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Case-control study shows IL-10 significantly associates with serum hepcidin in β-thalassemia major, suggesting inflammation affects iron regulation.
β-thalassemia major is a chronic, transfusion-dependent disorder marked by severe iron overload and systemic inflammation. However, the interplay among inflammatory cytokines, iron chelation therapy, and hepcidin regulation remains incompletely understood. In this case–control study, 140 participants (100 patients, 40 healthy controls) were examined for associations between inflammatory and biochemical parameters and serum hepcidin. Hematological and biochemical parameters, inflammatory cytokines (IL-10 and TNF-α), and serum hepcidin levels were evaluated using nonparametric tests, Spearman’s correlation, and bootstrapped multiple linear regression, with adjustment for serum ferritin, hemoglobin, TNF-α, and age to account for potential confounding. Patients had significantly higher levels of ferritin, liver enzymes, blood glucose, inflammatory cytokines, and hepcidin than controls (p < 0.05). IL-10 and hepcidin showed a strong positive correlation (r = 0.838, p < 0.001). Bootstrapped Multiple regression showed that IL-10 was significantly associated with serum hepcidin in the adjusted model (B = 1.078, 95% CI: 0.876–1.288, p < 0.001), whereas ferritin was not independently associated with hepcidin. The model explained 74.2% of the variance (Adjusted R2 = 0.742). Moreover, significant variations in these parameters were observed across iron chelation therapy groups. These findings suggest a potential association between inflammatory activity and hepcidin-related iron regulation in β-thalassemia major, but longitudinal studies are needed to clarify the clinical relevance of this relationship.
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Salih et al. (2026) studied this question.
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