Association of Serum Ferritin with Hepatic, Renal, and Endocrine Markers in β-Thalassemia Major: A Cross-Sectional Study
DOI:
https://doi.org/10.31185/bsj.Vol22.Iss43.1719Keywords:
Keywords: β-Thalassemia Major; Iron Overload; Endocrine Dysfunction; Hepatocellular Injury.Abstract
Abstract
Background: Chronic iron overload from frequent transfusions remains the primary driver of multi-organ morbidity in β-thalassemia major (β-TM). Objective: This study evaluated the interplay between serum ferritin, thyroid function, and biochemical markers (hepatic and renal) in β-TM patients. Methods: A cross-sectional analysis of 179 patients (101 males, 78 females; ages 5–50) was conducted at Al-Kut Hospital for Gynecology and Pediatrics (Hereditary Hematology Center-Thalassemia Unit), Iraq. Serum ferritin and thyroid profiles (TSH, T3, T4) were quantified via CLIA, while liver and renal parameters were analyzed using the Abbott Architect c4000 system (significance at p < 0.001). Results: Critical systemic iron overload was observed, with significantly higher mean ferritin in males (4241.23 ± 233.13 ng/mL) than females (3329.60 ± 261.11 ng/mL; p = 0.010). In abnormal subgroups, significant elevations (p < 0.001) were found in TSB (2.14 ± 0.11 mg/dL), AST (71.22 ± 4.91 U/L), and ALT (83.82 ± 8.50 U/L). Correlation analysis revealed a profound positive association between AST and ALT (r = 0.90) and a significant link between ferritin and AST (r = 0.44). Notably, ferritin showed an inverse relationship with T4 (r = -0.30) and T3 (r = -0.23), reflecting iron-induced endocrine suppression. while urea (46.94 ± 0.81 mg/dL) and RBS (163.30 ± 9.81 mg/dL) showed marked disturbances in affected groups. Conclusion: Iron overload is the central pathogenic driver of synchronized hepatic and endocrine dysfunction. These findings necessitate integrated, personalized chelation protocols and rigorous multi-organ monitoring to mitigate progressive clinical deterioration.
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