Key result
Pleural adenosine deaminase effectively diagnoses inflammatory exudates with an AUC of ~0.81.
Why the study?
Mechanisms of action in pleural inflammatory diseases remain unclear, prompting investigation into the role of total pleural ADA levels in their diagnosis.
Does total pleural ADA (P-ADA) level accurately diagnose pleural inflammatory diseases?
Cohort (n=157)
Yes
Does total pleural ADA (P-ADA) level accurately diagnose pleural inflammatory diseases?
Pleural ADA levels ≥ 9.00 U/L demonstrate high diagnostic performance for identifying pleural inflammatory exudates.
P-ADA ≥9 U/L may aid pleural exudate diagnosis; leaves open prospective validation before clinical adoption.
BACKGROUND Although inflammatory diseases commonly affect the pleura and pleural space, their mechanisms of action remain unclear. The presence of several mediators emphasizes the concept of pleural inflammation. Adenosine deaminase (ADA) is an inflammatory mediator detected at increased levels in the pleural fluid. AIM To determine the role of total pleural ADA (P-ADA) levels in the diagnosis of pleural inflammatory diseases. METHODS 157 patients with inflammatory pleural effusion (exudates, n = 124, 79%) and non-inflammatory pleural effusion (transudates, n = 33, 21%) were included in this observational retrospective cohort study. The P-ADA assay was tested using a kinetic technique. The performance of the model was evaluated using the area under the receiver operating characteristic (ROC) curve (AUC). The ideal cutoff value for P-ADA in pleural inflammation was determined using the Youden index in the ROC curve. RESULTS The transudates included congestive heart failure (n = 26), cirrhosis of the liver with ascites (n = 3), chronic renal failure (n = 3), and low total protein levels (n = 1). The exudate cases included tuberculosis (n = 44), adenocarcinoma (n = 37), simple parapneumonic effusions (n = 15), complicated parapneumonic effusions/empyema (n = 8), lymphoma (n = 7), and other diseases (n = 13). The optimal cutoff value of P-ADA was ≥ 9.00 U/L. The diagnostic parameters as sensitivity, specificity, positive and negative predictive values, positive and negative likelihood values, odds ratio, and accuracy were 77.69 (95%CI: 69.22-84.75); 68.75 (95%CI: 49.99-83.88); 90.38 and 44.90 (95%CI: 83.03-95.29; 30.67-59.77); 2.48 and 0.32 (95%CI: 2.21-11.2; 0.27-0.51); 7.65 (95%CI: 0.78-18.34), and 75.82 (95%CI: 68.24-82.37), respectively (χ² = 29.51, P = 0.00001). An AUC value of 0.8107 (95%CI: 0.7174-0.8754; P = 0.0000) was clinically useful. The Hosmer-Lemeshow test showed excellent discrimination. CONCLUSION P-ADA biomarker has high diagnostic performance for pleural inflammatory exudates.
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Maranhão et al. (2025) conducted a cohort in Pleural effusion syndrome (n=157). Total pleural adenosine deaminase (P-ADA) vs. Non-inflammatory pleural effusion (transudates) was evaluated on Diagnosis of pleural inflammatory diseases (exudates) (AUC 0.8107, 95% CI 0.7174-0.8754, p=0.0000). Total pleural adenosine deaminase at a cutoff of ≥ 9.00 U/L effectively diagnosed pleural inflammatory exudates with an AUC of 0.8107.
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