From CT to Cytokines: Evaluating the Role of Systemic Inflammation and Metabolic Markers in Epiploic Appendagitis

Epiploic appendagitis (EA) is an underrecognized cause of acute abdominal pain. While its localized inflammatory nature is well described, potential systemic inflammatory responses and underlying metabolic contributions remain poorly understood. This study aimed to investigate the association between EA and systemic inflammatory and metabolic markers—Triglyceride-Glucose (TyG) index, Systemic Immune-Inflammation Index (SII), and Systemic Inflammation Response Index (SIRI). In this retrospective case–control study, we evaluated 85 patients with CT-confirmed EA and 79 age- and sex-matched controls. Biomarker data (TyG, SII, SIRI) were obtained from routine laboratory tests. Inflammatory severity and lesion volume were assessed via CT. Comparative, correlation, and logistic regression analyses were conducted. The TyG index did not significantly differ between EA and control groups (p = 0.354). However, both SII and SIRI were significantly elevated in EA patients (p < 0.001 for both). The strongest predictor of EA was log-transformed SII (OR = 3.85; 95% CI: 1.35–11.0), followed by SIRI (OR = 2.94; 95% CI: 1.25–6.91). While no significant correlation was found between biomarker levels and lesion volume, SII and SIRI values showed an increasing trend with radiological severity, though not statistically significant. Although CRP was a significant univariate predictor, our focus remained on novel indices (SII/SIRI) for their clinical applicability. SII and SIRI may serve as useful, readily available and inexpensive biomarkers to support the diagnosis and monitoring of EA, particularly in diagnostically challenging cases. Although the TyG index did not reach statistical significance, future studies with larger, prospectively collected cohorts excluding confounding metabolic conditions are warranted to further explore its role. Overall, systemic inflammatory indices could enhance understanding of EA’s pathophysiology beyond localized inflammation.