• 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.80 no.4
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• pp.344-350
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• 2017

Bronchial asthma is a disease characterized by the condition of airway hyper-responsiveness, which serves to produce narrowing of the airway secondary to airway inflammation and/or various spasm-inducing stimulus. Nonspecific bronchoprovocation testing is an important method implemented for the purpose of diagnosing asthma; this test measures the actual degree of airway hyper-responsiveness and utilizes direct and indirect bronchoprovocation testing. Direct bronchoprovocation testing using methacholine or histamine may have superior sensitivity as these substances directly stimulate the airway smooth muscle cells. On the other hand, this method also engenders the specific disadvantage of relatively low specificity. Indirect bronchoprovocation testing using mannitol, exercise, hypertonic saline, adenosine and hyperventilation serves to produce reactions in the airway smooth muscle cells by liberating mediators with stimulation of airway inflammatory cells. Therefore, this method has the advantage of high specificity and also demonstrates relatively low sensitivity. Direct and indirect testing both call for very precise descriptions of very specific measurement conditions. In addition, it has become evident that challenge testing utilizing each of the various bronchoconstrictor stimuli requires distinct and specific protocols. It is therefore important that the clinician understand the mechanism by which the most commonly used bronchoprovocation testing works. It is important that the clinician understand the mechanism of action in the testing, whether direct stimuli (methacholine) or indirect stimuli (mannitol, exercise) is implemented, when the testing is performed and the results interpreted.

• 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.71 no.1
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• pp.24-29
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• 2011

Background: The rising prevalence of asthma worldwide may be associated with the rising prevalence of obesity in developed nations. Although several studies have suggested a relationship between asthma and obesity, controversy still remains. The aim of this study was to examine the relationship between obesity and asthmatic factors such as atopy, eosinophilia, serum total Ig E and bronchial hyperresponsiveness in chronic cough patients. Methods: This study was a retrospective, observational study in two centers done between January 2007 and June 2008. The subjects included individuals who had a chronic cough. We examined body mass index (BMI) to measure obesity and pulmonary function. We did a metacholine provocation test for airway hyperresponsiveness (AHR), a skin prick test for atopy, and tests for blood eosinophils and serum IgE. Results: A total of 1022 subjects were included. Airway hyperresponsiveness was not related with obesity (p=0.06), and atopy incidence was significant higher in non obese patients (p=0.00). There was no significant difference in serum IgE and blood eosinophil counts between obese and non obese patients. Forced expiratory volue in one second ($FEV_1$)/forced vital capacity (FVC) was significantly reduced in obese patients (p=0.03), but FEV1 and FVC were no significant difference between obese and non obese patients. Conclusion: There is no relationship between obesity and bronchial hyperresponsiveness. The nonobese group appears to have more atopy. The relationship between obesity and bronchial hyperresponsiveness and atopy need further investigation.

• Tuberculosis and Respiratory Diseases
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• v.60 no.2
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• pp.221-227
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• 2006

Background : Cough may be a consequence of bronchial hyperresponsiveness or inflammation. Empirical treatment is important in this context because it difficult to verify the obvious cause of cough using laboratory tests, Corticosteroid has a nonspecific anti-inflammatory effect, and can be used for cough management. However, its response rate has not yet been fully elucidated. This study investigated the short- term effects of inhaled corticosteroid on chronic cough Methods : Patients with chronic cough with a normal chest radiograph and a pulmonary function test were enrolled. Cases with a prior respiratory infection within 8 weeks, a history of bronchial asthma, objective wheezing on examination, subjective symptoms of gastroesophageal reflux or taking an ACE inhibitor were excluded. On the first visit, a methacholine bronchial provocation test, spontaneous sputum eosinophil count performed twice and a paranasal sinus radiograph were checked, and the patients were treated with budesonide turbuhaler $800{\mu}g/day$ for ten days. The primary outcome measure was a decrease in the cough score after treatment. Results : Sixty nine chronic coughers were finally analyzed. The final diagnoses by the routine tests were as follows: bronchial asthma 13.0%, eosinophilic bronchitis 18.8%, paranasal sinusitis 23.2% and non-diagnostic cases 53.6%. The following responses to the inhaled corticosteroid were observed: definite responders, 76.8%, possible responders, 2.9% and non-responders, 20.3%. The response rate was not affected by the final diagnosis even in the non-diagnostic cases. There were minimal adverse drug related effects during the empirical treatment. Conclusion : Routine objective tests such as methacholine provocation, sputum eosinophil count and simple radiographs were notare not suitable for diagnosing chronic cough Therefore, empirical treatment is important. Short term inhaled corticosteroid is effective and can guide a further treatment plan for chronic cough.

• Tuberculosis and Respiratory Diseases
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• v.58 no.1
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• pp.25-30
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• 2005

Background : An insertion-deletion polymorphism of angiotensin converting enzyme (ACE) gene has been shown to be associated with enzyme activity levels of ACE. Reported results that have been mutually contradictory about asthmatic hypersensitiveness and occurrence according to ACE gene insertion (I)/deletion (D) polymorphism. Also, the involvement of the ACE genes as the genetic basis of bronchial asthma is currently controversy. We investigated whether there was any association between polymorphisms of the ACE genes and airway hyper-responsiveness in chronic obstructive pulmonary disease (COPD). Methods : A total of 100 patients with COPD were enrolled in this study. The ACE genotypes were determined in all subjects by polymerase chain reaction. Pulmonary function test including bronchodilator response (BDR), methacholine bronchial provocation test (MBPT) were done in those patients. Airway hyper-responsiveness include any findings of positive BDR or MBPT. Results : In COPD patients, the ACE genotype distribution did not differ significantly among groups of patients with severities of COPD, and with or without airway hyper-responsiveness. Conclusions : These results suggest that polymorphisms of the ACE gene may not be associated with airway hyper-responsiveness, development and severity of COPD.

• Tuberculosis and Respiratory Diseases
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• v.50 no.2
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• pp.196-204
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• 2001

Background : Bronchial asthma is characterized by a reversible airway obstruction, airway hyperresponsiveness, and eosinophilic airway inflammation. The bronchodilator response(BDR) after short acting beta agonist inhalation and PC20 with methacholine inhalation are frequently used for diagnosing bronchial asthma. However, the relationship between the presence of a bronchodilator response and the degree of airway hyperresponsiveness is uncertain. Therefore, the availability of a eosinophil cationic protein (ECP) and a correlation ECP with a bronchodilator response and airway hyperresponsiveness was investigated. Method : A total 71 patients with a moderate to severe degree of bronchial asthma were enrolled and divided into two groups. 31 patients with a positive bronchodilator response and 38 patients with a negative bronchodilator response were evaluated. In both groups, the serum ECP, peripheral blood eosinophil counts, and total IgE level were measured and the methacholine bronchial provocation test was examined. Results : There were no differences observed in age, sex, atopy, and baseline spirometry in both groups. The peripheral eosinophil counts showed no difference in both groups, but the ECP level in group 1 (bronchodilator responder group) was higher than in group 2(non-bronchodilator responder group) ($22.4{\pm}20.7$ vs $14.2{\pm}10.4$, mean$\pm$SD). The PC20 in group 1 was significantly lower than in group 2 ($1.14{\pm}1.68$ vs $66{\pm}2.98$). There was a significant positive correlation between the BDR and ECP, and a negative correlation between the bronchial hyperresponsiveness and ECP. Conclusion : The bronchodilator response significantly correlated with the bronchial hyperresponsiveness and serum ECP in the moderate to severe asthma patients. Hence, the positive bronchodilator response is probably related with active bronchial inflammation and may be used as a valuable index in treatment, course and prognosis of bronchial asthma.

• Tuberculosis and Respiratory Diseases
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• v.57 no.6
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• pp.535-542
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• 2004

Background : Despite the clinical clues of bronchial asthma, some chronic coughers fail to be diagnosed due to negative test results. This study was aimed at evaluating the diagnostic performance of routine objective tests and identifying a cost-effective approach for asthmatics with a chronic cough. Methods : Patients with a chronic cough of more than 3 weeks duration, and showing normal chest radiograph and spirometry were enrolled. On the first visit, objective tests, composed of serum total IgE, peripheral blood eosinophil count, spontaneous sputum eosinophil count, methacholine bronchial provocation test (MBPT) and paranasal sinus radiograph, were performed, with the simultaneous administration of oral prednisolone (0.5mg/kg) for one week. The final diagnoses were made on the basis of the test results, and the patients grouped according to their steroid responsiveness. The role of the etiologic diagnosis tests was evaluated, and the medical costs of the final management plan simulated with respect to three assumed models. Results : Sixty chronic coughers were finally analyzed. The final diagnoses were as follows: bronchial asthma 21.7%, eosinophilic bronchitis 6.7%, paranasal sinusitis 18.3%, presumptive allergy 8.3% and non-diagnostic case 45.0%. Ninety percent were steroid responder. With the bronchial asthma cases, the positive rate of MBPT was 38.5%, with sputum eosinophil count in 84.6%, serum total IgE in 38.5%, and a peripheral blood eosinophil count rate of 30.8%. When the test results and steroid responsiveness data were applied to the 3 models, the chest radiograph, spirometry, sputum eosinophil count and paranasal sinus radiograph test results, and simultaneous short term steroid treatment seemed to have acceptable diagnostic performances, which could be used as a further guide to cost-effective planning. Conclusion : Objective tests, composed of chest radiograph, spirometry, paranasal sinus radiograph and sputum eosinophil count, with simultaneous short term steroid treatment, are suggested as cost-effective approaches for asthmatics with a chronic cough.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.568-573
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• 1994

Corticosteroids are widely used in the treatment of various diseases because of its potent antiinflammatory effect. According to recent knowledge, bronchial asthma is also chronic inflammatory disease. Therefore antiinflammtory agent such as cromoyln sodium and corticosteroid is highly recommended for treament of chronic bronchial asthma. Especially hydrocortisone succinate (Solu-Cortef) is commonly used for treament to acute asthmatic attack via intravenous injection due to have rapid therapeutic onset and short duration. Since Sunaga et al. reported acute asthma attack after hydrocortisone injection in 1973, several cases of bronchospam with or without angioedema and urticaria after intravenous injection of hydrocortisone have been reported. We experienced a case of severe bronchospasm and acute respiratory failure after intraveous injection of hydrocortisone succinate in 64 year-old female asthmatic patient who visited to emergency room for acute asthmatic attack. About 5 minites after Solu-Cortef injection, a severe bronchospasm with arterial hypoxemia was developed. In order to confirm the suspected relationship between the offending drug(Solu-Cortef) and acute bronchospasm, we examed intravenous and inhalation provocation test by hydrocortisone succinate and methylprednisolone(control). After administration of hydrocortisone succinate via intravenous and inhalation route, severe asthmatic attack occurred. But administration of intravenous methylprednisolone and orall triamcinolone and saline were not provoke bronchospasm. Skin test using hydrocortisone sodium succinate was also positive. Administration of hydrocortisone is very serious to asthmatic patient with hydrocortisone hypersensitivity. Therefore, the clinician must be have history taking about previous adverse reaction of steroid before its clinical use. And methylprednisone may be useful and safe drug to the treatment of acute asthmatic patient with hydrocortisone hypersensitivity.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1188-1198
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• 1998

Background : The purpose of the present study was to determine the protective effect of antiasthmatic activity of inhaled heparin, cromolyn sodium, budesonide, furosemide in exercise-induced asthma(EIA). The other important considerable point of this study was the mechanism of bronchoconstriction on EIA. Methods : Eight subjects with a history of EIA were studied on 5 different experiment days. After obtaining baseline $FEV_1$ and FVC, subjects performed a standardized exercise challenge. EIA was assessed by measurement of $FEV_1$ before and after exercise. On experiment day 4, the exercise challenge was performed after the subjects inhaled either heparin (1,000 units/kg/day for 5 days), furosemide (1mg/kg for 5 days), cromolyn (4mg/day for 5 days), or budesonide ($400{\mu}g/day$ for 5 days). On experiment day 5, the methacholine bronchial provocation test was performed. On experiment day 3, activated partial thromboplastine time(aPTI) was checked. Results : Maximum decrements of $FEV_1$ (mean${\pm}$SE) among 0 to 120 minutes after exercise were as follows : heparin was $83.1{\pm}4.81%$ (p=0.010), furosemide was $80.5{\pm}6.87%$ (p=0.071), cromolyn was $86.8{\pm}6.53%$ (p=0.340), and budesonide was $79.4{\pm}7.31%$ (p=0.095). Above medications were compared to the control value ($72.5{\pm}18.2%$) by paired t-test. No medications had effect on $PD_{20}$ of methacholine bronchial provocation test The results were control $1.58{\pm}0.49{\mu}mol$), heparin ($4.17{\pm}1.96{\mu}mol$), furosemide ($1.85{\pm}0.86{\mu}mol$), cromolyn ($2.19{\pm}0.89{\mu}mol$), and budesonide ($3.38{\pm}1.77{\mu}mol$), respectively(p>0.05). The inhaled heparin had no effect of anticoagulation. Conclusion : These data demonstrate that inhaled heparin has a protective effect on EIA. The effect of inhaled cromolyn was statistically absent with manufacture's recommended dosage on EIA. So, the dosage of cromolyn should be carefully evaluated in future. Although inhalation of budesonide and furosemide have no statistical significance compared to control, these drugs also have some protective effects on EIA.