use. Presentation: Saturday, July 12, 2025