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Impact of iron chelation therapy on thyroid function in beta-thalassemia major patients from Pakistan
Arsalan Waqas Ahmad Shah1, Sulaiman Shams2, Muhammad Jaseem Khan3
1Institute of Health Sciences Swabi, Khyber Medical University Peshawar, Peshawar, 25000, Pakistan.
Transfusion-Dependent Thalassemia (TDT) causes severe anemia requiring chronic transfusions, leading to iron overload and endocrine complications, including hypothyroidism. Iron chelation therapy (ICT) mitigates iron toxicity, but its effects on thyroid function remain understudied in resource-limited settings like Pakistan. This cross-sectional study compared 100 TDT patients receiving ICT (deferasirox, deferoxamine, or deferiprone) for ≥ 6 months with 100 Control group who have not taken ICT. Thyroid function tests (free T3, free T4, TSH), serum ferritin, and hepatic/renal biomarkers were analyzed. Statistical analyses included t-tests, ANOVA, Pearson correlation, and multivariate regression (SPSS v25). ICT-treated patients had significantly lower TSH (3.10 ± 0.62 vs. 9.95 ± 3.19 μIU/mL, p < 0.001) and higher free T3/T4 levels than controls (p < 0.001). Deferasirox users exhibited the lowest TSH (2.43 ± 0.06 μIU/mL) among chelators (p < 0.001). Ferritin strongly correlated with TSH (r = 0.94, p < 0.001) and independently predicted TSH levels (coefficient = 0.0010, p = 0.048). ICT also preserved hepatic (ALT: 50.55 ± 41.87 vs. 291.36 ± 161.99 U/L, p < 0.001) and renal function (creatinine: 0.97 ± 0.22 vs. 1.65 ± 0.34 mg/dL, p < 0.001). ICT, particularly deferasirox, protects against thyroid dysfunction in TDT, with ferritin as a key predictor. These findings support personalized chelation strategies and routine endocrine monitoring in thalassemia management.
Transfusion-Dependent Thalassemia (TDT) causes severe anemia requiring chronic transfusions, leading to iron overload and endocrine complications, including hypothyroidism. Iron chelation therapy (ICT) mitigates iron toxicity, but its effects on thyroid function remain understudied in resource-limited settings like Pakistan. This cross-sectional study compared 100 TDT patients receiving ICT (deferasirox, deferoxamine, or deferiprone) for ≥ 6 months with 100 Control group who have not taken ICT. Thyroid function tests (free T3, free T4, TSH), serum ferritin, and hepatic/renal biomarkers were analyzed. Statistical analyses included t-tests, ANOVA, Pearson correlation, and multivariate regression (SPSS v25). ICT-treated patients had significantly lower TSH (3.10 ± 0.62 vs. 9.95 ± 3.19 μIU/mL, p < 0.001) and higher free T3/T4 levels than controls (p < 0.001). Deferasirox users exhibited the lowest TSH (2.43 ± 0.06 μIU/mL) among chelators (p < 0.001). Ferritin strongly correlated with TSH (r = 0.94, p < 0.001) and independently predicted TSH levels (coefficient = 0.0010, p = 0.048). ICT also preserved hepatic (ALT: 50.55 ± 41.87 vs. 291.36 ± 161.99 U/L, p < 0.001) and renal function (creatinine: 0.97 ± 0.22 vs. 1.65 ± 0.34 mg/dL, p < 0.001). ICT, particularly deferasirox, protects against thyroid dysfunction in TDT, with ferritin as a key predictor. These findings support personalized chelation strategies and routine endocrine monitoring in thalassemia management.
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