Endocrine Abstracts

JOINT1206

Introduction: Growth hormone (GH) has been shown to play a protective role against liver steatosis by reducing visceral adipose tissue. Liver fibrosis has been observed in cases of GH resistance and impairment of GH signaling pathways. In this study, we aimed to evaluate liver steatosis and liver fibrosis in patients with acromegaly.

Materials and Methods: This cross-sectional study included 58 patients diagnosed with acromegaly, followed up at the endocrinology outpatient clinic of Marmara University Hospital, along with 79 age-, sex-, and BMI-matched control patients. Hepatic steatosis and liver fibrosis were evaluated using controlled attenuation parameter (CAP) and liver stiffness measurements (LSM) via FibroScan, performed by a single experienced operator. Increased hepatic steatosis was defined as a CAP >260 dB/m (>34% fat), and increased liver fibrosis was defined as an LSM ≥8 kPa (F ≥2).

Results: The acromegaly and control groups showed a similar distribution in terms of age, gender, body mass index (BMI), and the prevalence of diabetes, hypertension, and hyperlipidemia. No significant differences were observed between the groups regarding fasting blood glucose (FBG), LDL cholesterol levels, or liver function tests (P >0.05). The CAP score, a marker of hepatic steatosis, was significantly lower in the acromegaly group compared to the control group (241.8 ± 50.0 dB/m vs. 289.8 ± 65.3 dB/m, P <0.001). Similarly, the LSM score, used to assess hepatic fibrosis, was lower in the acromegaly group compared to controls (4.7 ± 1.4 kPa vs. 6.4 ± 4.5 kPa, P = 0.007). Moderate-to-severe hepatic steatosis was present in 36.2% of the acromegaly patients and 60.7% of the control group (P = 0.005). Fibrosis stage F2 or higher was detected in 5.1% of patients with acromegaly, compared to 17.7% of the control group (P = 0.035). A negative correlation was found between CAP score and GH levels (r: -0.311, P = 0.017), while positive correlations were identified between CAP score and FBG, BMI, and waist circumference (r: 0.298, P = 0.020; r: 0.447, P <0.001; and r: 0.447, P = 0.001, respectively). Positive correlations were observed between LSM and both age and BMI (r: 0.400, P = 0.001; r: 0.540, P <0.001).

Discussion: Hepatic steatosis and hepatic fibrosis were observed less frequently in patients with acromegaly compared to the control group. A negative correlation was identified between hepatic steatosis and GH levels. Elevated GH may have a potential protective role against fatty liver development in acromegaly patients, regardless of comorbid conditions such as diabetes and hyperlipidemia, which are major contributors to fatty liver disease.