• 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.49 no.2
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• pp.198-206
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• 2000

Background : Pulmonary complications following bonemarrow transplantation (BMT) are common and associated with a high mortality rate. We investigated the yield, safety, and impact of fiberoptic bronchoscopy (FOB) for diagnosis of postBMT pneumoniae. Methods : From May 1997 to April 2000, 56 FOBs were performed in 52 post BMT patients for clinical pneumoniae. BMT patients with respiratory symptoms and/or pulmonary infiltrates had a thoracic HRCT(high resolution computed tomography) and bronchoscopic examination including BAL (bronchoalveolar lavage), TBLB (transbronchial lung biopsy), PSB (protected specimen brush). Results : The characteristics of the subjects were as follows : 37 males, 15 females, mean age of 31.3 years(l7-45), 35 sibling donor allogenic BMTs, 15 nonrelated donor allogenic BMTs, and 2 autologous BMTs. Fiftynine percent of FOBs (33 FOBs, 31 patients) were diagnostic. Isolated pathogens included the following : 12 cytomegalovirus (CMV) (21.4 %), 7 pneumocystis carinii (PC) (12.5 %), 11 CMV with PC (19.6 %), 2 Mycobacaterium tuberculosis (3.6%), and 1 streptococcus (1.8%). Most of the radiographic findings were diffuse interstitial lesions. CMV pneumoniae had mainly diffuse interstitial nodular lesion, and PC pneumoniae had diffuse, interstitial ground glass opacity(GGO). When CMV was accompanied by PC, a combined pattern of nodular and GGO was present. Of the 56 cases (23.2%), 13 died of CMV pneumoniae (n=2), PCP (n=2),mixed infection with CMV and PC (n=3), underlying GVHD (n=1), underlying leukemia progression (n=1), or respiratory failure of unknown origin (n=4). There was no major complication by bronchoscopy. Only 3 cases developed minor bleeding and 1 episode temporary hypoxemia. Conclusion : Based on our findings, CMV and PC are the major causes of postBMT pneumoniae. In addition, BAL can be considered a safe and accurate procedure for the evaluation of pulmonary complications after BMT.

• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.639-648
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• 1997

Background : Arterial hypoxemia has been noted in patients with liver cirrhosis because of bronchial vessel dilatation. Cabenes et al. reported that bronchial hyperresponsiveness to the metacholine inhalation was observed in patients of left side heart failure, he suggested that one of the mechanism was bronchial vessel dilatation. We hypothesized that patients of liver cirrhosis might have bronchial hyperresponsiveness to metacholine inhalation due to portal hypertension. We evaluate the relationship between bronchial responsiveness and severity of liver cirrhosis, severity of portal hypertension. Methods : In the 22 patients of the liver cirrhosis with clinical portal hypertension, metacholine provocation test was done and determined $PC_{20}FEV1$. We classified liver cirrhosis according to Pugh-Child classification. Esophagogastroscopies were performed for the evaluation of the relationship between bronchial hyperresponsiveness and severity of esophageal varix. Results : In the 22 cases of the liver cirrhosis with clinical portal hypertension. The causes of liver cirrhosis, alcoholic hepatitis was 9 cases, hepatitis B virus was 12 cases, hepatitis C virus was 1 case, and 151 cases (68.18%) of total 22 cases were positive in metacholine provocation test. In positive cases. There was no significant relationship between $PC_{20}FEV1$ and severity of liver cirrhosis which were classified by Pugh-Child classification or severity of esophageal varix(p<0.05). Conclusion : we observed that bronchial responsiveness to metacholine increased in the patients of liver cirrhosis and there was no significant relationship between the severity of liver cirrhosis and the severity of esophageal varix.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.404-415
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• 1998

Background: Sleep apnea syndrome, which occurs in 1~4 % of the adult population, frequently has different cardiovascular complications such as hypertension, ischemic heart disease, cardiac arrythmia as well as sleep-wake disorder such as excessive daytime hypersomnolence or insomnia. Mortality and vascular morbidity are reported to be significantly higher in sleep apnea syndrome patients than in normal population. According to the recent studies, autonomic dysfunction as well as hypoxemia, hypercapneic acidosis, and increased respiratory effort, may playa role in the high prevalence of cardiovascular complications in patients with sleep apnea syndrome. However the cause and mechanism of autonomic neuropathy in patients with sleep apnea syndrome are not well understood. We studied the existence of autonomic neuropathy in patients with sleep apnea syndrome and factors which influence the pathogenesis of autonomic neuropathy. Method: We used the cardiovascular autonomic neuropathy(CAN) test as a method for evaluation of autonomic neuropathy. The subjects of this study were 20 patients who diagnosed sleep apnea syndrome by polysomnography and 15 persons who were normal by polysomnography. Results: Body mass index and resting systolic blood pressure were higher in sleep apnea group than control group. Apnea index(Al), respiratory disturbance index(RDI) and snoring time percentage were significantly higher in sleep apnea group compared with control group. But there were no significant differences in saturation of oxygen and sleep efficiency in two groups. In the cardiac autonomic neuropathy test, the valsalva ratio was significantly low in sleep apnea group compared with control group but other tests had no differences between two groups. The CAN scores and corrected QT(QTc) interval were calculated significantly higher in sleep apnea group, but there were no significant correlations between CAN scores and QTc interval. There were no significant data of polysomnography to correlate to the CAN score. It meant that the autonomic neuropathy in patients with sleep apnea was affected by other multiple factors. Conclusion: The cardiovascular autonomic neuropathy test was a useful method for the evaluation of autonomic neuropathy in patients with sleep apnea syndrome and abnormalities of cardiovascular autonomic neuropathy were observed in patients with sleep apnea syndrome. However, we failed to define the factors that influence the pathogenesis of autonomic neuropathy of sleep apnea syndrome. This study warrants futher investigations in order to define the pathogenesis of autonomic neuropathy in patients with sleep apnea syndrome.

• Tuberculosis and Respiratory Diseases
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• v.42 no.1
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• pp.58-66
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• 1995

Background: Acute interstitial pneumonia is a relatively rare form of interstitial pneumonia, since the vast majority of interstitial pneumonia have a more chronic course. It corresponds to the lesion described by Hamman and Rich, as Hamman-Rich disease in 1944. Another name in the clinical literature is accelerated interstitial pneumonia, idiopathic acute respiratory distress syndrome (idiopathic ARDS), and the organizing stage of diffuse alveolar damage. Acute interstitial pneumonia differs from chronic interstitial pneumonia by clinical and pathologic features. Clinically, this disease is characterized by a sudden onset and a rapid course, and reversible disease. Method and Purpose: Five cases of pathologically proven acute interstitial pneumonia were retrospectively studied to define the clinical, radiologic, and pathologic features. Results: 1) The five cases ranged in age from 31 to 77 years old. The onset of illness was acute in all patients, it began with viral-like prodrome 6~40 days prior to shortness of breath, and respiratory failure eventually developed in all patients. In 2 cases, generalized skin rash was accompanied with flu-like symptoms. Etiologic agent could not be identified in any case. 2) All patients had leukocytosis and severe hypoxemia. Pulmonary function test of 3 available cases shows restrictive ventilatory defect, and one survived patient(case 5) has a complete improvement of pulmonary function after dismissal. 3) Diffuse bilateral chest infiltrates were present radiologically. Theses were the ground-glass, consolidation, and reticular densities without honeycomb fibrosis in all patients. The pathologic abnormalities were the presence of increased numbers of macrophages and the formation of hyaline membranes within alveolar spaces. There was also interstitial thickening with edema, proliferation of immature fibroblast, and hyperplasia of type II pneumocyte. In the survived patient(case5), pathologic findings were relatively early stage of acute interstitial pneumonia, such as hyaline membrane with mild interstitial fibrosis. 4) Of the 5 patients, four patients died of respiratory failure 14~90 days after onset of first symptom, and one survived and recovered in symptoms, chest X ray, and pulmonary function test Conclusion: These results emphasize that acute interstitial pneumonia is clinically, radiologically, and pathologically distinct form of interstitial pneumonia and should be separated from the group of chronic interstitial pneumonia. Further studies will be needed to evaluate the pathogenesis and the treatment of acute interstitial pneumonia.

• Tuberculosis and Respiratory Diseases
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• v.66 no.3
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• pp.192-197
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• 2009

Background: Despite the benefits of home oxygen therapy in patients suffering chronic respiratory failure, previous reports in Korea revealed lower compliance to oxygen therapy and a shorter time for oxygen use than expected. However, these papers were published before oxygen therapy was covered by the national insurance system. Therefore, this study examined whether there were some changes in compliance, using time and other clinical features of home oxygen therapy after insurance coverage. Methods: This study reviewed the medical records of patients prescribed home oxygen therapy in our hospital from November 1, 2006 to September 31, 2008. The patients were interviewed either in person or by telephone to obtain information related to oxygen therapy. Results: During study period, a total 105 patients started home oxygen therapy. The mean age was 69 and 60 (57%) were male. The mean oxygen partial pressure in the arterial blood was 54.5 mmHg and oxygen saturation was 86.3%. Primary diseases that caused hypoxemia were COPD (n=64), lung cancer (n=14), Tb destroyed lung (n=12) and others. After oxygen therapy, more than 50% of patients experienced relief of their subjective dyspnea. The mean daily use of oxygen was 9.8${\pm}$7.3 hours and oxygen was not used during activity outside of their home (mean time, 5.4${\pm}$3.7 hours). Twenty four patients (36%) stopped using oxygen voluntarily 7${\pm}$4.7 months after being prescribed oxygen and showed a less severe pulmonary and right heart function. The causes of stopping were subjective symptom relief (n=11), inconvenience (n=6) and others (7). Conclusion: The prescription of home oxygen has increased since national insurance started to cover home oxygen therapy. However, the mean time for using oxygen is still shorter than expected. During activity of outside their home, patients could not use oxygen due to the absence of portable oxygen. Overall, continuous education to change the misunderstandings about oxygen therapy, more economic support from national insurance and coverage for portable oxygen are needed to extend the oxygen use time and maintain oxygen usage.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.795-804
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• 1998

Background: Chronic eosinophilic pneumonia(CEP) is interstitial lung disease characterized by multiple infiltration on radiographic study, accumulation of eosinophils in the alveolar space and interstitium of the lung, chronic persistent symptoms and possible relapse. Acute eosinophilic pneumonia(AEP) is a recently described illness, characterized by rapid clinical course, acute respiratory insufficiency and no relapse. Method : To better characterize acute and chronic eosinophilic pneumonia, we studied the clinical and laboratory features of 16 patients(AEP : 7 patients, CEP : 9 patients), which were clinico-pathohistologically diagnosed and not to be associated with organic disorders producing peripheral blood eosinophilia. Results: The mean age was higher for patients with CEP than for patients with AEP ($55.4{\pm}15.1$ vs. $24.6{\pm}7.9$ years, p<0.05). High fever(above $38^{\circ}C$) was presented in all patients of AEP and in one patient(11%) of CEP. All patients of AEP and eight patients (89%) of CEP showed bilateral pulmonary infiltrates, and 6 patients(86%) of AEP and 2 patients(22%) of CEP showed pleural effusion in chest radiograph. The mean white blood cell count of AEP and CEP were $17,186/mm^3$ and $12,867/mm^3$, respectively. The mean peripheral blood eosinophil count of AEP and CEP were $939/mm^3$ and $2,104/mm^3$, respectively. The mean eosinophil fraction of BAL fluid of AEP and CEP were 32.4% (range: 18~47%) and 35.8% (range: 15.3~88.2%), respectively. The mean $PaO_2$ was lower for patients with AEP than for patients with CEP ($44.1{\pm}15.5$ vs. $62.7{\pm}6.9$mmHg, p<0.05). All patients of AEP and CEP were initially treated with antibiotics. All patients of CEP and one patients of AEP were finally required systemic steroid therapy. 6 patients of AEP were improved without steroid therapy. Relapse was observed in 3 patients(33%) of CEP. Conclusion : Compair with of chronic eosinophilic pneumonia, acute eosinophilic pneumonia was characterized by relatively young age, acute onset, high fever, severe hypoxemia, diffuse pulmonary infiltrates with pleural effusion, steroid therapy is effective but spontaneous improvement with conservative therapy was frequent.