β-thalassemia major (b-TM) is a severe hereditary hemoglobinopathy that remains a significant public health concern in Azerbaijan due to its relatively high carrier frequency and regional prevalence. In addition to chronic anemia resulting from defective hemoglobin synthesis, the disease is characterized by profound disturbances in iron metabolism and mineral homeostasis, largely driven by ineffective erythropoiesis and long-term transfusion therapy. This review aims to summarize current evidence on alterations in iron regulatory and calcium-phosphorus metabolism markers in patients with b-TM. Recent studies have highlighted the central role of iron metabolism markers, including ferritin, hepcidin, and ferroportin, in assessing iron overload and dysregulated iron homeostasis in transfusion-dependent thalassemia. Suppression of hepcidin and increased ferroportin activity contribute to excessive iron absorption and systemic iron accumulation, leading to multisystem complications. In parallel, growing evidence indicates that disturbances in calcium-phosphorus homeostasis represent a major non-hematological complication of b-TM. Alterations in parathyroid hormone and vitamin D metabolism, along with emerging regulators such as fibroblast growth factor-23 (FGF-23), play a critical role in bone and mineral disorders observed in affected patients.
Hamidova et al. (Wed,) studied this question.