# Role of Saroglitazar in Improving Transient Elastography Parameters in Significant and Advanced Metabolic Dysfunction-Associated Steatohepatitis

## TL;DR

Saroglitazar improves liver stiffness and other health markers in patients with metabolic dysfunction-associated liver disease over 52 weeks.

## Contribution

Demonstrates real-world efficacy of Saroglitazar in improving liver and metabolic parameters in MASLD/MASH patients.

## Key findings

- Liver stiffness decreased by 39.1% in significant fibrosis patients after 52 weeks of Saroglitazar treatment.
- Transaminase levels and lipid parameters also showed significant reductions in both fibrosis groups.
- Saroglitazar was well-tolerated with no serious adverse events reported.

## Abstract

Introduction: Metabolic dysfunction-associated steatohepatitis (MASH) contributes significantly to liver-related and cardiometabolic morbidity. Saroglitazar, a dual peroxisome proliferator-activated receptor (PPAR)-α/γ agonist, targets both hepatic and metabolic pathways. This study evaluated its real-world efficacy in improving liver stiffness, steatosis, hepatic transaminases, and lipid parameters.

Methods: This retrospective, single-center, observational study included 204 adults with metabolic dysfunction-associated steatotic liver disease (MASLD)/MASH treated with saroglitazar 4 mg once daily for 52 weeks. Patients were categorized as Significant Fibrosis (<14 kPa; n = 104) or Advanced Fibrosis (≥14 kPa; n = 100) based on baseline liver stiffness measurement (LSM). Changes in LSM, controlled attenuation parameter (CAP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol, and low-density lipoprotein cholesterol (LDL-C) were analyzed at baseline, 24 weeks, and 52 weeks.

Results: In the Significant Fibrosis group, mean LSM reduced from 10.31 ± 2.01 to 6.27 ± 1.44 kPa (-39.1%, p < 0.001) and CAP from 295.82 ± 49.34 to 241.01 ± 63.61 dB/m (-18.4%). ALT and AST declined by 49.5% and 43.4%, respectively, with total cholesterol and LDL-C reductions of 17.6% and 25.9%. In the Advanced Fibrosis group, LSM decreased from 17.96 ± 1.85 to 13.83 ± 1.42 kPa (-23.0%) and CAP from 317.05 ± 61.28 to 272.36 ± 52.38 dB/m (-14.1%), accompanied by ALT and AST reductions of 46.6% and 45.1%, and total cholesterol and LDL-C reductions of 18.3% and 25.7% (p < 0.001 for all). Saroglitazar was well-tolerated without serious adverse events.

Conclusion: Saroglitazar 4 mg daily was associated with significant improvements in liver stiffness, steatosis, transaminases, and lipid parameters over 52 weeks. These findings support its hepatometabolic potential across both early and advanced MASLD/MASH stages in real-world practice.