Ferritin as a Dual-Purpose Biomarker: Unraveling its Role in Iron Storage and as a Surrogate for Tumor Burden in CML

Background: Hyperferritinemia observed in patients with chronic myeloid leukemia (CML) presents an interpretive challenge, as its underlying cause may be attributable to either iron overload or an inflammatory response associated with the tumor. Accurate identification of the primary driver is essential for precise clinical assessment. Objective: This investigation sought to elucidate the principal cause of elevated ferritin levels in patients with newly diagnosed chronic myeloid leukemia (CML) and to assess the diagnostic effectiveness and utility of the calculated Iron/Ferritin and TIBC/Ferritin ratios. Materials and Methods: This retrospective, cross-sectional study involved 90 adult patients with untreated chronic-phase CML. At diagnosis, serum ferritin, lactate dehydrogenase (LDH), iron levels, and total iron-binding capacity (TIBC) were measured. The relationships between ferritin, LDH, and iron parameters were examined using Spearman’s correlation and multiple linear regression, with ferritin log10-transformed. Patients were divided at the median LDH level, and the Mann-Whitney U test was used to compare the proposed ratios between groups with high and low disease burden. Results: The cohort demonstrated pronounced hyperferritinemia, with a median ferritin level of 339.5 μg/L, and elevated lactate dehydrogenase (LDH), with a median of 269.2 U/L. Concurrently, serum iron and total iron-binding capacity (TIBC) were markedly reduced. A moderate positive correlation was observed between ferritin and LDH (ρ=0.52, p