Risk Factors for Impaired Glucose Metabolism in Transfusion-Dependent Patients with β-Thalassemia: A Single-Center Retrospective Observational Study

Abstract

Background/Objectives: B-thalassemia is a genetic disorder that leads to reduced or absent β-globin chains, often resulting in endocrine abnormalities due to iron overload, chronic anemia, and hypoxia. This study investigates the prevalence and risk factors for glucose metabolism disturbances in transfusion-dependent β-thalassemia (TDT) patients, focusing on pancreatic iron overload and its association with other iron biomarkers. Methods: We studied two groups of TDT patients (2018–2022) at Hippokration General Hospital: Group 1 (no glucose metabolism impairment, n = 46) and Group 2 (with impaired glucose tolerance or diabetes mellitus, n = 18). Patients were assessed for factors contributing to glucose disturbances, and laboratory data were analyzed. Type 2 diabetes was diagnosed per American Diabetes Association criteria, and impaired glucose tolerance was defined by OGTT results. A multivariate logistic regression identified potential independent risk factors. In a subset of patients on iron chelation therapy, we examined the relationship between pancreatic, liver, and heart iron overload (T2* MRI) and glucose/ferritin levels. Results: Age and elevated serum GGT levels were significantly associated with impaired glucose metabolism (p = 0.02). Beta-blocker use was correlated with glucose disturbances (p = 0.02), but multivariate analysis revealed no significant independent risk factors. A significant relationship was found between pancreatic and heart iron overload (r = 0.45, p = 0.04). Conclusions: Elevated GGT levels suggest that oxidative stress and liver dysfunction play a key role in glucose metabolism disturbances. Pancreatic MRI T2* may help predict heart iron overload. Further research is needed to identify reliable biomarkers for glucose regulation in TDT.