• Title/Summary/Keyword: the surface markers

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The Predictors of Effectiveness on Urokinase Instillation Therapy into Loculated Pleural Effusion. (소방이 형성된 흉막질환에서 유로키나제 주입치료의 예후인자)

  • Song, Kee-San;Bang, Jei-So;Kwak, Seung-Min;Cho, Chul-Ho;Park, Chan-Sup
    • Tuberculosis and Respiratory Diseases
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    • v.44 no.3
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    • pp.621-628
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    • 1997
  • Background : As the pleural inflammation progresses, exudative pleural fluid becomes loculated rapidly with pleural thickening. Complete drainage is important to prevent pleural fibrosis, entrapment and depression of lung function. Intrapleural urokinase instillation therapy has been advocated as a method to facilitate drainage of gelatinous pleural fluid and to allow enzymatic debriment of pleural surface. This study was designed to investigate the predictors of effectiveness of intrapleural urokinase in the treatment of loculated pleural effusion. Method : Thirty-five patients received a single radiographically guided pig-tail catheter ranging in size from 10 to 12 French. Twenty-two patients had tuberculous pleural effusions, and 13 had non-tuberculous postpneumonic empyemas. A total of 240,000 units of urokinase was dissolved in 240 ml of normal saline and the aliquots of 80mL was instilled into the pleural cavity via pig-tail catheter per every 8hr. Effectiveness of intrapleural urokinase instillation therapy was assessed by biochemical markers, ultrasonography, and technical details. A greater than 50% improvement on follow-up chest radiographs was defined as success group. Result : Twenty-seven of 35 (77.1%) patients had successful outcome to urokinase instillation therapy. Duration of symptoms before admission was shorter in success group ($11.8{\pm}6.9day$) than in failure group ($26.62{\pm}16.5day$) (P<0.05). Amount of drained fluid during urokinase therapy was larger in success group ($917.1{\pm}392.7ml$) than in failure group ($613.8{\pm}259.7ml$) (P<0.05). Pleural fluid glucose was higher in success group ($89.7{\pm}35.9mg/dl$) than in failure group ($41.2{\pm}47.1mg/dl$) (P<0.05). Pleural fluid LDH was lower in success group ($878.4{\pm}654.3IU/L$) than in failure group ($2711.1{\pm}973.1IU/L$) (P<0.05). Honeycomb septated pattern on chest ultrasonography was observed in six of eight failure group, but none of success group (P<0.05). Conclusion : Longer duration of symptoms before admission, smaller amount of drained fluid during urokinase therapy, lower glucose value, higher LDH value in pleural fluid examination, and honeycomb septation pattern on chest ultrasonograph were predictors for failure group of intrapleural urokinase instillation therapy.

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Soluble IL-2R, IFN-$\gamma$ and Neopterin as Immunologic Markers in Patients with Tuberculosis (결핵 환자에서 면역학적 지표로서의 sIL-2R, IFN-$\gamma$, Neopterin에 관한 연구)

  • Ryu, Yon-Ju;Ryu, Kum-Hei;Kim, Su-Hyun;Lee, Jong-Soo;Cheon, Seon-Hee;Seoh, Ju-Young
    • Tuberculosis and Respiratory Diseases
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    • v.53 no.3
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    • pp.294-308
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    • 2002
  • Background : The cell-mediated immune response plays an important role in tuberculosis. After being activated by mycobacterial antigens, T lymphocytes express a high affinity receptor (IL-2R) for interleukin-2 (IL-2) on their own surface and release a soluble fraction of the IL-2 receptor (sIL-2R) from the cell membrane into the circulation. Neopterin is a metabolite of guanosine-triphosphate, which is produced by stimulated macrophages under the influence of IFN-$\gamma$ with a T lymphocyte origin. Therefore, the utility of sIL-2R, IFN-$\gamma$ and the neopterin levels as immunologic indices of the cell-mediated immune response and severity of disease in patients with pulmonary tuberculosis was assessed. Methods : The serum sIL-2R, IFN-$\gamma$ and neopterin levels were measured in 39 patients with pulmonary tuberculosis, 6 patients with tuberculous lymphadenitis prior to treatment and 10 healthy subjects. The serum and pleural sIL-2R, neopterin and ADA levels were measured in 22 patients with tuberculous pleurisy. The patients with pulmonary tuberculosis were divided into a mild, moderate and severe group according to the severity by ATS guidelines. To compare the results from these patients with those of the pretreatment levels, the sIL-2R, IFN-$\gamma$ and neopterin levels were measured in 36 of the 39 patients(1 patient, expired; 2 patients were referred to a sanitarium) with pulmonary tuberculosis after 2 months of treatment. Results : 1) the serum sIL-2R and IFN-$\gamma$ levels were elevated in patients with tuberculosis when compared to those of healthy subjects (p>0.05). The neopterin concentration in the serum was significantly lower in patients with pulmonary tuberculosis($2967{\pm}2132.8$ pg/ml) than in healthy controls($4949{\pm}1242.1$ pg/ml)(p<0.05). 2) In the pulmonary tuberculosis group, the serum sIL-2R and IFN-$\gamma$ levels were higher in patients with severe disease than those in patients with mild and moderate disease. However, the neopterin levels declined as the pulmonary tuberculosis became more severe (p<0.01). 3) The mean serum sIL-2R and IFN-$\gamma$ levels declined from $1071{\pm}1139.4$ U/ml to $1023{\pm}1920.9$ U/ml(p>0.05), $41{\pm}52.8$ pg/ml to $22{\pm}23.9$ gm/ml(p<0.05), respectively, after 2 month of treatment. The mean serum neopterin levels increased from $3158{\pm}2272.6$ pg/ml to $3737{\pm}2307.5$ pg/ml(p>0.05) after a 2 month of treatment. These findings were remarkable in the severe group of pulmonary tuberculosis with a clinical correlation. 4) In the patients with tuberculous pleurisy, the serum sIL-2R and ADA were significantly higher than those in the pleural fluid, However, the neopterin levels in the sera and pleural effusion were similar. Conclusion : On the basis of this study, sIL-2R, IFN-$\gamma$ and neopterin measurements may not only provide an insight into the present state of the cell-mediated immune response, but also serve as parameters monitoring of the prognosis of the disease, particularly in patients with severe pulmonary tuberculosis. In addition, an assay of the pleural sIL-2R levels might signal a stimulated local immunity including T cell activation in the tuberculous pleural effusion.