• Tuberculosis and Respiratory Diseases
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• v.49 no.2
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• pp.179-188
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• 2000

Background : The decision to institute mechanical ventilation for patients with COPD is very difficult. The accurate information regarding weaning success and long-term survival will improve communication with patients and family and enhance informed consent. The aims of this study are to describe outcomes and identify variables associated with survival for patients experiencing mechanical ventilation with an acute respiratory failure of COPD. Methods : The 53 cases of mechanical ventilation in the intensive care unit in the National Medical Center from 1989 to 1998 were included. Data were collected retrospectively from medical records. Weaning success rate and 3 month and 1 year survival rates were estimated. Factors associated with weaning success and survival were determined. Results : Weaning sucess was 55%. For success group with 29 cases, 3 months survival rate was 61% and 1 year survival rate 37%. APACHE II scores in weaning success group were significantly lower than those in the failure group. Factors such as age, sex, comorbid-illnes. previous steroid use, causes of respiratory failure, RVH or arrhythmia on EKG, serum albumin level, arterial blood pH, $PaO_2$, $PaCO_2$, $FEV_1$ duration of mechanical ventilation and steroid use during mechanical ventilation were not associated with weaning success. Only age and serum albumin level were associated with 3 month and 1 year survival. No COPD patients of age more than 75 years and serum albumin level less than 3g/dl had survived at 1 year after weaning success. Conclusion : While weaning success from mechanical ventilation can be predicted by APACHE II score in COPD patients, long-term outcomes of survivors may be influenced by nutritional status and age.

• Tuberculosis and Respiratory Diseases
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• v.40 no.4
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• pp.410-415
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• 1993

Background: The lung abscess predominantly occurs on a dependent region, because its major predisposing factor is aspiration. However, a lung abscess appeared on a nondependent region occasionally. Traditionally bronchoscopy has been performed in patients with lung abscess on a nondependent region for evaluating the endobronchial obstruction such as bronchogenic carcinoma. But the clinical characteristics and necessities of bronchoscopy in patients with lung abscess located at nondependent region have not been discussed previously. Thus, we investigated the underlying etiologies and the necessities of bronchoscpy in patients with lung abscess in a nondependent region. Method: Fifteen patients with cavitary lesion on a nondependent location have been studied retrospectively by reviewing their clinical records, chest PAs, computerized tomograms, and bronchoscopic findings. Results: 1) Most patients were older than 30 years except one, and their mean age was 51 years. The ratio of male to female was 6.5:1. 2) The underlying etiologies were bacterial infections in 13 cases, and tuberculous infection in two cases. However, bronchogenic carcinoma was not found as its etiology. 3) Among thirteen bacterial lung abcess, tweleve cases located at right middle lobe. 4) The findings of bronchoscopy were non-speicifc mucosal change in 8 cases and segmental obstructions in 2 cases. There were no malignant evidences in the finings of cytology and bronchscopic biopsy. 5) Among thirteen bacterial lung abcess, eleven patients showed good clinical reponse to antibiotic therapy. Conclusion: The necessity of early bronchoscopy may need to be re-evaluated in the lung abscess on a nondependent region, unless evidences of bronchial obstruction or bronchogenic carcinoma exist. The pulmonary tuberculosis shoud be regarded as the underlying etiology of the nondependent lung abscess.

• Tuberculosis and Respiratory Diseases
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• v.44 no.2
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• pp.329-337
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• 1997

Background : Since endotracheal tube is the most important factor involved in the imposed work of breathing during mechanical ventilation, extubation of endotracheal tube is supposed to reduce respiratory work of patient. However, some patients show labored breathing after extubation despite acceptable blood gases. We investigated the changes of work of breathing before and after extubation and the factors involved in the change of WOB after extubation. Methods : The subjects were 34 patients(M : F = 20 : 14, mean age = $61{\pm}17yre$) who recovered from respiratory failure after ventilatory support and were considered to be ready for extubation. The patients with clinical or radiologic evidences of upper airway obstruction before endotracheal intubation for mechanical ventilation were excluded. Vital sign, physical examination, chest X-ray, work of breathing and other respiratory mechanic indices were measured prior to, immediately, 6, 24 and 48 hours after extubation serially. Definition of weaning failure after extubation was resumption of ventilatory support or reintubation of endotracheal tube within 48 hour after extubation because of respiratory failure. The patients were classified into group 1(decreased work of breathing), group 2(unchanged work of breathing) and group 3(increased work of breathing) depending on the statistical difference in the change of work of breathing before and after extubation. Results : Work of breathing decreased in 33%(11/34, group 1), unchanged in 41%(14/34, group 2) and increased in 26%(9/34, group 3) of patients after extubation compared with before extubation. Weaning failure occurred 9%(1/11) of group, 1, 28.6%(4/14) of group 2 and 44%(4/9) of group 3 after extubation(p = 0.07). The change of work of breathing after extubation was positively correlated with change of mean airway resistance(mRaw). (r = 0.794, p > 0.01). In three cases of group 3 whose respiratory indices could be measured until 48 hr after extubation, the change in work of breathing paralleled with the sequential change of mRaw. The work of breathing was peaked at 6 hr after extubation, which showed a tendency to decrease thereafter. Conclusions : Reversible increase of work of breathing after extubation may occur in the patients who underwent extubation, and the increase in mRaw could be responsible for the increase in work of breathing. In addition, the risk of weaning failure after extubation may increase in the patients who have increased WOB immediately after extubation.

• Tuberculosis and Respiratory Diseases
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• v.49 no.5
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• pp.594-600
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• 2000

Background : Positive end expiratory pressure (PEEP) ventilation is well established as an integral part of the management of patients with the acute lung injury. PEEP is a key element in the treatment of hypoxemia resulting from pulmonary edema. Pulmonary capillary pressure (Pcap) is the most important factor influencing lung edema formation, and an understanding of how Pcap is altered by variations of PEEP or pulmonary arterial occlusion pressure (PAOP) is important to improve the treatment of acute lung injury patients. This study was performed to evaluate the effects of PEEP on the pulmonary capillary pressure in acute lung injury patients. Methods : This was a prospective study of 11 acute lung injury patients. The effect of PEEP on pulmonary circulation at four different levels (0,4,8, and 12cm$H_2O$) was analyzed. Pcap was estimated visually at bed side with Swan Ganz catheters. The pulmonary vasculature was analyzed by calculating the pressure difference at the arterial and venous parts of the circulation. Results: As PEEP increased from 0 to 12 cm$H_2O$, the mean pulmonary arterial pressure (PAP) and Pcap increased respectively from $22.7{\pm}7.4$ to $25.3{\pm}7.3$ mmHg and $15.3{\pm}3.3$ to $17.8{\pm}3.2$ mmHg (p<0.05). Similarly, PAOP increased from $9.8{\pm}2.1$ to $12.8{\pm}2.1$ mmHg and the central venous pressure increased from $6.1{\pm}1.6$ to $9.3{\pm}2.3$ mmHg(p<0.05). However, the pressure gradient at the arterial (PAP-Pcap) and venous (Pcap-Pcwp) parts of pulmonary circulation remained unchanged at all evaluated PEEP levels. Conclusion : Although Pcap increased gradually with increased the pressure gradient at the arterial and venous part of the pulmonary vasculature remained unchanged at all evaluated PEEP levels in acute lung injury patients.

• Tuberculosis and Respiratory Diseases
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• v.48 no.6
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• pp.887-897
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• 2000

Background : Since the exact pathogenesis of sepsis-induced ARDS has not been elucidated, the mechanisms of enhanced neutrophilic respiratory burst were probed in endotoxin primed neutrophils associated with the roles of phospholipase A2(PLA2), platelet activating factor(PAF) and apoptosis. Methods : In isolated fresh human neutrophils, effects of the inhibition of PLA2 and PAF on the apoptosis were examined by the method of Annexin-FITC/dual PIflow cytometry. The roles of PLA2 and PAF on the neutrophilic respiratory burst were also examined by measuring oxidant generation in cytochrome-c reduction assay. Activities of the PLA2 and lysoPAF acetyltransferase (lysoPAF AT) of the neutrophils were determined to understand the effect of endotoxin on these enzymatic activities which may be related to the neutrophilic respiratory burst and apoptosis. In addition, the role roles of PLA2 and PAF in neutrophilic adhesion to bovine endothelial cells were examined in vitro by neutrophil adhesion assay. To investigate the effect of oxidants on pulmonary surfactant, cytochemical ultrastructural microscopy was performed. To inhibit PLA2 and PAF, non-specific PLA2 inhibitor mepacrine (100 nM) and WEB 2086 (100 nM) or ketotifen fumarate (10 ${\mu}g$/ml) were used respectively in all in vitro experimental sets. WEB 2086 is PAF receptor antagonist, and ketotifen fumarate is a lyso PAF AT inhibitor. Results: The mapacrine treatment, provided and the endotoxin (ETX) treatment, resulted in increased apoptosis of neutrophils (p<0.001) while treatments of WEB 2086 and ketotifen did not. The inhibition of PLA2 and PAF decreased (p<0.001) production of oxidants from PMA-stimulated neutrophils. While endotoxin increased the PLA2 activity of neutrophils (p<0.01), mepacrine supressed (p<0.001) the activity, provided after treatment of ETX. The lyso PAF actyltransferase activity (lyso PAF AT) increased (p<0.01) after treatment of ETX. In contrast, mepacrine, WEB 2086 and ketotifen showed a tendency of decreasing the activity after treatment of ETX. The treatment of ETX incresed (p<0.001) neutrophil adhesion to endothelial cells, which was reversed by inhibition of PLA2 and PAF (p<0.01). The binding of oxidants to pu1monary surfactant was identified histologically. Conclusions : The enhanced neutrophilic respiratory burst by ETX plays a pivotal role in the pathogenesis of ARDS in terms of oxidayive oxidative stress. Increased production of oxidants from neutrophils is mediated by the activations of PLA2 and lyso PAF AT.

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.347-355
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• 1999

Background: Phospholipase C(PLC) plays a central role in cellular signal transduction and is important in cellular growth, differentiation and transformation. There are currently ten known mammalian isozymes of PLC reported to this date. Hydrolysis of phosphatidylinositol 4,5-bisphosphate($PIP_2$) by PLC produces two important second messengers, inositol 1,4,5-trisphosphate($IP_3$) and diacylglycerol. PLC-${\gamma}1$, previously, was known to be activated mainly through growth factor receptor tyrosine kinase. Other mechanisms of activating PLC-yl have been reported such as activation through tau protein in the presence of arachidonic acid in bovine brain and activation by $IP_3$, phosphatidic acid, etc. Very recently, another PLC-${\gamma}1$ activator protein such as tau has been found in bovine lung tissue, which now is considered to be AHNAK protein. But there has been no report concerning AHNAK and its associated disease to this date. In this study, we examined the expression of the PLC-${\gamma}1$ activator, AHNAK, in lung cancer specimens and their paired normal. Methods: From surgically resected human lung cancer tissues taken from twenty-eight patients and their paired normal counterparts, we evaluated expression level of AHNAK protein using immunoblot analysis of total tissue extract Immunohistochemical stain was performed with primary antibody against AHNAK protein. Results: Twenty-two among twenty-eight lung cancer tissues showed overexpression of AHNAK protein (eight of fourteen squamous cell lung cancers, all of fourteen adenocarcinomas). The resulting bands were multiple ranging from 70 to 200 kDa in molecular weight and each band was indistinct and formed a smear, reflecting mobility shift mainly due to proteolysis during extraction process. On immunohistochemistry, lung cancer tissues showed a very heavy, dense staining with anti-AHNAK protein antibody as compared to the surrounding normal lung tissue, coresponding well with the results of the western blot Conclusion: The overexpression of PLC-${\gamma}1$ activator protein, AHNAK in lung cancer may provide evidence that the AHNAK protein and PLC-${\gamma}1$ act in concerted manner in carcinogenesis.

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.374-382
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• 1999

Background: The aim of this study was to investigate etiologic factor, treatment, prognosis of spontaneous pneumothorax (SP). Material and Methods: The medical records of 225 cases of SP experienced at Kyungpook University Hospital from Jan. 1996 to Dec. 1997 were retrospectively analyzed. Results: The patients were 128 primary SP and 97 secondary SP. The mean age was $30{\pm}15.5$ years in primary SP and $51{\pm}7.4$ years in secondary SP. The ratio of male to female was 8:1 in primary SP and 5.5:1 in secondary SP. Smoker was more common in seconday SP (71.1 %) than primary SP (34.4%). About 70% of patients with primary and secondary SP was underweighted. The previous history of SP was present in 28.9% and 25.8% of primary and secondary SP, respectively. The main underlying lung diseases in secondary SP were inactive tuberculosis (68%), active tuberculosis (12.4%) and COPD (11.3%). Tube thoracostomy was performed in 96.8% and 97.9% of primary and secondary SP, respectively. The duration of chest tube insertion was longer in seconday SP ($18.2{\pm}19.59$ days) than primary SP ($7.5{\pm}6.57$ days). The open thoracotomy were performed in 22.7% and 10.3% of primary and secondary SP, respectively. The most com- mon indication of open thoracotomy was recurrence in primary SP and persistent air leak in secondary SP. During following-up of $17{\pm}7.8$ months, the recurrence rate in patients with conservative treatment was 16.5% and 11.8% of primary and secondary SP, respectively. The recurrence was most common within 1 month after discharge. Conclusion: Greater attention and research about SP are necessary for more efficient patient care.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.835-845
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• 1998

Background: Silica-induced lung diseases is characterized by the accumulation of inflammatory cells at early stage and fibrosis in pulmonary parenchyma and interstitium at late stage. As a consequence of inflammation, silicosis is accompanied with the expansion of interstitial collagen and the formation of fibrotic nodule. In this process, several kinds of lung cells produce cytokines which can amplify and modulate pulmonary fibrosis. The alveolar macrophage is a potent source of proflammatory cytokines and growth factor. But in the process of silicotic inflammation and fibrosis, there are many changes of the kinetics in cytokine network. And the sources of cytokines in each phase are not well known. Method: 2.5 mg of silica was instillated into the lung of C57BL/6J mice. After intratracheal instillation of silica, the lungs were removed for imunohistochemical stain at 1, 2, 7 day, 2, 4, 8, 12 week, respectively. We investigated the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$ in lung tissue. Results: 1) The expression of IL-6 increased from 1 day after exposure to 8 weeks in vascular endothelium. Also peribronchial area were stained for IL-6 from 7 days and reached the peak level for 4 weeks. 2) The IL-1 $\beta$ was expressed weakly at the alveolar and peribronchial area through 12 weeks. 3) The TNF-$\alpha$ expressed strongly at alveolar and bronchial epithelia during early stage and maintained for 12 weeks. 4) TGF-$\beta$ was expressed strongly at bronchial epithelia and peribronchial area after 1 week and the strongest at 8 weeks. Conclusion: The results above suggests IL-6, TNF-$\alpha$ appear to be a early inflammatory response in silica induced lung fibrosis and TGF-$\beta$ play a major role in the maintenance and modulation of fibrosis in lung tissue. And the regulation of TNF-$\alpha$ production will be a key role in modultion of silica-induced fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.169-175
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• 1998

Background: Heliox is known to decrease $PaCO_2$ in patients with increased airway resistance by increasing minute ventilation and reducing work of breathing(WOB). Besides these effect, heliox is expected to decrease functional anatomic dead space owing to improvement of peak expiratory flow rate(PEFR) and enhancement of gas distribution. We investigated whether heliox can decrease $PaCO_2$ even at the same minute ventilation (VE) and WOB with $N_2-O_2$ to speculate the effect of the heliox on the anatomic dead space. Material and Method: The subjects were 8 mechanically ventilated patients with asthma or upper airway obstruction(M : F=5 : 3, $68{\pm}10$years) who were under neuromuscular paralysis. The study was consisted of three 15-minutes phases: basal $N_2-O_2$ heliox and washout Heliox was administered via the low pressure inlet of servo 900C, and respiratory parameters were measured by pulmonary monitor(CP-100 pulmonary monitor, Bicore, Irvine, CA, USA). To obtain the same tidal volume(Vt) in heliox phase, the Vt on monitor was adjusted by the factor of relative flow rate of heliox to $N_2-O_2$. Dead space was calculated by Bohr equation. Results: 1) Vt, VE, peak inspiratory pressure(PIP) and peak inspiratory flow rate(PIFR) were not different between $N_2-O_2$ and heliox. 2) PEFR was higher on heliox($0.52{\pm}0.19$L/sec) than $N_2-O_2$($0.44{\pm}0.13$L/sec)(p=0.024). 3) $PaCO_2$(mmHg) were decreased with heliox($56.1{\pm}14.1$) compared to $N_2-O_2$($60.5{\pm}15.9$)(p=0.027). 4) Dead space ventilation(%) were decreased with heliox($73{\pm}9$ with $N_2-O_2$ and $71{\pm}10$ with heliox)(p=0.026). Conclusion: Heliox decreased $PaCO_2$ even at the same VE and WOB with $N_2-O_2$, and the effect was considered to be related with the reduction of anatomic dead space.

• Tuberculosis and Respiratory Diseases
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• v.64 no.5
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• pp.362-368
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• 2008

Background: LKB1(STK11) is a serine/threonine kinase that functions as a tumor growth suppressor. The functions of LKB1 in lung cancer are not completely understood. This study evaluated the relationship between LKB1 protein expression and the clinicopathological features in lung cancer tissues. Methods: The expression of LKB1 was studied in paraffin-embedded tumor blocks, which were obtained from 77 patients who had undergone surgery at Wonkwang University Hospital. The expression of the LKB1 protein was considered positive if the staining intensity in the tumor tissue adjacent to the normal airway epithelium was >30%. Results: The LKB1 expression was positive in 31 (40%) of samples. Loss of LKB1 expression was significantly associated with being male, smoking history, and squamous cell carcinoma. In the peripheral sites, the loss of LKB1 expression was strongly associated with a smoking history. A loss of LKB1 expression was more frequently associated with progression according to TNM staging, particularly more than T2, N progression. Conclusion: There was a significant relationship between the loss of the LKB1 protein and gender, smoking history, and histological type in primary lung cancer. Although LKB1 expression was not found to be a significant prognostic factor, further studies with a larger cohort of patient's lung cancer tissue samples will be needed to confirm this.