Background: Ineffective erythropoiesis is a predominant feature in β-thalassemia major (β-TM), causing marked erythroid expansion leading to highly raised levels of growth differentiation factor-15 (GDF-15), which, in turn, suppresses hepcidin production in liver resulting in increased iron absorption from gut. We aim to study the serum GDF-15 in polytransfused β-TM patients and its correlation with serum ferritin and serum hepcidin.
Method: Thirty-nine polytransfused β-TM children aged between 5 and 17 years and 33 age- and gender-matched healthy controls were enrolled in the study. Complete blood count, serum GDF-15, serum ferritin, and serum hepcidin were performed.
Results: The mean serum GDF-15, serum hepcidin, and serum ferritin levels were 638.65 ± 306.96 pg/ml, 108.21 ± 191.30 ng/ml, and 2274.60 ± 1216.08 ng/ml, respectively, which were significantly higher than control group (P < 0.001, P = 0.003, P < 0.001, respectively). There was significant positive correlation of GDF-15 with blood transfusions (r = 0.415, P = 0.009), positive correlation with serum ferritin (r = 0.653, P = 0), and significant negative correlation with serum hepcidin (r = -0.508, P = 0.001).
Conclusion: The findings of the present study suggest that GDF-15 is an important regulator of hepcidin in β-TM patients. GDF-15 and serum hepcidin together can be used to monitor iron overload and its related complications in such patients.
Keywords: GDF-15; ferritin; hepcidin; β-Thalassemia.