• Tuberculosis and Respiratory Diseases
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• v.75 no.6
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• pp.244-249
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• 2013

Background: Conventional biomarkers cannot always establish the cause of pleural effusions; thus, alternative tests permitting rapid and accurate diagnosis are required. The primary aim of this study is to assess the ability of pentraxin-3 (PTX3) in order to diagnose the cause of pleural effusion and compare its efficacy to that of other previously identified biomarkers. Methods: We studied 118 patients with pleural effusion, classified as transudates and exudates including malignant, tuberculous, and parapneumonic effusions (MPE, TPE, and PPE). The levels of PTX3, C-reactive protein (CRP), procalcitonin (PCT) and lactate in the pleural fluid were assessed. Results: The levels of pleural fluid PTX3 were significantly higher in patients with PPE than in those with MPE or TPE. PTX3 yielded the most favorable discriminating ability to predict PPE from MPE or TPE by providing the following: area under the curve, 0.74 (95% confidence interval, 0.63-0.84), sensitivity, 62.07%; and specificity, 81.08% with a cut-off point of 25.00 ng/mL. Conclusion: Our data suggests that PTX3 may allow improved differentiation of PPE from MPE or TPE compared to the previously identified biomarkers CRP and PCT.

• The Korean Journal of Cytopathology
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• v.6 no.2
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• pp.106-115
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• 1995

Reactive humsn mesothelial cells were examined by immunocytochemical stain with intermediate filaments (cytokeratin [CK1, CK7, CK8, CK18, CD19), vimentin, desmin, actin), epithelial membrane antigen, carcinoembryonic antigen (CEA), MHC class II antigen (HLA-DR), LeuM-1 (CD15), $\alpha1-antitrypsin$(ACT), $\alpha1-antichymotrypsin$ (ACHT), CD68(KP-1) and FcyRIII(CD16). The mesothelial cells were isolated from patients with liver cirrhosis and pleural effusion, and short-term cultured in RPMI 1640 media containing 10% heat inactivated fetal calf serum and 1% identical supernatant fluid of the patients' transudates. The results obtained are as follows 1. The cultured-reactive mesothelial cells were positive for the protein of cytoskeleton such as cytokeratin and vimentin, but negative for desmin and actin. The resting mesothelial cells showed positive reactions for cylokeratin, but negative for vimentin, desmin and actin. 2. The primary antibodies to the cytokeratin were strongly reactive for CK1, CK8 and CK18 but negative for CK7 and CK19 in both reactive and resting mesothelial cells. 3. Resting mesothelial cells showed negative reactions for CEA, but strong positive reactions in cultured-reactive mesothelial cells. 4. The markers for the monocytes/histiocytes(CD11b, CD14, CD16, CD68, Iysozyme and $\alpha1-antitrypsin$ and $\alpha1-antichymotrypsin$) were nonreactive in resting mesothelial cells, but lysozyme and $\alpha1-antitrypsin$ were weakly reactive in reactive and proliferative mesothelial cells. 5. MHC Class II molecule(HLA-DR antigen) was negative in both resting and reactive mesothelial cells. These results suggest that the short-term cultured, reactive mesothelial cells show a newly aberrant expression of the vimentin and calcine-embryonic antigen. The reason of the aberrant expression of the intermediate filament and oncofetal antigen in reactive and proliferative mesothelial cells should be further evaluated.

• Tuberculosis and Respiratory Diseases
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• v.63 no.4
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• pp.353-361
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• 2007

Background: Malignancies are a common and important causes of exudative pleural effusions. Several tumor markers have been studied because the pleural fluid cytology and pleural biopsy specimens do not provide a diagnosis in a high percentage of malignant effusions. In an attempt to overcome this limitation, procalcitonin and C-reactive protein (CRP) in pleural effusions and serum, which are known to be inflammation markers, were measured to determine if they can differentiate an exudate from trasndate as well as the diverse causes of exudative pleural effusion. Methods: 178 consecutive patients with pleural effusion (malignant 57, tuberculous 51, parapneumonic 31, empyema 5, miscellaneous benign 7, transudative 27)were studied prospectively. The standard parameters of pleural effusion and measured serum and pleural procalcitonin were examined using in immunoluminometric assay. The level of CRP in serum and pleural fluid was determined by turbidimetric immunoassay. Results: The pleural procalcitonin levels in the exudate were significantly higher than those in the transudate, $0.81{\pm}3.09ng/mL$ and $0.12{\pm}0.12ng/mL$, respectively (p=0.007). The pleural CRP levels were significantly higher in the exudate than the transudate, $2.83{\pm}3.31mg/dL$ and $0.74{\pm}0.67mg/dL$, respectively (p<0.001). The pleural procalcitonin levels in the benign effusion were significantly higher than those in the malignant effusion, $1.15{\pm}3.82ng/mL$ and $0.25{\pm}0.92ng/mL$, respectively (p=0.032). The pleural CRP levels were significantly higher in the benign effusion than in the malignant effusion, $3.68{\pm}3.78mg/dL$ and $1.42{\pm}1.54mg/dL$, respectively (p<0.001). The pleural procalcitonin levels in the non-tuberculous effusion were significantly higher than those in the tuberculous effusion, $1.16{\pm}3.75ng/mL$ and $0.13{\pm}0.37ng/mL$, respectively (p=0.008). Conclusion: Measuring the level of procalcitonin and CRP in the pleural fluid is helpful for differentiating between transudates and exudates. In addition, it is useful for differentiating between benign and malignant pleural effusions.

• Tuberculosis and Respiratory Diseases
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• v.65 no.1
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• pp.7-14
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• 2008

Background: Residual pleural thickening (RPT) is the most frequent complication of tuberculous pleurisy (TP), and this can happen despite of administering adequate anti-tuberculous (TB) therapy. Yet there was no definite relation between RPT and other variables. The aim of this study was to examine matrix metalloproteinases (MMPs) and the inhibitors of metalloproteinases (TIMPs) and to identify the factors that can predict the occurrence of RPT. Methods: The patients with newly-detected pleural effusions were prospectively enrolled in this study from January 2004 to June 2005. The levels of MMP-1, -2, -8 and -9, and TIMP-1 and -2 were determined in the serum and pleural fluid by ELISA. The residual pleural thickness was measured at the completion of treatment and at the point of the final follow-up with the chest X-ray films. Results: The study included 39 patients with pleural fluid (PF). Twenty-three had tuberculous effusion, 7 had parapneumonic effusion, 7 had malignant effusion and 2 had transudates. For the 17 patients who completed the anti-TB treatment among the 23 patients with TP, 7 (41%) had RPT and 10 (59%) did not. The level of PF TIMP-1 in the patients with RPT ($41,405.9{\pm}9,737.3ng/mL$) was significantly higher than that of those patients without RPT ($29,134.9{\pm}8,801.8$) at the completion of treatment (p=0.032). In 13 patients who were followed-up until a mean of $8{\pm}5$ months after treatment, 2 (15%) had RPT and 11 (85%) did not. The level of PF TIMP-2 in the patients with RPT ($34.4{\pm}6.5ng/mL$) was lower than that of those patients without RPT ($44.4{\pm}15.5$) at the point of the final follow-up (p=0.038). Conclusion: The residual pleural thickening in TP might be related to the TIMP-1 and TIMP-2 levels in the pleural fluid.

• Tuberculosis and Respiratory Diseases
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• v.62 no.4
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• pp.290-298
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• 2007

Background: The currently available diagnostic markers for pleural effusion have a limited role. The soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is a molecule recently reported to play an important role in the myeloid cell mediated inflammatory response, and is up regulated in the body fluid by bacterial or fungal products. This study examined the expression of sTREM-1 in pleural effusion. Methods: Between April 2004 and December 2005, 48 patients with pleural effusions were enrolled in this study. The pleural fluids were taken and analyzed for the total protein, glucose, lactate dehydrogenase (LDH), adenosine deaminase (ADA), and sTREM-1. Bacterial cultures and cytology tests were also performed. Results: The clinical diagnoses were 17 parapneumonic, 14 tuberculous, and 13 malignant effusions. Four patients presented with transudates. The mean ages of the parapneumonic, tuberculous and malignant effusion groups were $57.1{\pm}19.7$, $49.5{\pm}18.6$, $66.9{\pm}15.5$, and $76.0{\pm}18.1$. respectively. The level of sTREM-1 expression was significantly higher in the parapneumonic effusions ($344.0{\pm}488.7$) than in the tuberculous effusions ($81.7{\pm}56.6$) and malignant effusions ($39.3{\pm}19.6$). With a cut-off value of 55.4pg/ml, the sensitivity and specificity for a parapneumonic effusion was 70.6% and 74.1%. Conclusion: sTREM-1 expression is significantly higher in parapneumonic effusions, suggesting its potential role as an additional diagnostic marker for pleural effusions.