• Tuberculosis and Respiratory Diseases
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• v.63 no.3
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• pp.294-298
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• 2007

Pulmonary alveolar proteinosis is a rare disorder that is characterized by the abundant accumulation of surfactant-derived material within the alveolar spaces and distal bronchioles. Although the findings of homogenous ground-glass opacities overlaid by thickened septa, which form a "crazy paving" pattern on high-resolution computed tomography, can assist in making a diagnosis, a lung biopsy is usually required. This disorder has a variable clinical course, from spontaneous resolution to respiratory failure and death. While a whole lung lavage has been the standard treatment since the early 1960s, GM-CSF therapy has been attempted based on the recently suggested pathogenetic mechanism. We report a case of pulmonary alveolar proteinosis that resolved spontaneously after an open lung biopsy.

• Tuberculosis and Respiratory Diseases
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• v.45 no.3
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• pp.519-528
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• 1998

Background: Diagnosis of pulmonary tuberculosis is not easy when the sputum smear for Mycobacterium tuberculosis(M. Tb) is negative. We evaluated the clinical utility of polymerase chain reaction(PCR) for detecting M. Tb in bronchoalveolar lavage(BAL) samples. Methods: We recruited 84 patients whose sputum smear for M. Tb were negative or not available due to no production of sputum. We performed bronchoalveolar lavage for acid-fast stain, culture of mycobacteria, and PCR assay of BAL fluid. We analyzed the results of microbiologic examination. Results: The sensitivity of BAL fluid smear, culture, and PCR were 20%, 38%, and 40%, respectively. The specificity of BAL fluid PCR was 95%. The positive predictive value of PCR was 89%. The smear of BAL fluid was positive in 17%. The PCR of BAL fluid was the only diagnostic test in 17%. Therefore, the BAL fluid analysis including smear and PCR was diagnostic in 34 % within 24 hours. The BAL fluid analysis including smear, PCR, and culture was diagnostic in 55% within 2 month. Conclusion: The BAL fluid PCR was valuable method in the diagnosis of pulmonary tuberculosis in patients whose sputa were not available or reveal negative smear.

• Tuberculosis and Respiratory Diseases
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• v.53 no.4
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• pp.409-419
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• 2002

Background : The therapeutic effects of surfactant on acute lung injury derive not only from its recruiting action on collapsed alveoli but also from its anti-inflammatory effects. Pro-apoptotic action on alveolar neutrophils represents one of the important anti-inflammatory mechanisms of surfactant. In the present study, we evaluated the effects of sufactant on the apoptosis of human peripheral and rat alveolar neutrophils. Methods : In the (Ed- the article is not definitely needed but it helps to separate the two prepositions 'in') in vitro study, human neutrophils were collected from healthy volunteers. An equal number of neutrophils ($1{\times}10^6$) (Ed-confirm) was treated with LPS (10, 100, 1000ng/ml), surfactant (10, 100, $1000{\mu}g/ml$), or a combination of LPS (1000ng/ml) and surfactant (10, 100, $1000{\mu}g/ml$). After incubation for 24 hours, the apoptosis of neutrophils was evaluated by Annexin V method. In the in vivo study, induction of acute lung injury in SD rats by intra-tracheal instillation of LPS (5mg/kg) was followed by intra-tracheal administration of either surfactant (30mg/kg) or normal saline (5ml/kg). Tenty-four hours after LPS instillation, alveolar neutrophils were collected and the apoptotic rate was evaluated by Annexin V method. In addition, changes of the respiratory mechanics of rats (respiratory rate, tidal volume, and airway resistance) were evaluated with one chamber body plethysmography before, and 23 hours after, LPS instillation. Results : in the in vitro study, LPS treatment decreased the apoptosis of human peripheral blood neutrophils (control: $47.4{\pm}5.0%$, LPS 10ng/ml; $30.6{\pm}10.8%$, LPS 100ng/ml; $27.5{\pm}9.5%$, LPS 1000ng/ml; $24.4{\pm}7.7%$). The combination of low to moderate doses of surfactant with LPS promoted apoptosis (LPS 1000ng/ml + Surf $10{\mu}g/ml$; $36.6{\pm}11.3%$, LPS 1000ng/ml +Surf $100{\mu}g/ml$; $41.3{\pm}11.2%$). The high dose of surfactant ($1000{\mu}g/ml$) decreased apoptosis ($24.4{\pm}7.7%$) and augmented the anti-apoptotic effect of LPS (LPS 1000ng/ml + Surf $1000P{\mu}g/ml$; $19.8{\pm}5.4%$). In the in vivo study, the apoptotic rate of alveolar neutrophils of surfactant-treated rats was higher than that of normal saline-treated rats ($6.03{\pm}3.36%$ vs. $2.95{\pm}0.58%$). The airway resistance (represented by Penh) of surfactant-treated rats was lower than that of normal saline-treated rats at 23 hours after LPS injury ($2.64{\pm}0.69$ vs. $4.51{\pm}2.24$, p<0.05). Conclusion : Surfactant promotes the apoptosis of human peripheral blood and rat alveolar neutrophils. Pro-apoptotic action on neutrophils represents one of the important anti-inflammatory mechanisms of surfactant.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.942-952
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• 1998

The aim of this study was to evaluate spontaneous and LPS stimulated proinflammatory cytokines and chemokine release of alveolar macrophages in the patients with pulmonary tuberculosis and healthy individuals, as a control. Alveolar macrophages recovered from bronchoalveolar lavage fluids were cultured with or without LPS 0.1, 1, or 10 ${\mu}g/ml$ for 24 and 48 hours in 37C, 5% CO2. TNF-$\alpha$, IL-1$\beta$, IL-6 and IL-8 amount were evaluated using ELISA kit from the supernatants. There were a significant increase in the spontaneous 24 hours release of TNF-$\alpha$ and IL-6 from the involved segments of tuberculosis patients compared with uninvolved segments and normal control There were also increasing trends of release of them after LPS stimulation in involved segments, but not significant. IL-1$\beta$ and IL-8 were not evaluated from the involved segments of tubeculosis and there were not significant differences of them between uninvolved segments of tuberculosis and normal control. It is concluded that cytokine release of alveolar macrophages in the pulmonary tuberculosis was markedly increased, and it was localized to the alveolar macrophages from the involved segments.

• Tuberculosis and Respiratory Diseases
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• v.39 no.1
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• pp.55-61
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• 1992

Background: The lung is the most common site of metastasis and usually it manifests as a single or multiple nodules in chest X-ray. But less commonly the cancer spreads through the lymphatics and X-ray shows diffuse reticulonodular densities. Sometimes, patient is presented with respiratory symptoms only with interstitial lung infiltration before the signs of primary tumor and in that cases, the differential diagnosis with other interstitial lung disease is required. We have experienced 5 such cases, who were diagnosed as lymphangitic carcinomatosis by transbronchial lung biopsy. Methods: Clinical manifestation, pulmonary function test, modified thin section CT, bronchoalveolar lavage and transbronchial lung biopsy were done. Results: The primary tumor was gastric cancer in 3, lung cancer in 2. Pulmonary function test showed restrictive pattern with low DLco in 2 patients and obstructive pattern in one. Bronchoalveolar lavage showed lymphocytosis in 4 patients and malignant cells were found in one patient. Transbronchial lung biopsy revealed malignant cells localized to the lymphatics (peribronchial, perivascular and perialveolar). Cell type was adenocarcinoma in 4 and squamous cell carcinoma in one. Conclusion: Rarely lymphangitic carcinomatosis can be presented as diffuse interstitial lung disease and easily diagnosed by transbronchial lung biopsy.

• Tuberculosis and Respiratory Diseases
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• v.43 no.1
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• pp.46-53
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• 1996

Background: Endotoxin or lipopolysaccharide(LPS) can prime phagocytic cells such as polymorphonuclear leukocytes, monocytes or animal peritoneal macrophages to generate increased amounts of secretory products such as oxygen free radicals and tumor necrosis factor, which play an important role in developing adult respiratory distress syndrome in gram negative sepsis. Human alveolar macrophages(HAM) are continuously exposed to various stimuli inhaled into the alveoli, and the response to LPS might be different in HAM. Therefore, we investigated the effect of LPS pre-exposure on HAM adhered to plastic surface and A549 cell(type II human alveolar epithelial cell line) monolayer. Methods: HAM were isolated from bronchoalveolar lavage fluid from normal lung of the patients with localized lung cancer and esophageal cancer. LPS was exposed to HAM for 2hrs before or after adherence to plastic surface of 24-well Linbro plate and A549 cell monolayer. And then HAM was stimulated with PMA(phorbol myristate acetate) or fMLP(N-formyl-methionylleucyl-phenylalanine). The amount of hydrogen peroxide($H_2O_2$) production in the supernatant was measured on the principle of peroxidase-dependent oxidation of phenol red by hydrogen peroxide. Results: LPS pre-exposure could not enhance $H_2O_2$ production in neither HAM adhered to plastic surface nor one to A549 cell monolayer. But LPS even in the absence of PMA or fMLP stimulation directly increased $H_2O_2$ release in HAM if added after the adherence to A549 cell monolayer. Conclusion: Endotoxin does not prime HAM, but may directly activate HAM adhered to alveolar epithelial cells. Further investagation will be necessary.

• Tuberculosis and Respiratory Diseases
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• v.43 no.2
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• pp.210-220
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• 1996

Background : Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. In the process of surface adherence, adhesion molecules have a clear role in intracellular signal pathway of cellular activation. Human alveolar macrophages(HAM) are frequently purified by the adherence procedure after bronchoalveolar lavage. But the experimental data of many reports about alveolar macrophages have ignored the possibility of adhesion-induced cellular activation. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be normal by chest CT. With the measurement of hydrogen peroxide release from adherent HAM to plastic surface and non-adherent HAM with or without additional stimulation of phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP), we observed the effect of the adherence to plastic surface. We also evaluated the effect of various biological surfaces on adhesion-induced activation of HAM. Then, to define the intracellular pathway of signal transduction, pretreatment with cycloheximide, pertussis toxin and anti-CD11/CD18 monoclonal antibody was done and we measured hydrogen peroxide in the culture supernatant of HAM. Results : 1) The adherence itself to plastic surface directly stimulated hydrogen peroxide release from human alveolar macrophages and chemical stimuli such as phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine(fMLP) colud not increase hydrogen peroxide release in these adherent macrophages which is already activated. 2) PMA activated human alveolar macrophages irrespective of the state of adhesion. However, fMLP stimulated the release of hydrogen peroxide from the adherent macrophages, but not from the non-adherent macrophages. 3) HAM adherent to A549 cell(type II alveolar epithelium-like human cell line) monolayer released more hydrogen peroxide in response to both PMA and fMLP. This adherence-dependent effect of fMLP was blocked by pretreatment of macrophages with cycloheximide, pertussis toxin and anti-CD18 monoclonal antibody, Conclusion : These results suggest that the stimulatory effect of PMA and fMLP can not be found in adherent macrophage because of the activation of human alveolar macrophage by the adherence to plastic surface and the cells adhered to biologic surface such as alveolar epithelial cells are appropriately responsive to these stimuli. It is also likely that the effect of fMLP on the adherent macrophage requires new protein synthesis via G protein pathway and is dependent on the adhesion between alveolar macrophages and alveolar epithelial cells by virtue of CD11/CD18 adhesion molecules.

• Tuberculosis and Respiratory Diseases
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• v.52 no.4
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• pp.411-418
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• 2002

Pulmonary alveolar proteinosis(PAP) is a disorder in which an insoluble, proteinaceous material, rich in phospholipids, is deposited in the alveoli and bronchioles. The deficiency in the clearance and degradation of the intra-alveolar phospholipoproteinaceous material in PAP most likely represents a dysfunction of the type II pneumocytes. Although the pathogenesis and causative treatment of PAP is unclear a whole lung bronchopulmonary lavage is a relatively safe and effective treatment. Here we experienced a case of pulmonary alveolar proteinosis in a 62 year old female patient who had pulmonary tuberculosis approximately 20 years ago. She complained of aggravated dyspnea and chronic cough, and presented fine inspiratory crackles at both lung fields, diffuse ground glass opacity with some area of consolidation and smooth interlobular septal thickenings in both upper, right middled lobes, and a portion of right lower lobe. Optical microscopy of the lung tissue obtained by and open lung biopsy revealed many granulomas containing acid-fast smear positive bacilli and diffuse homogeneous PAS-positive fluid in the alveolar space. Immunohistochemical stain showed surfactant. A in the alveolar space. Antituberculosis drugs with bronchoalveolar lavage were used to treat the disease. Thereafter she showed improvement in her symptoms and a partial improvement in the chest X-ray and HRCT findings. We present a case of PAP associated with pulmonary tuberculosis.

• Journal of Chest Surgery
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• v.29 no.1
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• pp.43-51
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• 1996

From march 1989 to October 1993, 57 patients were diagnosed and operated for primary non-small cell lung cancer, and evaluated clinically. 1. There were 45 males and 12 females (M:F=3.8:1), and the peak incidence of age was 6th decade of life (45.6%). In the preoperative diagnostic methods and their positive rate, sputum cytology was 11%, bronchial washing cytology 50%, bronchoscopic biopsy 73%, and CT guided percutaneous needle aspiration biopsy 83%. 3. Histopathologically, squamous cell carcinoma was 56.1%, adenocarcinoma 22.8%, bronchioloal veolar cell carcinoma 1%, and undifferentiated large cell carcinoma 1.8%. 4. In the operation, pneumonectomy was 35.1%, lobectomy 38.6%, bilobectomy 3.5%, segmentec tony 7%, and exploratory thoracotomy 15.8%, and overall resectability was 84.2%. 5. In postoperative stagings, stage I was 28.1%, st ge II 22.8%, stage IIIa 31.6% and stage IIIb 17.5%. 6. Postoperative complications were developed in 11 cases (19.3%) and operative mortality was none. 7. One year survival rate in rejectable cases was 87.0%, 2 year 61.6% and 5 year 44.9%. According to stage, 3 year survival rate was 75.8% in stage I, 16.9% in stage II, 60.9% in stage IIIa, 50% in stage IIIb.

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.321-330
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• 1999

Background : Early diagnosis and proper antibiotic treatment are very important in the management of ventilator-associated pneumonia (VAP) because of its high mortality. Bronchoscopy with a protected specimen brush (PSB) has been considered the standard method to isolate the causative organisms of VAP. However, this method burdens consumer economically to purchase a PSB. Another useful method for the diagnosis of VAP is quantitative cultures of aspirated specimens through bronchoscopic bronchoalveolar lavage (BAL), for which the infusion of more than 120 m1 of saline has been recommended for adequate sampling of a pulmonary segment. However, occasionally it leads to deterioration of the patient's condition. We studied the diagnostic efficacy of minibronchoalveolar lavage (miniBAL), which retrieves only 25 ml of BAL fluid, in the isolation of causative organisms of VAP. Methods: We included 38 consecutive patients (41 cases) suspected of having VAP on the basis of clinical evidence, who had received antibiotics before the bronchoscopy. The two diagnostic techniques of PSB and miniBAL, which were performed one after another at the same pulmonary segment, 'were compared prospectively. The cut-off values for quantitative cultures to define causative bacteria of VAP were more than $10^3$ colony-forming units (cfu)/ml for PSB and more than $10^4$ cfu/ml for BAL. Results: The amount of instilled normal saline required to retrieve 25 ml of BAL fluid was $93{\pm}32 ml$ (mean${\pm}$SD). The detection rate of causative agents was 46.3% (19/41) with PSB and 43.9% (18/41) with miniBAL. The concordance rate of PSB and miniBAL in the bacterial culture was 85.4% (35/41). Although arterial blood oxygen saturation dropped significantly (p<0.05) during ($92{\pm}10%$) and 10 min after ($95{\pm}3%$) miniBAL compared with the baseline ($97{\pm}3%$), all except 3 cases were within normal ranges. The significantly elevated heart rate during ($l25{\pm}24$/min, p<0.05) miniBAL compared with the baseline ($1l1{\pm}22$/min) recovered again in 10 min after ($111{\pm}26$/min) miniBAL. Transient hypotension was developed during the procedure in two cases. The procedure was stopped in one case due to atrial flutter. Conclusion: MiniBAL is a safe and effective technique to detect the causative organisms of VAP.