Pancreatic dysfunction in thalassemia major: The impact of iron overload on exocrine and endocrine functions

The pancreas is a critical organ with dual endocrine and exocrine functions, integral to digestion and glucose regulation. In thalassemia major, chronic blood transfusions lead to systemic iron overload, resulting in pancreatic hemosiderosis. This condition causes significant structural and functional damage, including acinar cell atrophy, fibrosis, exocrine pancreatic insufficiency (EPI), and beta-cell dysfunction, which predisposes patients to diabetes. Advanced imaging modalities like MRI T2* have revealed a strong correlation between pancreatic iron overload and these complications, demonstrating superior accuracy over traditional markers such as serum ferritin. Results: It indicate that 85% of patients with pancreatic iron overload exhibited signs of EPI, characterized by malabsorption, steatorrhea, and severe nutrient deficiencies. Similarly, endocrine dysfunction was observed in 75% of cases, manifesting as impaired insulin secretion and glycemic abnormalities. MRI T2* imaging proved 90% effective in detecting subclinical pancreatic dysfunction, outperforming serum ferritin as a predictive tool. Chelation therapy was effective in reducing pancreatic iron levels in 80% of cases, but therapeutic response varied depending on the adherence and intensity of treatment regimens. Enzyme replacement therapy for EPI and glycemic control interventions improved the quality of life in patients with advanced dysfunction. Discussion: Explores the interplay between iron overload and pancreatic dysfunction. Pancreatic hemosiderosis disrupts digestive enzyme secretion, leading to nutritional deficiencies and exocrine dysfunction. Concurrently, beta-cell damage impairs glucose metabolism, heightening the risk of diabetes, particularly in patients with prolonged iron exposure. MRI T2* has revolutionized early detection, enabling the identification of subclinical pancreatic dysfunction and informing targeted interventions. Chelation therapy remains the cornerstone of management, but its effectiveness is influenced by patient compliance and the choice of agents. Adjunctive treatments such as enzyme replacement and insulin therapy are critical for addressing the multifaceted burden of pancreatic dysfunction. This review underscores the need for an integrated approach combining early diagnostic imaging, tailored chelation strategies, and supportive therapies to mitigate complications and improve outcomes in thalassemia major patients. Longitudinal studies are essential to further understand the progression of pancreatic dysfunction and refine therapeutic strategies.