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Ann Thorac Surg 2009;87:251-254. doi:10.1016/j.athoracsur.2008.09.047
© 2009 The Society of Thoracic Surgeons

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Original Articles: General Thoracic

Soluble Triggering Receptor Expressed on Myeloid Cells-1 for Diagnosing Empyema

Jihad Bishara, MDa,*, Elad Goldberg, MDa, Shai Ashkenazi, MDd,e, Yael Yuhas, PhDd, Zmira Samra, PhDb, Milton Saute, MDc, Hila Shaked, MDa

a Infectious Diseases Unit, Tel Aviv University, Petah-Tiqwa, Israel
b Laboratory of Clinical Microbiology, Tel Aviv University, Petah-Tiqwa, Israel
c Department of Thoracic Surgery, Rabin Medical Center, Beilinson Hospital, Sackler Faculty of Medicine, Tel Aviv University, Petah-Tiqwa, Israel
d Laboratory of Infectious Diseases, Felsenstein Medical Research Center, Petah-Tiqwa, Israel
e Infectious Diseases Unit, Schneider Children's Medical Center of Israel, Petah-Tiqwa, Israel

Accepted for publication September 19, 2008.

* Address correspondence to Dr Bishara, Infectious Diseases Unit, Rabin Medical Center, Beilinson Hospital, Petah-Tiqwa, 49100, Israel (Email: bishara{at}netvision.net.il).

Background: Studies have shown that soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is upregulated by microbial products in the bronchoalveolar lavage fluid, and cerebrospinal fluid of patients with pneumonia and bacterial meningitis, respectively. Our goal was to evaluate whether sTREM-1 in pleural fluid can distinguish pleural empyema from postthoracotomy-related pleural effusion and effusions of other etiologies.

Methods: Patients who presented with pleural effusion were identified through laboratory records. In addition to routine biochemical markers, differential white blood cells, cytology, Gram stain, and pleural fluid culture, pleural fluid sTREM-1 was measured by enzyme-linked immunosorbent assay using a commercial kit (R&D Systems, Minneapolis, MN).

Results: Eighty-nine patients were included in the study: 17 with empyema, 7 simple parapneumonic effusion, 18 transudate, 12 postthoracotomy pleural effusion, 22 malignancy, 1 connective tissue disease, and 12 with undetermined effusion. Mean levels of sTREM-1 were significantly higher in empyema than in postthoracotomy pleural effusion (687 ± 479 pg/mL vs 34 ± 81 pg/mL, p < 0.0001, respectively) and in effusions of other etiologies (15 ± 54 pg/mL, p < 0.0001). A cutoff value of 114 pg/mL for pleural sTREM-1achieved a sensitivity of 94% and a specificity of 93% in differentiating empyema from pleural effusions of other etiologies. The area under the receiver operating characteristic curve for pleural effusion sTREM-1 as a predictor for empyema was 0.966.

Conclusions: Our findings suggest that sTREM-1 in the pleural fluid can potentially assist clinicians in the differentiation of bacterial from nonbacterial pleural effusion, particularly in postthoracotomy pleural effusion.







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