title: Diagnostic role of inflammatory and anti-inflammatory cytokines and effector molecules of cytotoxic T lymphocytes in tuberculous pleural effusion.
abstract: OBJECTIVE
  Early diagnosis of tuberculous pleural effusion (TPE) remains difficult. While some inflammatory markers in pleural effusion (PE) are helpful in diagnosis, the roles of anti-inflammatory cytokines and effector molecules of cytotoxic T lymphocytes have not been investigated.
  
  
  METHODS
  Lymphocyte-predominant exudative PE samples were assayed for inflammatory and anti-inflammatory cytokines and effector molecules of cytotoxic T lymphocytes. Logistic regression analysis was used to predict the probability of TPE and identify independently associated factors. Receiver operating characteristic (ROC) curve analysis was applied to determine the optimal cut-off value for the predicted probability.
  
  
  RESULTS
  Of 95 patients enrolled, 35 had TPE, 46 had malignant PE and 14 had PE due to other aetiologies. Interferon-γ (IFN-γ), adenosine deaminase (ADA), decoy receptor (DcR) 3, monocyte chemo-attractant protein (MCP)-1, IFN-induced protein (IP)-10, granzyme A and perforin were higher in TPE than in PE of other aetiologies. By logistic regression analysis, IFN-γ ≥ 75 pg/mL, ADA ≥ 40 IU/mL, DcR3 ≥ 9.3 ng/mL and soluble tumour necrosis factor receptor 1 (TNF-sR1) ≥ 3.2 ng/mL were independent factors associated with TPE. The predicted probability based on the four predictors had an area under the ROC curve of 0.920, with 82.9% sensitivity and 86.7% specificity under the cut-off value of 0.303. In the TPE group, patients with positive PE/pleural culture for Mycobacterium tuberculosis had higher pleural IFN-γ, MCP-1, IP-10 and perforin than those with positive sputum but negative PE culture.
  
  
  CONCLUSIONS
  While pleural interferon-γ and ADA are conventional markers for diagnosing TPE, simultaneous measurements of DcR3 and TNF-sR1 can improve the diagnostic efficacy.
authors.affiliation: Department of Traumatology, National Taiwan University Hospital, Taipei, Taiwan; Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan; Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
authors.forename: Chin-Chung
authors.initials: CC
authors.lastname: Shu
authors.forename: Jann-Yuan
authors.initials: JY
authors.lastname: Wang
authors.forename: Chia-Lin
authors.initials: CL
authors.lastname: Hsu
authors.forename: Li-Ta
authors.initials: LT
authors.lastname: Keng
authors.forename: Kochung
authors.initials: K
authors.lastname: Tsui
authors.forename: Jeng-Feng
authors.initials: JF
authors.lastname: Lin
authors.forename: Hsin-Chih
authors.initials: HC
authors.lastname: Lai
authors.forename: Chong-Jen
authors.initials: CJ
authors.lastname: Yu
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Lee
authors.forename: Kwen-Tay
authors.initials: KT
authors.lastname: Luh
mesh_terms: D000243:Adenosine Deaminase / Q000378:metabolism; D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007371:Interferon-gamma / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009169:Mycobacterium tuberculosis / Q000302:isolation & purification / Q000472:pathogenicity; D054353:Perforin / Q000378:metabolism; D010996:Pleural Effusion / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D012372:ROC Curve; D053323:Receptors, Tumor Necrosis Factor, Member 6b / Q000378:metabolism*; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood*; D012680:Sensitivity and Specificity; D013602:T-Lymphocytes, Cytotoxic / Q000473:pathology*; D014396:Tuberculosis, Pleural / Q000150:complications / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D053323:Receptors, Tumor Necrosis Factor, Member 6b; D047888:Receptors, Tumor Necrosis Factor, Type I; D054353:Perforin; D007371:Interferon-gamma; D000243:Adenosine Deaminase
keywords: adenosine deaminase; decoy receptor 3; interferon-γ; soluble tumour necrosis factor receptor 1; tuberculous pleural effusion