Association Between the Monocyte-to-Lymphocyte Ratio and Hemoglobin Levels in Lung Cancer Patients

Cancer-related anemia is common and associated with reduced quality of life, treatment intolerance, and poorer outcomes. Inflammation plays a central role in anemia of chronic disease, yet the specific inflammatory phenotype linked to reduced erythropoiesis remains poorly defined. The monocyte-to-lymphocyte ratio (MLR) reflects chronic macrophage-driven inflammation and may offer insight into erythropoietic suppression in cancer. The aim of this study was to evaluate the association between complete blood count (CBC)-derived inflammatory ratios and erythropoietic parameters in lung cancer patients, with particular focus on the monocyte-to-lymphocyte ratio.

This retrospective cross-sectional study included 90 adult lung cancer patients with CBC data, including neutrophils, lymphocytes, monocytes, platelets, hemoglobin, and hematocrit. The first available laboratory panel for each patient was analyzed. Derived inflammatory ratios included MLR, neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR). Correlations between inflammatory markers and erythropoietic parameters (hemoglobin, hematocrit) were evaluated using Spearman's rank correlation coefficient in a complete-case cohort.

MLR showed a moderate inverse correlation with hemoglobin (ρ=-0.34, p=0.001) and hematocrit (ρ=-0.31, p=0.003). PLR demonstrated weaker inverse correlations with hemoglobin (ρ=-0.24, p=0.026) and hematocrit (ρ=-0.25, p=0.019). NLR showed minimal correlation with hemoglobin (ρ=-0.12, p=0.251) and hematocrit (ρ=-0.12, p=0.248). Hemoglobin and hematocrit were strongly correlated (ρ=0.97, p<0.001), consistent with their physiological relationship.

Monocyte-associated inflammation is selectively linked to erythropoietic suppression in cancer patients. CBC-derived inflammatory ratios may serve as practical indicators of anemia of chronic disease and support the role of macrophage-driven inflammation in cancer-related anemia. These findings warrant further investigation into the inflammation-erythropoiesis axis and its clinical implications.