EP1204 - ECE_3109 - Evaluation of serum IL-1β levels in acromegalic patients with hepatic steatosis

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Abstract Introduction Acromegaly is a chronic endocrine disorder caused by excessive secretion of growth hormone (GH) and insulin-like growth factor-1 (IGF-1), and is frequently associated with metabolic complications, including hepatic steatosis. Hepatic involvement in acromegaly is considered a manifestation of metabolic syndrome and may progress to fibrosis, commonly assessed using non-invasive indices such as the Fibrosis-4 (FIB-4) score. Although chronic low-grade inflammation has been proposed as a contributing mechanism in acromegaly-related metabolic dysfunction, the role of circulating inflammatory mediators remains incompletely understood. This study aimed to evaluate inflammatory markers in patients with acromegaly and controls to explore their relationship with hepatic and metabolic parameters. Methods A total of 90 participants were included: 48 patients with acromegaly (53.3%) and 42 healthy controls (46.7%). Demographic characteristics, hormonal and metabolic parameters, and abdominal ultrasonography findings were recorded. Serum interleukin-1 beta (IL-1β) and nuclear factor kappa B (NF-κB) levels were measured using enzyme-linked immunosorbent assay. Patients with acromegaly were additionally evaluated according to disease activity (controlled vs uncontrolled). Group comparisons were performed using non-parametric statistical methods. Correlation analyses and exploratory receiver operating characteristic (ROC) analyses were conducted. Results Patients with acromegaly were older than controls (median 54 vs 45 years, P < .001), while sex distribution was similar (P = .343). Markers of metabolic burden were higher in the acromegaly group, including fasting glucose (P = .009) and HbA1c levels (P < .001). The FIB-4 index was significantly elevated in patients with acromegaly (median 0.94 vs 0.63, P < .001), and ultrasonographic hepatic steatosis was more frequent (P = .030). Serum IL-1β levels were significantly lower in patients with acromegaly compared with healthy controls (median 866 vs 2006 pg/mL, P < .001). NF-κB levels were also significantly lower in the acromegaly group (P = .013). Overall correlation analyses demonstrated weak associations between IL-1β and hepatic or hormonal parameters, which were not consistently maintained in subgroup analyses. In ROC analysis, IL-1β showed good distinctive ability for distinguishing acromegaly from controls (AUC = 0.80), whereas FIB-4 demonstrated modest performance (AUC = 0.72). The ability of FIB-4 to distinguish controlled from uncontrolled acromegaly was limited (AUC = 0.68). Conclusion Despite increased hepatic and metabolic burden in acromegaly, circulating inflammatory markers did not indicate classical inflammatory activation. This pattern may reflect immunomodulatory effects of chronic GH/IGF-1 excess rather than a conventional pro-inflammatory state. Given the age difference between groups, findings should be interpreted with caution. These results highlight the complexity of immune–metabolic interactions in acromegaly.

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