Background/Objectives: Imatinib, a first-generation tyrosine kinase inhibitor, is the standard treatment for chronic myeloid leukemia (CML). Although generic formulations have improved access, concerns regarding their efficacy and safety remain. This study aimed to compare the clinical outcomes and adverse events of original and generic imatinib in patients with CML in Thailand. Methods: We conducted a retrospective cohort study of patients with chronic-phase CML receiving frontline imatinib at Chiang Mai University Hospital between January 2012 and September 2022. Treatment responses, event-free survival (EFS), overall survival (OS), and adverse events were also analyzed. Results: Among the 71 patients, 46 (64.8%) received original imatinib, and 25 (35.2%) received generic imatinib. The median follow-up period was 80.3 months (IQR: 52.0–106.4). At 12 months, there were no significant differences in the cumulative complete cytogenetic response (73.3% vs. 70.8%, p = 0.825) or major molecular response (35.6% vs. 41.7%, p = 0.618). Although EFS was not significantly different between the groups, OS was significantly longer in patients receiving original imatinib (p < 0.001). Conclusions: Although early treatment responses and EFS were similar, generic imatinib was associated with an inferior OS. These findings highlight the need for close monitoring and further evaluation of long-term outcomes when using generic formulations.

Thalassemia is a hereditary hemoglobinopathy characterized by ineffective erythropoiesis, chronic hemolysis, and transfusion-related iron overload, which collectively contribute to oxidative stress and organ dysfunction. The present study aimed to investigate the relationships between iron metabolism, oxidative stress biomarkers, and immune cell function across different clinical conditions. Peripheral blood samples were obtained from healthy individuals and patients with iron deficiency anemia, obesity, thalassemia trait (TT), β-thalassemia HbE (BTE), and β-thalassemia major (BTM). Hematological parameters were measured using automated hematology analyzers, while biochemical indicators, including liver enzymes and bilirubin, were determined using clinical chemistry assays. Iron overload was evaluated using serum iron parameters and T2*-weighted magnetic resonance imaging. Oxidative stress biomarkers, including reduced glutathione, thiobarbituric acid-reactive substances, and total antioxidant capacity, were assessed spectrophotometrically. Flow cytometric analysis was used to measure reactive oxygen species, redox-active iron, and lipid peroxide levels in granulocytes and lymphocytes. Thalassemia patients exhibited severe anemia, elevated liver enzymes, increased bilirubin levels, and significant alterations in iron metabolism compared with healthy controls. Hepatic iron accumulation was more common than cardiac iron deposition, particularly in BTE patients. Granulocyte oxidative burst activity was significantly reduced in thalassemia patients, whereas lymphocyte responses remained relatively preserved. Increased variability in glutathione levels suggested activation of intracellular antioxidant defense mechanisms in response to chronic oxidative stress. These findings highlight the complex interplay between iron overload, oxidative stress, and the immune cell dysfunction associated with thalassemia, thereby providing insights into improved monitoring and therapeutic strategies.