ArticleJournal of thoracic disease2026
Pleural fluid C-C motif chemokine ligand 2 as a diagnostic biomarker for malignant pleural effusion.
Article in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Accurate diagnosis of malignant pleural effusion (MPE) using biomarkers remains challenging. C-C motif chemokine ligand 2 (CCL2) is involved in immune regulation and has been implicated in the pleural immune microenvironment associated with MPE. This study aimed to evaluate the diagnostic accuracy of CCL2 for MPE. Methods: From June 2019 to April 2022, 184 patients with exudative pleural effusion admitted to our hospital were enrolled and randomly divided into a training group (70.1%, n=129) and an internal validation group (29.9%, n=55). Clinical indicators, including pleural fluid carcinoembryonic antigen (CEA), were collected. Pleural fluid CCL2 concentrations were determined using enzyme-linked immunosorbent assay. Analyses included receiver operating characteristic (ROC) curves, univariate logistic regression, and nomogram construction. Model performance was evaluated by the area under the curve (AUC), concordance index (c-index), and calibration plots. Results: Pleural fluid CCL2 levels were significantly higher in MPE than in non-MPE cases (cut-off value =612.5 pg/mL, AUC =0.734, sensitivity =61.7%, specificity =74.1%), whereas adenosine deaminase (ADA) levels were lower. Compared with other pleural fluid biochemical indicators, pleural fluid CCL2 showed competitive diagnostic accuracy, particularly for exclusion diagnosis (negative predictive value =76.9%). In addition, CCL2 exerts a significant stratification effect on the diagnosis of MPE subgroups, especially in the ADA ≥26.5 U/L group, chloride ≥109.25 mmol/L group, and CEA ≥2.62 ng/mL group, where its diagnostic efficacy is more prominent. A nomogram incorporating pleural fluid CCL2, age, and ADA demonstrated strong discriminative performance in the training cohort (AUC =0.981; sensitivity =92.7%; specificity =100%). The c-index was 0.981, indicating good agreement between predicted and observed outcomes. Internal validation analyses further supported the robustness of the model, with AUC values exceeding 0.90. Conclusions: Pleural fluid CCL2 may serve as a useful adjunctive biomarker for the diagnostic evaluation of MPE. A CCL2-based nomogram integrating age and ADA demonstrated strong discriminative performance in internal analyses, suggesting its potential value as a minimally invasive aid for MPE identification.
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