title: Pleural effusion and serum soluble fas-ligand levels are elevated in different clinical conditions.
abstract: Fas ligand (FasL) plays an important role in the regulation of apoptosis. Soluble FasL (sFasL) is produced by a cleavage of FasL from the cell surface by metalloproteinase. Whether or not sFasL exists or is elevated in the pleural effusion of different etiologies is unknown. The present study is designed to determine pleural effusion and serum sFasL levels under different clinical conditions, and ascertain if there exists a significant difference in the levels found in different clinical conditions, and whether this difference can be used as a tool for differential diagnosis. Soluble FasL levels in the pleural effusion and serum of 103 patients, including 37 with malignant pleural effusion, 24 with uncomplicated parapneumonic effusion, 8 with bacterial empyema, 16 with tuberculous pleurisy, and 18 with transudate effusion (8 with congestive heart failure and 10 with viral liver cirrhosis), were analyzed with ELISA assays. Pleural effusion from patients with bacterial empyema (median 79.4 pg/ml) and TB pleurisy (median 31.9 pg/ml) contained significantly higher amounts of sFasL than the pleural effusion from all other conditions studied (p <0.001). Viral liver cirrhosis had a significantly higher serum sFasL level (median 53.6 pg/ml, p = 0.025, when compared with other patients). Patients with congestive heart failure had the lowest serum sFasL levels when compared with other patients (p = 0.014). There was no significant correlation between pleural effusion sFasL levels and other parameters, such as effusion LDH, cell count, neutrophil, and lymphocyte percentage. In conclusion, soluble FasL is a useful marker for the differentiation of bacterial empyema and TB pleurisy from other disease entities. In addition, the elevation of serum sFasL levels in viral liver cirrhosis can also be used to differentiate cirrhosis from congestive heart failure, in which both effusions are transudate.
authors.affiliation: Chest Department, School of Medicine, Taipei Veterans General Hospital, National Yang-Ming University, Taipei, Taiwan, R.O.C.
authors.forename: P S
authors.initials: PS
authors.lastname: Wang
authors.forename: Y M
authors.initials: YM
authors.lastname: Chen
authors.forename: Y L
authors.initials: YL
authors.lastname: Hsieh
authors.forename: C F
authors.initials: CF
authors.lastname: Yu
authors.forename: C M
authors.initials: CM
authors.lastname: Tsai
authors.forename: R P
authors.initials: RP
authors.lastname: Perng
mesh_terms: D000368:Aged; D017209:Apoptosis; D015415:Biomarkers; D003937:Diagnosis, Differential; D053222:Fas Ligand Protein; D005260:Female; D006333:Heart Failure / Q000175:diagnosis; D006801:Humans; D008103:Liver Cirrhosis / Q000175:diagnosis; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism*; D010996:Pleural Effusion / Q000378:metabolism*; D016066:Pleural Effusion, Malignant / Q000378:metabolism*
chemical_list: D015415:Biomarkers; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins