The Relationship Between Acromegaly and Hepatic Steatosis: Insights from FibroScan Imaging

Purpose: The relationship between metabolic dysfunction-associated steatotic liver disease (MASLD) and acromegaly is unclear due to the complex metabolic effects of growth hormone (GH). GH stimulates gluconeogenesis, glycogenolysis, and lipolysis, increasing free fatty acids, a risk factor for MASLD, but may also protect against hepatic fat accumulation. In this study, we aimed to evaluate the impact of acromegaly and GH levels on liver steatosis and fibrosis using non-invasive FibroScan imaging. Methods: This cross-sectional study included 58 acromegaly patients and 61 age-sex-matched controls. Hepatic steatosis and fibrosis were assessed via controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) by vibration-controlled transient elastography. Moderate to severe steatosis was defined as CAP > 260 dB/m, and significant fibrosis as LSM ≥ 8.0 kPa. Results: The acromegaly group showed significantly lower mean CAP scores than controls (241.8 ± 50.0 vs. 281.7 ± 61.2 dB/m; p < 0.001), indicating less liver fat. LSM was also lower (4.7 ± 1.4 vs. 5.5 ± 1.8 kPa; p = 0.008). Moderate to severe steatosis occurred in 36.2% of acromegaly patients vs. 68.8% of controls (p = 0.005). Significant liver fibrosis was detected in 5.1% of acromegaly patients vs. 14.7% of controls (p = 0.152). GH levels were lower in acromegaly patients with MASLD (p < 0.001) compared to those without. CAP negatively correlated with GH but positively with BMI, waist circumference, and triglycerides. LSM correlated positively with age, BMI, and triglycerides. Conclusion: Hepatic steatosis is less frequent and severe in acromegaly, with GH inversely associated with liver fat, suggesting a protective role of GH independent of metabolic comorbidities.