THU068 Evaluation Of Nonalcoholic Fatty Liver Disease, Liver Fibrosis And Serum Angiopoietin-like Protein Levels In Patients With Acromegaly

Abstract

Abstract Disclosure: I. Eroglu: None. B. Gonul Iremli: None. I. Idilman: None. D. Yuce: None. I. Lay: None. D. Akata: None. T. Erbas: None. Background: Due to their impaired glucose and lipid metabolism, acromegaly patients are potentially at risk for NAFLD. However, limited data exist about acromegaly and NAFLD relation. In this study (cross-sectional, case-controlled), we evaluated the risk of NAFLD and hepatic fibrosis in acromegalic patients and its association with noninvasive hepatosteatosis scores (NS) and angiopoietin-like protein-8 (ANGPTL-8) level for the first time in the literature. Methods: Thirty-two (15F/17M - median age=50.15 yrs) acromegalic patients (n=15 active acromegaly - AA and n=17 controlled acromegaly - CA) compared to 19 healthy controls (C) in terms of liver fat ratio (LFR), liver stiffness measurement (LSM), and ANGPTL-8 levels. Subjects had MRI-PDFF to determine LFR and MR elastography to quantify LSM. NAFLD was confirmed in those with LFR of ≥5%, and increased LSM in those with LSM of ≥2.5 kPa. VAI (visceral adipocity index), FLI (fatty liver index), HSI (hepatic steatosis index), and TyG (Triglyceride-glucose index) were calculated as NS. Results: Age, gender and BMI were similiar across groups. The GH and IGF-1 levels in AA group was greater than in CA, and C (p< 0.001). The CA had greater frequency of NAFLD than AA (p<0.001). Increased LSM was detected in three (21.4%) of AA, four (23.5%) of CA, and two (10.5%) of C.The median LFR was 1.75% in the AA group, 6.5% in the CA group, and 3.5% in the control group. LFR was lower in the AA group than in the CA (p=0.026). According to MRI-PDFF results, none of the patients in the AA group were diagnosed with NAFLD, while 58.8% (n=10) in the CA group and 26.3% (n=5) in the control group were diagnosed with NAFLD. The prevalence of NAFLD was found to be higher in the CA group than in the AA group (p<0.001). In acromegaly patients, LFR was positively correlated with TyG (r=0.675, p<0.001), VAI (r=0.508, p=0.004), and FLI (r=0.482, p=0.006). However, no correlation was seen between LFR and traditional risk factors for NAFLD (including BMI, waist circumference, Hba1c, HOMA-IR, and CRP) in acromegalics.ANGPTL-8 was lower in CA group (0.61 ng/mL) than in AA group (0.89 ng/mL) (p=0.006). When all acromegaly patients were evaluated independently, those with NAFLD had lower ANGPTL-8 levels than those without NAFLD (p=0.036). Conclusion: In conclusion, high GH levels seem to be protective against fatty liver in patients with active acromegaly, even if the metabolic profileis impaired. There was no relation observed between LFR and conventional risk factors in acromegaly patients. The strongest connection was found between LFR and TyG index among the noninvasive hepatosteatosis scores. ANGPTL-8 levels were lower in acromegaly patients with NAFLD, suggesting that high levels represent a reaction to insulin resistance rather than a cause of NAFLD. Treatment planning at a level that does not cause GH deficiency while maintaining disease control may be helpful to prevent NAFLD in acromegaly. Presentation: Thursday, June 15, 2023