Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing public health concern, with projections indicating that over half of the global population could be affected by 2040. MASLD is strongly linked to cardiometabolic risk factors and can progress to advanced liver diseases such as fibrosis, cirrhosis, and hepatocellular carcinoma. It is characterized by lipid accumulation within hepatocytes, leading to oxidative stress and inflammation. Gilbert’s syndrome (GS), a benign hereditary condition marked by elevated unconjugated bilirubin, is known for its antioxidant and anti-inflammatory properties. These properties have been associated with a reduced risk of several cardiometabolic conditions, raising the question of whether GS may influence the progression or severity of liver disease in MASLD.

Aims & Methods

This study aimed to investigate the potential relationship between GS and MASLD, focusing specifically on the impact of bilirubin’s effects on liver fibrosis and disease severity. A retrospective cohort study was conducted at Nawaloka Hospital, Colombo, Sri Lanka. Medical records from January 2022 to December 2024 were reviewed to extract sociodemographic, anthropometric, and biochemical data. Liver fibrosis was assessed using Fibro Scan® 502. Data analysis was performed using SPSS version 28, employing univariate analyses including t-tests, chi-square tests, and simple linear regression. A P-value <0.05 was considered statistically significant.

Results

A total of 180 patients with MASLD were included, of whom 36 were identified as having GS (defined by total bilirubin >1 mg/dL with elevated unconjugated bilirubin) and 144 without. No statistically significant difference in liver stiffness measurements (LSM) was observed between patients with and without GS (P = 0.8919). GS was not significantly associated with the presence or severity of liver fibrosis. Increasing age (P = 0.0278), body mass index (BMI) (P = 0.0330), and blood sugar levels (P = 0.0257) were positively associated with liver fibrosis. Demographic and clinical characteristics of the participants are summarized in Table 1.

Conclusion

There was no difference in the presence of fibrosis in MASLD patients with GS without GS in our population. This is in keeping with the view that GS is a benign condition. The significant associations of age, BMI, and blood sugar with increased fibrosis are well documented.