Diagnostic Performance of D-dimer in Predicting Pulmonary Embolism in Tuberculosis Pleural Effusion Patients.

Abstract Background: Tuberculosis pleural effusion patients always have elevated D-dimer levels. How D-dimer performance in predicting pulmonary embolism in TPE population is unclear. The aim of this study was to assess the diagnostic performance of D-dimer for pulmonary embolism in TPE population and explore the potential mechanism of PE in TPE patients.Methods: We retrospectively analyzed patients who were admitted to Xinhua hospital and Weifang Respiratory Disease Hospital with a final diagnosis of TPE between March 2014 and January 2020. Data including demographics, history, symptoms, D-dimer, C-reactive protein (CRP), white blood cell (WBC) and erythrocyte sedimentation rate (ESR) as well as the cytokines such as IL-6, IL-8, TNF-α, IL-2 receptor of the first blood test, imaging results including computed tomography pulmonary angiography (CTPA) and compression ultrasound (CUS) with Doppler were collected and analyzed. Results: 248 patients (male=170, female=78) at the age of 43±20.6 years were final included in this study. Elevated D-dimer (≥0.5mg/L) was detected in 186/248 (75%) patients. 150 patients received CTPA examination. PE was diagnosed in 29/150 (19.3%) patients. Among the TPE population, PE patients had significantly higher DD level than that of non-PE patients (2.26±0.96 mg/L VS 1.06±0.73 mg/L) (P＜0.05). An optimized cut off value for D-dimer in predicting PE in TPE was 1.18 mg/L, with a sensitivity of 89.7% and a specificity of 77.8 % ( area under curve was 0.893; 95% CI: 0.839-0.947; P＜0.01). PE patients had lower median WBC and IL-8 values (5.14Ⅹ109/L VS 6.1Ⅹ109/L, P＜0.05 ; 30.2 pg/ml VS 89.7 pg/ml, P＜0.05) but higher median IL-2 receptor value (1964.8 pg/ml VS 961.2 pg/ml, P＜0.01) than that of non-PE patients.Conclusions: D-dimer is still an objective biomarker to predict PE in TPE patients. In order to avoid unnecessary radiological test, the cut off value of D-dimer in TPE patients should be set at 1.18 mg/L. In addition, the imbalance of prothrombotic and antithrombotic cytokines may partly attribute to the formation of pulmonary embolus in TPE patients.