Abstract 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 patients with acromegaly, 61 age- and sex-matched metabolically comparable controls, and 82 healthy 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 Both acromegaly patients and metabolically healthy individuals exhibited lower CAP (241.8 ± 50.0 and 231.7 ± 51.9 dB/m) and LSM (4.7 ± 1.4 and 4.8 ± 1.8 kPa) scores than metabolically matched controls (CAP 281.7 ± 61.2 dB/m; LSM 5.5 ± 1.8 kPa; CAP p < 0.001; LSM p = 0.012). Moderate-to-severe steatosis was observed in 36.2% of acromegaly patients, 27.7% of healthy individuals, and 68.8% of metabolically matched controls ( p < 0.001), while significant liver fibrosis occurred in 5.2%, 7.3%, and 14.7%, respectively ( p = 0.154). GH levels were lower in acromegaly patients with MASLD ( p < 0.001) compared to those without. CAP correlated negatively with GH and positively with BMI, waist circumference, and triglycerides, whereas LSM correlated positively with age, BMI, and triglycerides. Conclusions Hepatic steatosis was less frequent in acromegaly than in metabolically comparable individuals, and GH was inversely associated with hepatic steatosis scores, possibly suggesting a protective role of GH independent of metabolic comorbidities.
Apaydin et al. (2026) studied this question.