• Tuberculosis and Respiratory Diseases
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• v.67 no.6
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• pp.565-568
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• 2009

Yellow nail syndrome is a rare cause of pleural effusions. This syndrome is characterized by yellow discoloration of nails, lymphedema, and respiratory disorders, including pleural effusion, chronic bronchitis, bronchiectasis, and chronic sinusitis. The etiology of this syndrome is obscure, but the pathogenesis seems to be related with impaired lymphatic drainage. We report a case of yellow nail syndrome in a 70-year-old female with the typical clinical findings (yellow discoloration of nails, lymphedema, and chronic pleural effusion) of this disorder and with proven lymphatic obstruction on lymphoscintigraphy.

• Tuberculosis and Respiratory Diseases
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• v.64 no.4
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• pp.314-317
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• 2008

We report the patient presented with a left-sided pleural effusion. Pleural fluid analysis revealed lymphocyte-dominant exudates with lower level of adenosine deaminase and negative cytologic malignancy. Thoracoscopic examination and histologic examination revealed metastatic nodules on pleurae, proven to be from the papillary thyroid cancer. There were no other sites of distant metastases. Though papillary thyroid cancer is characterized with slow progression and relatively good prognosis, metastatic pleural effusion as an initial manifestation of undiagnosed papillary thyroid cancer can be considered.

• Tuberculosis and Respiratory Diseases
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• v.64 no.5
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• pp.379-382
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• 2008

Eosinophilic pleural effusions (EPE) are defined as those effusions that contain at least 10% eosinophils, and EPE can be associated with peripheral blood eosinophilia in a variety of systemic diseases. There have been a few cases that have addressed the association of peripheral blood eosinophilia and posttraumatic EPE, and this condition can be misdiagnosed as being the result of other causes due to the delayed presentation. We report here on a case of 47-year-old male who presented with eosinophilic pleural effusion associated with peripheral blood eosinophilia at 2 months after minor chest trauma. We excluded the other possible causes such as consumption of drugs, parasite infection, malignancy, diseases of pulmonary eosinophilic infiltration, autoimmune diseases and pulmonary thromboembolism. We observed his clinical course without specific treatment. Three months later, the pleural effusion completely disappeared and the number of peripheral eosinophils returned to normal.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.301-310
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• 1998

Background: Cell mediated immune response mediated by interaction between CD4+ T lymphocytes and macrophagies is thought to play an important role in tuberculous pleurisy. This interaction is dependent on the interplay of various cytokines. The immunologic response of tuberculous pleurisy is thought to depend on the balance between helper T cell(Th1) cytokine Interleukin-12, Interferon gamma and Th2 cytokine IL-4, IL-10. To understand immunologic mechanism in tuberculous pleurisy and evaluate diagnostic value of these cytokines, the concentrations of Th1 cytokine IL-12, IFN -$\gamma$ and Th2 cytokine IL-10 were measured in tuberculous pleurisy and malignant pleural effusion group. Material and Methods: The concentrations of IL-10, IL-12 and IFN-$\gamma$ were measured by ELISA method in pleural fluids and serums of 20 patients with tuberculous pleurisy and 20 patients with malignant pleural effusion ADA activities were measured by spetrophotomery in pleural fluids of both groups. Results: In tuberculous pleurisy, the mean concentrations of IL-10, IL-12 and IFN-$\gamma$ of pleural fluids showed $121.3{\pm}83.7$ pg/mL, $571.4{\pm}472.7$ pg/mL and $420.4{\pm}285.9$ pg/mL. These were significantly higher than that of serum, $21.2{\pm}60.9$ pg/mL, 194.5 pg/mL, $30.1{\pm}18.3$ pg/mL respectively(p< 0.01). In malignant pleural effusion, the mean concentrations of IL-10, IL-12 and IFN-$\gamma$ of pleural fluids showed $88.4{\pm}40.4$ pg/mL, $306.5{\pm}271.1$ pg/mL and $30.5{\pm}54.8$ pg/mL respectively. Compared with that of serum ($43.4{\pm}67.2$ pg/mL, $206.8{\pm}160.6$ pg/mL, $14.6{\pm}3.3$ pg/mL), only IL-10 was significantly higher (p<0.001), but IL-12, IFN-$\gamma$ were not significant. In tuberculous pleural effusion compared with malignant pleural effusion, the concentration of IL-12, IFN-$\gamma$, ADA were significantly higher (p=value 0.046, <0.001, <0.001), but IL-10 was not significant. For differential diagnosis of tuberculous pleurisy from malignant pleural effusion, using cut-off value of IL-12, IFN-$\gamma$, ADA as 300 pg/mL. 100 pg/mL, 45 U/L, the sensitivity/specificity were 60%/70%, 90%/87.5%, 85%/90% respectively. Conclusion: In tuberculous pleurisy, IL-10, IL-12 and IFN-$\gamma$ were selectively concentrated highly in pleural space than serum. Compared with malignant pleural effusion, IL-12 and IFN-$\gamma$ were significantly higher, but IL-10 were not in tuberculous pleural effusion. The results suggest that Th1 pathway contributes to immune resistant mechanism in tuberculous pleurisy. IFN-$\gamma$ and ADA revealed useful methods of differential diagnosis in tuberculous pleurisy from malignant pleural effusion.

• Tuberculosis and Respiratory Diseases
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• v.65 no.1
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• pp.49-51
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• 2008

We report a case of acute myeloid leukemia with multilineage dysplasia accompanying malignant pleural effusion. A 73 year-old male patient was admitted complaining of febrile sensations and right chest pain. The cytology of the pleural fluid revealed malignant pleural effusion showing many blasts, which had previously been identified in his bone marrow when he was diagnosed with acute myeloid leukemia with multilineage dysplasia two months earlier. His age and poor general condition had precluded chemotherapy with the exception of hydroxyurea and conservative treatment. Unfortunately, he succumbed to the disease 4.5 months after diagnosis. This case highlights the importance of determining if the pleural effusion of acute leukemia is malignant or not because it can suggest a pleural metastasis and influence the prognosis.

• Tuberculosis and Respiratory Diseases
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• v.76 no.5
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• pp.211-217
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• 2014

Malignant pleural effusions (MPEs) are the second leading cause of exudative pleural effusions after parapneumonic effusions. In the vast majority of cases, a MPE signifies incurable disease associated with high morbidity and mortality. Considerable advances have been made for the diagnosis of MPEs, through the development of improved methods in the specialized cytological and imaging studies. The cytological or histological confirmation of malignant cells is currently important in establishing a diagnosis. Furthermore, despite major advancements in cancer treatment for the past two decades, management of MPE remains palliative. This article presents a comprehensive review of the medical approaches for diagnosis and management of MPE.

• Journal of Chest Surgery
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• v.28 no.5
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• pp.510-512
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• 1995

Reexpansion pulmonary edema following treatment of pneumothorax and pleural effusion is a rare complication. However, because of possibility of its fatal outcome, physicians must be aware of this complication and every effort must be made to prevent its occurrence. We experienced 5 cases of reexpansion of pulmonary edema. One was complete tension pneumothorax and became death despite of intensive management. Remained four were 3 pneumothoraces and 1 pleural effusion and discharged without event, fortunately.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.3
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• pp.1411-1414
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• 2016

Background: Eosinophilic pleural effusion (EPE) is an eosinophil count more than 10% on cytology of pleural samples. Recently, it was reported that malignancy had been the most prevalent cause inducing EPE. Therefore, we conducted an analysis on the prevalence and etiology of EPE and investigated the relationship between EPE and malignancy. Materials and Methods: Data for pleural cell differential count from patients receiving thoracentesis during the period from January 2008 to December 2013 were compared with clinical data and established diagnosis of patients obtained via electronic chart review. Results: A total of 6,801 requests of pleural cytology from 3,942 patients with pleural effusion who had received thoracentesis were available at Far Eastern Memorial Hospital from 2008 to 2013, and of these subjects, 115 (2.9%) were found to have EPE. The most frequent cause of EPE was malignancy (33.0%, n=38), followed by parapneumonic effusions (27.8%, n=32), tuberculosis pleuritis (13.9%, n=16), transudate effusions (12.2%, n=14) and the presence of blood or air in pleural space (10.4%, n=12). Additionally, an inverse relationship of eosinophilia in pleural fluid was identified in patients with malignancy and EPE. The cut-off eosinophil count in pleural fluid was 15% for the most accurate discrimination between malignancy and benign disorders in patients with EPE. At the cut-off level, the sensitivity and specificity were 65.8% and 67.5%, respectively. Conclusions: Pleural fluid eosinophilia was a speculative negative predictor for malignancy, despite the fact that cancers, including lung cancers and metastatic cancers to lung, were the most leading cause of pleural fluid eosinophilia. An inverse correlation was observed between the pleural eosinophil percentage and the likelihood of malignancy in patients with EPE.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.1031-1038
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• 1998

Background: Most of malignant pleural effusions are serous but 8-33% of them are bloody. We wanted to evaluate the relationships between gross appearance and pleural CEA level or results of histocytology in malignancy associated pleural effusions. We also tried to reevaluate the meaning of CEA measurement in histocytologically proved or unproved malignancy associated pleural effusions. Methods: We studied 98 cases of malignancy associated pleural effusions, 50 cases of histocytologically proven malignant effusions and 48 cases of histocytologically unproven paramalignant effusions. We had observed gross appearance and conventional laboratory values and CEA levels for pleural effusions. Results: 44.9% of malignancy associated effusions were bloody(63.6% of bloody effusions were histocytologically proven malignant effusion). 65.0% of malignancy associated pleural effusions which have RBCs numbers over $100,000/mm^3$ were cytologically proven malignant effusions. 72.7% of cytologically proven malignant effusions had increased pleural fluid CEA level over 10 ng/ml. 58.2% of cases with pleural CEA over 10 ng/ml had positive results in pleural bistocytology. There was no definable relationships between pleural fluid CEA elevation and RBCs numbers and results of pleural fluid cytology. Conclusion: About half of the cases with malignancy associated pleural effusions were bloody. Histocytologically proven malignant effusions were more common in bloody effusion than non-bloody effusion(63.6% Vs 38.9%). But increased red blood cell numbers was not associated with positivity of pleural histocytology. Pleural fluid CEA elevation(over 10 ng/ml) was not correlated with positive pleural histocytology. But pleural fluid CEA elevation was rare in nonmalignant pleural effusions, and than pleural CEA measurement in uncertain pleural effusions maybe helpful to distinguishes its origin.

• Tuberculosis and Respiratory Diseases
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• v.50 no.2
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• pp.171-181
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• 2001

Background : Angiogenesis is an essential process for the growth and metastatic ability of solid tumors. One of the key factors known to be capable of stimulating tumor angiogenesis is the vascular endothelial growth factor (VEGF). The serum VEGF concentration has been shown to be a useful parameter related to the clinical features and prognosis of lung cancer and has been recently applied to a the malignant pleural effusion showing a correlation with the biochemical parameters. The VEGF has been shown to play a role in the inflammatory diseases, but rarely in the tuberculosis (TB). The serum and pleural fluid VEGF levels were measured in patients with lung cancer and TB. Their relationship with the clinical and laboratory parameters and repeated measurement 3 months after various anticancer treatments were evaluated to assess the utility of the VEGF as a tumor marker. Methods : Using a sandwich enzyme-linked immunosorbent assay, the VEGF conoentration was measured in both sera and pleural effusions collected from a total of 85 patients with lung cancer, 13 patients with TB and 20 healthy individuals. Results : The serum VEGF levels in patients with lung cancer ($619.9{\pm}722.8pg/ml$) were significantly higher than those of healthy controls ($215.9{\pm}191.1pg/ml$), However, there was no significant difference between the VEGF levels in the lung cancer and TB patients. The serum VEGF levels were higher in large cell and undifferentiated carcinoma than in squamous cell carcinoma and adenocarcinoma. The serum VEGF levels of lung cancer patients revealed no significant relationship with the various clinical parameters. The VEGF concentrations in the malignant effusion ($2,228.1{\pm}2,103.0pg/ml$) were significantly higher than those in the TB effusion ($897.6{\pm}978.8pg/ml$). In the malignant pleural effusion, the VEGF levels revealed significant correlation with the number of red blood cells (r=0.75), the lactate dehydrogenase (LDH)(r=0.70), and glucose concentration (r=-0.55) in the pleural fluid. Conclusion : The serum VEGF levels were higher in the lung cancer patients. The VEGF levels were more elevated in the malignant pleural effusion than in the tuberculous effusion. In addition, the VEGF levels in the pleural fluid were several times higher than the matched serum values suggesting a local activation and possible etiologic role of VEGF in the formation of malignant effusions. The pleural VEGF levels showed a significant correlation with the numbers of red blood cells, LDH and glucose concentrations in the pleural fluid, which may represent the tumor burden.