Long-Term Impact of Saroglitazar on Advanced Hepatic Fibrosis and Metabolic Dysfunction in MASLD patients: A Two-Year Case Series
Naresh Dang *
Max Super Speciality Hospital, Patparganj, New Delhi, India.
Meenakshi Jain
Max Super Speciality Hospital, Patparganj, New Delhi, India.
*Author to whom correspondence should be addressed.
Abstract
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent in individuals with type 2 diabetes mellitus (T2DM). However, it remains an often overlooked hepatic comorbidity in this population. This case series contributes to the literature by presenting real-world, longitudinal evidence of hepatic fibrosis regression and glucometabolic improvement with saroglitazar, a dual PPAR-α/γ agonist in combination with oral semaglutide (7 mg or 14 mg as tolerated), a GLP-1 receptor agonist in T2DM patients with MASLD over a 2-year follow-up period.
Case Summary: Saroglitazar 4 mg once daily was initiated in four adult patients with T2DM and imaging-confirmed MASLD. Baseline assessments revealed elevated HbA1c (6.4–8.2%), hypertriglyceridemia, and evidence of hepatic steatosis and fibrosis on transient elastography. CAP values ranged from 257 to 347 dB/m, corresponding to S1–S3 steatosis grades, while LSM values ranged from 14.3 to 38.5 kPa, indicative of F3–F4 fibrosis stages. No other hepatoprotective or antidiabetic agents with hepatic benefit were used. All patients experienced marked reductions in HbA1c, triglycerides, ALT, and AST after two years of Saroglitazar 4 mg therapy. Three patients demonstrated improvement in hepatic steatosis (from S2–S3 to S0–S1) and fibrosis (from F2–F3 to F0–F1); notably, one patient showed marked regression from advanced fibrosis (F3) to no fibrosis (F0). The therapy was well tolerated, with no adverse effects reported.
Conclusion: This case series highlights the potential of saroglitazar as a dual PPAR agent with semaglutide addressing both metabolic and hepatic derangements in MASLD associated with T2DM. The observed improvements in liver stiffness and glycemic-lipid profiles over two years, independent of weight loss or adjunct therapies, suggest a disease-modifying role. Clinicians managing diabetic patients should be vigilant for coexisting MASLD and consider saroglitazar as a promising therapeutic option pending further confirmatory trials.
Keywords: PPAR agonist, liver stiffness measurement, transient elastography, diabetic dyslipidemia, non-invasive biomarkers, fibrosis regression, GLP-1 receptor agonist