• Tuberculosis and Respiratory Diseases
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• v.57 no.3
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• pp.221-225
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• 2004

• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.165-174
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• 1995

Background: Exercise is one of the most common precipitants of acute asthma encountered in clinical practice. The development of airflow limitation that occurs several minutes after vigorous exercise, i. g. exercise-induced bronchoconstriction(EIB), has been shown to be closely correlated with the nonspecific bronchial hyperresponsiveness, which is the hallmark of bronchial asthma. All previous reports that assessed the correlation of EIB to nonspecific bronchial hyperresponsiveness have focused on airway sensitivity($PC_{20}$) to inhaled bronchoconstrictor such as methacholine or histamine. However, maximal airway narrowing(MAN), reflecting the extent to which the airways can narrow, when being exposed to high dose of inhaled stimuli, has not been studied in relation to the degree of EIB. Methods: Fifty-six children with mild asthma(41 boys and 15 girls), aged 6 to 15 years(mean${\pm}$SD, $9.9{\pm}2.5$ years) completed this study. Subjects attended the laboratory on two consecutive days. Each subject performed the high-dose methacholine inhalation test at 4 p.m. on the first day. The dose-response curves were characterized by their position($PC_{20}$) and MAN, which was defined as maximal response plateau(MRP: when two or three data points of the highest concentrations fell within a 5% response range) or the last of the data points(when a plateau could not be measured). On the next day, exercise challenge, free running outdoors for ten minutes, was performed at 9 a.m.. $FEV_1$ was measured at graduated intervals, 3 to 10 minutes apart, until 60 minutes after exercise. Response(the maximal ${\triangle}FEV_1$ from the pre-exercise value) was classified arbitrarily into three groups; no response((-) EIB: ${\triangle}FEV_1$<10%), equivocal response ($({\pm})$EIB:10%<${\triangle}FEV_1$<20%) and definite response($({\pm})$EIB:${\triangle}FEV_1$>20%). Results: 1) When geometric mean $PC_{20}$ of the three groups were compared, $PC_{20}$ of (+) EIB group was significantly lower than that of (-)EIB group. 2) There was a close correlation between $PC_{20}$ and the severity of EIB in the whole group(r=-0.568, p<0.01). 3) Of the total 56 subjects, MRP could be measured in 36 subjects, and the MRP of these subjects correlated fairly with the severity of EIB(r=0.355, p<0.05) 4) The MAN of (+) EIB group was significantly higher than that of (-)EIB group(p<0.01). 5) The MAN correlated well with the severity of EIB in the whole group(r=0.546, p<0.01). Conclusion: The degree of MAN as well as bronchial sensitivity($PC_{20}$) to methacholine is correlated well with the severity of EIB. The results suggest that the two main components of airway hyperresponsiveness may be equally important determinants of exercise reactivity, although the mechanism may be different from each other. The present study also provides further evidence that EIB is a manifestation of the increased airway reactivity characteristic of bronchial asthma.

• 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.52 no.1
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• pp.24-36
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• 2002

Background: Bronchial reactivity is known to be a component of airway hyperresponsiveness, a cardinal feature of asthma, with bronchial sensitivity, and is increments in response to induced doses of bronchoconstrictors as manifested by the steepest slope of the dose-response curve. However, there is some controversy regarding methods of measuring bronchial reactivity and clinical impact of such measurements. The purpose of this study was to evaluate the clinical significance and assess the clinical use by analyzing the relationship of the bronchial sensitivity, the clinical severity and the changes in pulmonary function with bronchial reactivity. Method: A total of 116 subjects underwent a methacholine bronchial provocation test. They were divided into 3 groups : mild intermittent, mild persistent, moderate and cough asthma. Severe patients were excluded. Methacholine PC20 was determined from the log dose-response curve and PC40 was determined by one more dose inhalation after PC20. The steepest slope of log dose-response curve, connecting PC20 with PC40, was used to calculate the bronchial reactivity. Body plethysmography and a single breath for the DLCO were done in 43 subjects before and after methacholine test. Results: The average bronchial reactivity was 38.0 in the mild intermittent group, 49.8 in the mild persistent group, 61.0 in the moderate group, and 41.1 in the cough asthma group. There was a weak negative correlation between PC20 and bronchial reactivity. A heightened bronchial reactivity tends to produce an increased clinical severity in patients with a similar bronchial sensitivity and basal spirometric pulmonary function. There were significant correlations between the bronchial reactivity and the initial pulmonary function before the methacholine test in the order of sGaw, Raw, $FEV_1$/FVC, MMFR. There were no correlations between the bronchial sensitivity and the % change in the pulmonary function parameters after the methacholine test. However, there were significant correlations between the bronchial reactivity and the PEF, $FEV_1$, DLCO. Conclusion: There was weak significant negative correlation between the bronchial reactivity and the bronchial sensitivity, and the bronchial reactivity closely reflected the severity of the asthma. Accordingly, measuring both the bronchial sensitivity and the bronchial reactivity can be of assistance in assessing of the ongoing disease severity and in monitoring the effect of therapy.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.341-350
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• 1998

Background: Airway hyperreponsiveness is a cardinal feature of asthma. It consists of both an increased sensitivity of the airways, as indicated by a smaller concentration of a constrictor agonist needed to initiate the brochoconstrictor response and an increased reactivity, increments in response induced subsequent doses of constrictor, as manifested by slopes of the dose-response curve. The purpose of this study is to observe the relationship between bronchial sensitivity and reactivity in asthmatic subjects. Method: Inhalation dose-response curves using methacholine were plotted in 56 asthmatic subjects. They were divided into three groups(mild, moderate and severe) according to clinical severity of bronchial asthma. PC20 were determined from the dose-response curve as the provocative concentration of the agonist causing a 20% fall in FEVl. PC40 were presumed or determined from the dose response curve, using the PC20 and the one more dose after PC20. Reactivity was calculated from the dose-response curve regression line, connecting PC20 with PC40. Results: PC20 were 1.83mg/ml in mild group, 0.96mg/ml in moderate, and 0.34mg/ml in severe. PC40 were 7.l7mg/ml in mild group, 2.34mg/ml in moderate, and 0.75mg/ml in severe. Reactivity were $24.7{\pm}17.06$ in mild group, $46.1{\pm}22.l0$ in moderate, and $59.0{\pm}5.82$ in severe. There was significant negative correlation between PC20 and reactivity (r= -0.70, P<0.01). Conclusion: Accordingly, there was significant negative correlation between bronchial sensitivity and brochial reactivity in asthmatic subjects. However, in some cases, there were wide variations in terms of the reactivity among the subjects who have similar sensitivity. So both should be assessed when the bronchial response tor bronchoconstrictor agonists is measured.

• Tuberculosis and Respiratory Diseases
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• v.39 no.5
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• pp.392-399
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• 1992

Background: Despite dyspnea is a predominant complaint of patients with respiratory disease, the mechanisms contributing to the sensation of breathlessness are poorly understood. Traditionally, physicians have measured objective pulmonary function to assess severity of dyspnea. But it will be also useful to measure subjective dyspnea index because dyspnea probably depends on a complex interplay of mechanical, experimental, emotional and other factors. Method: We measured breathlessness at rest, after Methacholine challenge and then bronchodilator inhalation using a Visual Analogue Scale (VAS) and Borg Scale Dyspnea Index (BSDI) in stable asthmatic patients. Spirometry was performed concomittently. Results: There was no correlation between dyspnea index and FEV1. There was also no correlation between the change in dyspnea index and change in FEV1. The change in dyspnea index after methacholine and bronchodilator was greater in clinically mild asthmatic patients than clinically severe symptomatic group. Conclusion: In asthmatic patients, there was a wide variation in sensory response for any given FEV1, and the change in perception of dyspnea was greater in those with clinically mild symptoms. The measurement of dyspnea index may yield information complementary to that obtained by spirometry.

• Tuberculosis and Respiratory Diseases
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• v.59 no.6
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• pp.664-669
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• 2005

Objectives : To evaluate the clinical significance of abnormal bronchi originating from the trachea or main bronchi. Methods : 21 patients (male:female ratio, 13:8; mean age, 58.2 years, range 34-77), who were diagnosed with major tracheobronchial anomalies by bronchoscopy from January 2001 to March 2005, were enrolled in this study. The anomalous bronchi consisted of 13 tracheal bronchi and 8 cardiac accessory bronchus. The clinical features, bronchoscopic findings, and outcomes were analyzed retrospectively. Results : Common symptoms, including hemoptysis, cough and dyspnea, resulted from the underlying lung disease regardless of the bronchial anomalies. In this series of 13 tracheal bronchi, 7 cases originated from the trachea within 1cm of the carina (carinal type) and 6 cases originated at a higher level(tracheal type). Most patients had favorable outcome with conservative treatment for the underlying lung disease. Conclusion : Most tracheobronchial anomalies are found incidentally in the process of diagnosing lung disease. The clinical outcome of patients with a bronchial anomaly depends on the underlying lung disease.

• Tuberculosis and Respiratory Diseases
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• v.47 no.4
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• pp.517-524
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• 1999

Background : Airway inflammation and hyperresponsiveness are recognized as major characteristics of bronchial asthma. Airway inflammation has usually been assessed by invasive methods, e.g. BAL or bronchial biopsy, but recent studies proposed induced sputum as another reliable and non-invasive tool to investigate airway inflammation in asthmatic patients. Thus, the relationship between airway inflammation assessed by induced sputum and airway hyperresponsiveness was investigated in asthmatic patient. Method : Airway responsiveness was determined by the concentration that caused a 20% decrease in $FEV_1$($PC_{20}$) after inhaling incremental concentrations of methacholine. The numbers of inflammatory cells and the concentration of eosinophilic cationic protein(ECP) were assessed in induced sputum obtained by inhalation of hypertonic saline(3%). Result: We analyzed sputum induced in 15 stable asthmatic patients. The differential cell count(%) of macrophages, neutrophils, eosinophils and lymphocytes in induced sputum were $39.1{\pm}27.0%$, $29.6{\pm}21.0%$, $28.8{\pm}18.8%$, $1.3{\pm}3.1%$ respectively. The mean value of baseline FEV1(predicted) and ECP were $76.3{\pm}30.3%$ and $1,101{\pm}833{\mu}g/L$ respectively. The geometric mean value of $PC_{20}$ was 0.56 mg/mL. The relationships between the sputum eosinophil and ECP in induced sputum, and between sputum eosinophil and degree of airway responsiveness($PC_{20}$) were found to be significantly correlated (r=0.81, p<0.05 and r=-0.78, p<0.05, respectively). Sputum neutrophils and $PC_{20}$ were not correlated to each other (r=0.11, p=0.69) and a significant negative correlation was found between ECP and baseline $FEV_1$(predicted)(r=-0.62, p<0.05). Conclusion : The results of this study suggest that an induced sputum via a inhalation of hypertonic saline is useful to determine a patient's status of airway inflammation, and airway inflammation is one of the major causal factors in the development of bronchial hyperresponsiveness in asthmatic patients.

• Tuberculosis and Respiratory Diseases
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• v.46 no.4
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• pp.555-563
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• 1999

Background: Chronic cough is a common symptom that requires the systematic diagnostic approach for proper evaluation. Postnasal drip syndrome(PNDS), bronchial asthma, gastroesophageal reflux disease(GERD), and chronic bronchitis are among the common causes. This study was conducted to evaluate the spectrum and the frequency of the causes of chronic cough. Methods: We prospectively evaluated 93 patients who had chronic cough despite normal chest radiographic finding. History and physical examination were done along with paranasal sinus radiograph, spirometry, bronchoprovocation test and 24-hours' ambulatory aesophageal pH monitoring as necessary. Results: Forty-nine(52%) of the 93 patients had PNDS, 15 patients(16%) bronchitis, 10 patients(11%) asthma, 4 patients (4%) GERD, 7 patients (8%) both PNDS and asthma, 4 patients (4%) undiagnosed condition and 4 patients(4%) were taking ACE inhibitor. Sixty-nine percent of the patients with PNDS improved after follow up, 73% patients with bronchitis, 80% patients with asthma, 50% patients with GERD, 100% patients with both PNDS and asthma, and 100% patients with ACE inhibitor. Conclusion: PNDS was the most common causes of chronic cough. Bronchitis was the second and asthma the third in frequency. The etiology of chronic cough can be determined easily by history and physical examination, successful therapy initiated in most patients. The response to specific therapy also was important in evaluation of chronic cough.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.752-759
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• 1995

Background: Bronchial asthma is characterized by noctunal dyspnea, cough and wheezing because of airway hyperresponsiveness to nonspecific stimuli. These symptoms and signs are also observed in patients with congestive heart failure. Therefore, this is so called "cardiac asthma". There are lots of experimental and clinical datas to suggest that airway dysfunctions occur in acute and chronic congestive heart failure. However, it is still controversial whether bronchial hyperresponsiveness is present in patients with congestive heart failure. To assess whether bronchial hyperresponsiveness is present in patients with congestive heart failure and to demonstrate the relationship between bronchial responsiveness and vascular pressure, we performed methacholine provocation test in 11 patients with mitral valvular heart disease. Methods: All patients were in the New York Heart Association functional class II and treated continuously with digoxin and/or dichlozid and/or angiotensin converting enzyme inhibitor except one patient. All patients were undergone right and left side heart catheterization for hemodynamic measurements. A 20 percent fall of peak expiratory flow rate were considered as positive response to methacholine provocation test. Results: 1) Only one patient who has normal pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac index was positive in methacholine provocation test. 2) Their mean pulmonary artery pressure, pulmonary capillary wedge pressure were $21.72{\pm}9.70mmHg$, $15.45{\pm}8.69mmHg$ respectively which were significantly higher. Conclusion: It is speculated that in stable congestive heart failure patients, bronchial responsiveness as assessed by methacholine provocation test may not be increased.