• The Korea Swine Journal
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• v.6 no.9 s.61
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• pp.116-116
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• 1984

• Journal of Veterinary Clinics
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• v.32 no.5
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• pp.454-458
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• 2015

This report describes the diagnostic radiographic and CT features of pleuropneumonia in a cat with wet type of feline infectious peritonitis (FIP). In a 1 year-old cat presented with respiratory distress, pulmonary mass, thickened pleural wall with mass-like structures, and a large amount of pleural effusion were identified on radiography, ultrasonography, and CT. About two months later, in addition to the pre-existing lesions, multiple nodules had developed on the intestine and left kidney. The cat was diagnosed with pleuropneumonia caused by FIP through histologic examination and immunohistochemistry. Pleuropneumonia is rarely reported in cats with FIP, and only one cat with non-effusive FIP had pyogranulomatous pneumonia as consolidated lung lobe. In the present case, pleuropneumonia was detected as multiple mass-like lesions on diagnostic imaging.

• Clinical and Experimental Pediatrics
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• v.49 no.1
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• pp.56-63
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• 2006

Purpose : This study was designed to document the etiologies and the characteristics of parapneumonic effusion in children. Methods : During a 17-year period from 1987 to 2004, parapneumonic effusion was confirmed in 86 children at Gyeongsang National University Hospital. The clinical records of these children were reviewed and radiological findings and laboratory data, especially results of thoracentesis, were analyzed retrospectively. Results : M. pneumoniae(34 subjects) was the most common pathogen at all over age, especially above 1-years-old. There were diagnosed with clinical characteristics and serologic tests. The $2^{nd}$ most common pathogen revealed non tuberculous bacteria(14 subjects). A species of bacteria at no tuberculous bacteria revealed S. aureus(5), S. pneumoniae(3), P. aeroginosa(3), other staphylococcus (2), and K. pneumoniae(1). There were confirmed with sputum culture or pleural fluid culture or blood culture. S. aureus was most common pathogen in infants. The $3^{rd}$ common pathogen was M. tuberculosis(7). There were confirmed with skin tuberculin tests and AFB stains. Another that was classified as a non bacteria was adenovirus(2). Complications of parapneumonic effusion such as pleural thickness occurred on M. tuberculosis(1). Non tuberculous bacteria, especially S. aureus revealed a serious predominance of polymorphocyte at pleural fluid, and lowest pleural pH and glucose, and highest pleural protein and LDH. Tuberculosis revealed high pleural protein and LDH. Conclusion : Age and chemistries of pleural fluid might be helpful in differentiating various etiologies of parapneumonic effusion. If there were suspicious of tuberculosis and non-tuberculous bacteria, more aggressive approaches were needed to prevent complication.

• Tuberculosis and Respiratory Diseases
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• v.44 no.1
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• pp.44-51
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• 1997

Background : The changes of the composition in the T-lymphocyte are important as an immunological abnormality in the pathogenesis of tuberculosis. Previously, the second type of TCR dimer(${\gamma}{\delta}$ T lymphocyte) that did not express CD4 or CD8 molecules was found. In other reports the presence of this type of lymphocytes was increased in the initial stage of tuberculous infections. Method : To determine whether there are some differences in the T-lymphocyte subsets in the peripheral blood or pleural effusion between pleural tuberculosis and other pleurisy. Thirty patients with pleural effusion among the forty-nine patients were examined T-lymphocyte subset analysis(CD4+T-cell,CD8+ T-cell,${\gamma}{\delta}$ T-lymphocytes) with anti- Leu4, anti-Leu3a, anti-Lea2a, anti HLA-DR and anti-TCR-${\gamma}{\delta}$-1(Becton & Dickinson Co.). Results : The average age of the patients was 50 years old(17-81year). There were 33 males and 16 female patients. Patiensts with tuberculosis are 30cases(tuberculous pleurisy 15), lung cancer 12cases(malignant effusion 9) and pneumonia 7cases(parapneumonic effusion 6cases) In T lymphocyte subsets of pleural effusion, helper T lymphocyte(54.6 + 13.8 %) of tuberculous pleurisy was higher than that(36.2 + 25.3 %) of non-tuberculous pleurisy(p=0.04). The peripheral blood ${\gamma}{\delta}$ T-lymphocytes in tuberculousis was insignificantly higher than non-tuberculous patients(p= 0.24). The peripheral blood ${\gamma}{\delta}$ T-lymphocytes and pleural ${\gamma}{\delta}$ T-Iymphocytes in tuberculous pleurisy was insignificantly higher than in non-tuberculous pleurisy(p= 0.16, p= 0.12). Conclusion : The percentage of -${\gamma}{\delta}$ T lymphocytes among the total T-lymphocytes is not significantly increased in the peripheral blood or pleural effusion of the pleural tuberculosis. ${\gamma}{\delta}$ T lymphocytes is less useful as a diagnostic method of pleural tuberculosis.

• The Korea Swine Journal
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• v.11 no.9 s.121
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• pp.144-147
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• 1989

• The Korea Swine Journal
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• v.29 no.2 s.330
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• pp.212-213
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• 2007

• Tuberculosis and Respiratory Diseases
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• v.63 no.1
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• pp.24-30
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• 2007

Background: Pleural effusion develops in approximately 40% of pneumonia patients. In 5-10% of these cases, it progresses to complicated parapneumonic effusion (CPPE) or empyema that requires drainage. The prognostic factors of CPPE and empyema remain to be clarified. We examined the treatment outcomes of CPPE and empyema and elucidating their prognostic factors. Methods: One hundred and fifteen patients with CPPE or empyema, who were diagnosed and treated in Kyungpook National University Hospital (Daegu, Korea) between September 2001 and December 2005, were retrospectively analyzed. All the data was acquired from their chart review, and regarding treatment results, the time to defervescence and the length of hospital stay were analyzed. Results: The treatment was successful in 101 patients with a success rate of 87.8%. Multivariate analysis showed the level of pleural fluid lactate dehydrogenase (LDH) to be a significant prognostic factor (odds ratio [OR] 7.37; 95% confidence interval [CI], 1.63 to 33.37; p=0.009). Pussy pleural fluid (r=0.236; p=0.01) and the frequency of urokinase use (r=0.257; p=0.01) correlated with the time to defervescence. However, there was no clinical factor that correlated with the length of hospital stay. Conclusion: The pleural fluid LDH level is a useful prognostic factor for monitoring treatment results of CPPE and empyema.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1214-1222
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• 1998

Background : The intrapleural hypofibrinolysis is caused by mainly excessive concentration of pleural plasminogen activator inhibitor-1 antigen(PAI-1 Ag), which binds tissue type plasminogen activator. In pleural inflammation induced by sclerosing agents for pleurodesis, levels of pleural PAI-1 antigen increase in relation to decreasing D-dimer levels. It has been known that the pleural mesothelial cells have the capability of secreting PAI-1 Ag in response to inflammation in vivo. Therefore, we estimated whether pleural inflammation changes the balance between fibrinolytic and coagulative properties in exudative pleural effusions. Method : The thirty cases was included in our study. We determined the pleural levels of glucose, lactic dehydrogenase(LDH), pH and the counts of white blood cell(WBC), polymorpho leukocyte(PMN), lymphocyte as the parameters of pleural inflammation and cellular components of pleural fluid. The plasma level of fibrinogen in fluid and the neutrophil count in blood were determined. The levels of D-dimer, PAI-1 Ag and thrombinantithrombin III complex(TAT) were determined by ELISA(Behring, Marburg, Germany). Result : The causes of pleural effusion were as following : tuberculous in 14 cases, malignant in 10 cases and parapneumonic in 6 cases. The levels of pleural D-dimer, PAI-1 Ag and TAT was significantly higher than that of plasma(p<0..001). The severity of pleural inflammation did not correlated with pleural D-dimer, PAI-1 Ag, TAT and their plasma levels. But the level of pleural TAT correlated with pleural WBC and lymphocyte count. Conclusion : We found that the severity of pleural inflammations did not correlated with pleural D-dimer, PAI-1 Ag, TAT and the possibility of local production of PAI-1 antigen is present.

• Proceedings of the Korean Society of Veterinary Service Conference
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• 2000.06a
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• pp.175.2-176
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• 2000

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.388-396
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• 1998

Background: Etiologic diagnosis of pleural effusion is usually made by clinical characteristics, pleural fluid analysis and pleural biopsy. But, despite careful diagnostic study, the cause of pleural effusion cannot be found in about 20 percent of patients, especially in loculated pleural effusions. Tuberculous pleurisy is one of the most common cause of pleural effusion in Korea. But, pleural fluid culture for Mycobacterium tuberculosis are positive in only 20 to 30 percent of patients and typical pleural biopsy finding in less than 50 percent of patients with this disease. In recent studies, adenosine deaminse(ADA) and its isoenzymes were proposed to be a useful diagnostic tool for differential diagnosis of pleural effusion. We investigated the pattern of ADA and its iscenzyme activities in various cause of pleural effusions to evaluate the diagnostic value of measuring ADA and its isoenzymes. Method: We measured total ADA and its isoenzyme activities in pleural fluid and serum from 54 patients with pleural effusion(25 tuberculous pleural effusion, 10 parapneumonic effusion, 14 malignant pleural effusion, 5 transudative pleural effusion), including 5 loculated tuberculous pleural effusions and 6 loculated parapneumonic effusions. Total ADA activity was measured by the spectrophotometric method and ADA2 isoenzyme activity was measured with same method using EHNA, potent inhibitor of ADA1 isoenzyme activity. Result: Total ADA activity of tuberculous pleural effusion was higher than malignant pleural effusion(p<0.01), but no significant difference was found between tuberculous pleural effusion and parapneumonic effusion(tuberculous pleural effusion: $148.9{\pm}89.9IU/L$, parapneumonic effusion: $129.0{\pm}119.4IU/L$, malignant pleural effusion: $48.7 {\pm}39.7IU/L$). Percentage of ADA2 activity to total ADA activity(ADA2%) of pleural effusion of tuberculous pleurisy was higher than parapneumonic effusion(p<0.05). but no significant difference was found between tuberculous pleural effusion and malignant pleural effusion(tuberculous pleural effusion: $57.2{\pm}10.7%$, parapneumonic effusion: $35.9{\pm}17.8%$, malignant pleural effusion: $60.7{\pm}4.1%$). In loculated pleural effusion, ADA2% of tuberculous pleural effusion was higher than parapneumonic effusion(tuberculous pleural effusion: $53.3{\pm}3.9%$, parapneumonic effusion: $27.8{\pm}7.9%$). Conclusion: Measurement of ADA isoenzyme activity is useful for differentiating tuberculous pleural effusion from parapneumonic effusion, especially in loculated pleural effusion.