Background: Atherosclerosis is a chronic inflammatory, immune-mediated disease that is a leading cause of global mortality and disability. Coronary artery calcification (CAC) is a key predictor of the severity of coronary artery disease (CAD). Interleukin-38 (IL-38), a newly identified anti-inflammatory cytokine, may modulate inflammation and prevent atherosclerosis progression.
Objective: This study aimed to evaluate the association between serum IL-38 levels and CAC severity among patients referred to the CT angiography unit at Razieh Firooz Hospital in Kerman City.
Methods: In this cross-sectional study, 151 patients aged 50–70 years were evaluated. The mean age of the participants was 60.1 ± 6.9 years. CAC severity was determined using the Agatston scoring method and multi-detector CT scanners. Serum IL-38 levels were measured via enzyme-linked immunosorbent assay (ELISA). Statistical analyses were performed using an independent T-test and multivariable logistic regression.
Results: Comparing serum IL-38 levels across CAC severity categories showed a statistically significant difference (P = 0.039). Mean serum IL-38 in patients with non-severe and severe calcification were 16.8 ± 5.5 pg/mL and 19.4 ± 4.9 pg/mL, respectively. However, in the multivariable regression analysis, adjusted for major risk factors including sex, age, diabetes, hypertension, and smoking, the association between serum IL-38 levels and CAC severity was not significant (P>0.05). In subgroup analyses, the significant association between IL-38 and CAC severity was observed only in older participants and in patients with established cardiovascular risk factors.
Conclusion: Although serum IL-38 levels were higher in patients with severe CAC, this association did not remain significant after adjustment for major cardiovascular risk factors. Therefore, the observed elevation may reflect age- or risk-related inflammatory changes rather than a direct role of IL-38 in calcification. So, this relationship remains unclear. Further investigation is needed to clarify the potential context-dependent function of IL-38 in atherosclerosis progression.