Impact of Beta-Thalassemia Trait on Clinical Outcomes and Treatment Response in Chronic Myeloid Leukemia

Background and aim The coexistence of beta-thalassemia trait and chronic myeloid leukemia (CML) is rare, and the clinical implications of this overlap remain poorly defined. Hematologic alterations associated with beta-thalassemia trait, such as microcytosis, elevated RBC counts, and compensatory marrow activity, may influence CML diagnosis, prognostic scoring, and treatment response. Understanding these interactions is clinically important for accurate risk stratification and individualized treatment planning. This study aimed to determine whether beta-thalassemia trait affects baseline clinical characteristics, tyrosine kinase inhibitor (TKI) treatment response, transfusion requirements, and survival outcomes in patients with chronic myeloid leukemia. Additionally, this study aimed to evaluate whether thalassemia-associated hematologic features influence established prognostic scoring systems. Methods This retrospective cohort study included patients diagnosed with CML who were treated at the National Hematology and Blood Transfusion Center in Baku, Azerbaijan. Patients were stratified by confirmed beta-thalassemia trait status. Baseline laboratory parameters, prognostic risk categories (Sokal, Hasford, European Treatment and Outcome Study {EUTOS} score), molecular response milestones, transfusion frequency, treatment modifications, and survival outcomes were compared. Statistical analyses included chi-square tests, Fisher's exact tests, independent t-tests, and Kaplan-Meier survival analysis. Effect estimates were reported with p-values and absolute differences where relevant. Ethics approval or waiver was obtained from the institutional review board. Results Among 848 CML patients, 15 (1.8%) had beta-thalassemia trait; 30 age- and sex-matched non-trait controls were selected. Trait prevalence was significantly lower than expected from the national background rate (p=0.00018). Trait carriers showed lower mean corpuscular volume (p<0.001), higher platelet counts (p=0.045), and more frequent Sokal low-risk classification (p=0.041). Time to major molecular response did not differ significantly (15.3 vs. 16.3 months; p=0.291). TKI switching was less common among trait carriers (46.7% vs. 66.7%; p=0.218). Transfusion needs were higher in the trait group (40% vs. 13.3%; p=0.099). No statistically significant differences were found in progression or survival outcomes. Conclusions and relevance Beta-thalassemia trait influences baseline hematologic profiles and risk stratification in CML but does not impair the effectiveness of tyrosine kinase inhibitors or survival. The higher transfusion rates suggest the need for closer anemia monitoring. Additional multicenter research is warranted to guide personalized management in CML patients with underlying hemoglobinopathies.