Tuberc Respir Dis > Volume 65(1); 2008 > Article
Tuberculosis and Respiratory Diseases 2008;65(1):7-14.
DOI:    Published online July 1, 2008.
The Relation of Residual Pleural Thickening with Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases of Pleural Effusion in Patients with Tuberculous Pleuritis.
Youngkwon Choi, Chang Hyeok An, Yu Jin Kim, Sun Young Kyung, Sang Pyo Lee, Jeong Woong Park, Sung Hwan Jeong
1Graduate School of Medicine, Gachon University of Medicine and Science, Incheon, Korea.
2Division of Pulmonology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, Korea.
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+/-9,737.3 ng/mL) was significantly higher than that of those patients without RPT (29,134.9+/-8,801.8) at the completion of treatment (p=0.032). In 13 patients who were followed-up until a mean of 8+/-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+/-6.5 ng/mL) was lower than that of those patients without RPT (44.4+/-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.
Key Words: Matrix metalloproteinase, Pleural effusion, Residual pleural thickening, Tissue inhibitor of metalloproteinase, Tuberculous pleuritis

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