• 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.

• The Korean Journal of Pain
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• v.8 no.2
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• pp.331-335
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• 1995

Asthma is a disease of the airways that is characterized by increased responsiveness of the tracheobronchial tree to a multiplicity of stimuli. A number of causes have been postulated for the increased airway reactivity of asthma is conservative as beta-adrenergic agonist, methylxanthines, glucocorticoids, anticholinergics and mast cell stabilizing agent. Stellate ganglion block for the treatment of bronchial asthma has its controversies. Stellate ganglion block was performed for the treatment of 3 patients with bronchial asthma. After stellate ganglion blocks, dyspnea, coughing and wheezing was markedly reduced. Lung function test improved with 1 st case. Two asthma cases were able to discontinue medication for asthma. No severe aggrevation of bronchial symptoms were noted after stellate ganglion blocks. It suggested that stellate ganglion block can be safely performed on bronchial asthmatic patients.

• 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.

• Journal of Haehwa Medicine
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• v.18 no.1
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• pp.1-8
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• 2009

This study analyzed the contents of the research papers of Complementary Medicine concerning the inhalation drug for asthma published in Pubmed during lately 10 years. As a result, the following conclusion was drawn. 1. There were 5 papers concerning 2 review articles, 2 experimental studies and 1 clinical study. 2. Interventions of research papers are glutathione, microorganism fermentation extract (EM-X), ginkgolide and compound Chinese herbal monomer recipe (ligustrazin, baicalin, ginkgolide). 3. There is no controlled study for effect of inhaled glutathione, on the contrary it induced bronchial constriction in sulfites sensitive asthmatics. 4. Inhalation of EM-X reduced airway hyper-reactivity and level of IL-4, IL-5 and IL-13 in OVA challenged asthmatic mice. 5. Ginkgolide nebulized inhalation reduced symptomatic scorings and eosinophil cationic protein, improved FEV1 and PEF. 6. Compound Chinese herbal monomer (CHM) recipe reduced blood eosinophil count, eosinophil count and total cell cound in BALF, depressed airway hyper-responsiveness and airway inflammation.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.1012-1021
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• 1998

Background : It is known that airway inflammation is present in most patients with asthma, but the relationship between symptoms and the severity and nature of airway inflammation has not been established. Cough variant asthma is defined as an asthma in which the dominant symptom is cough, and the condition can be successfully treated with inhaled steroids. This study was performed to evaluate the time course of bronchial responsiveness according to an inhaled anti-inflammatory therapy and the factors which affect the resolution of bronchial responsiveness, and an efficacy of nedocromil to cough asthma. Method: A prospective study for the investigation of bronchial responsiveness according to an inhaled anti-inflammatory treatment in sixty-one cough asthmatics was performed. Twenty-three entered budesonide ($400{\mu}g{\times}2/day$), twenty-two entered nedocromil ($4mg{\times}2/day$) and sixteen patients entered combined group. The bronchial hyperresponsiveness (BHR) was estimated by methacholine challenge test using counted breath method. The symptom was estimated by 'symptom score'. Reevaluation of BHR and symptom was performed at 2 month after treatment, and if BHR was not resoluted at this time, regarded as a non-responder, and then follow-up of BHR and symptom was performed at 4- and/or 6 month after treatment. Results: The improvement of BHR and symptom was significant in 2 month (p<0.05), but there was no change of them during follow-up period of 4- and/or 6 month in non-responders. In comparison of allergic markers such as serum total IgE, peripheral eosinophil count and skin test reactivity between responders and non-responders, there was no difference in each other. However, in comparison of other factors such as cumulative pack-years, symptom duration, age, gender, and the initial degree of PC20, there was a significant difference in each other(p<0.05). The percent of patients with the resolution of BHR in 2 month was not different in each group(p=0.95). There was no significant difference in the degree of improvement of BHR and symptom in each group. Conclusion: Bronchial responsiveness and symptom was not significantly improved in non-responders during follow-up period of 4- and/or 6 month. The effect of inhaled nedocromil was equivalent to that of inhaled steroid in cough asthmatics, and the response to combined treatment is not superior to that achieved by either of these agents used alone.

• Tuberculosis and Respiratory Diseases
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• v.39 no.3
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• pp.219-227
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• 1992

Background: Acute and chronic airway inflammation are important in the pathogenesis of bronchial asthma. Corticosteroids have proved to be very effective in the management of asthma. Although the mechanism by which they produce this effect is still debated, suppression of the inflammatory response is thought to be the most likely. Although inhaled steroids are known to be safe and have less side effects than oral steroids, the extent which inhaled steroids have beneficial and the detrimental effects in the treatment of asthma has remained open to question. Budesonide is a recently developed corticosteroid for inhalation treatment with a strong local effect combined with rapid inactivation in the systemic circulation. We set out to look in more detail at the time course of change in bronchial reactivity, clinical symptoms and the effects on the adrenal function during 6 weeks of treatment with budesonide (800 ug per day). Methods: Clinical symptoms, pulmonary function test, histamine $PC_{20}$, serum ACTH and cortisol (8 AM and 4 PM) were measured in 23 allergic asthmatic patients before and after 6 weeks of treatment with budesonide. Results: 1) Pulmonary function test; PEFR, FEV1 and FVC after 6 weeks of treatment with budesonide were higher than those before treatment. 2) Clinical symptoms; Clinical symptoms were significantly improved after 3 weeks and 6 weeks of treatment with budesonide. 3) Histamine provocation; Histamine $PC_{20}$ after 6 weeks of treatment with budesonide was significantly higher than that before treatment. 4) Adrenal function; 6 weeks of budesonide therapy did not significantly affect the level of serum ACTH and cortisol. Conclusion: From these results, it is concluded that budesonide therapy improved the clinical symptoms, pulmonary function and bronchial hyperreactivity after 3 weeks of treatment and the improvement after 6 weeks of treatment was higher than that after 3 weeks of treatment. During 6 weeks of treatment with budesonide, the inhibitory effect on the adrenal function was not obvious.

• Clinical and Experimental Pediatrics
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• v.46 no.5
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• pp.495-499
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• 2003

Purpose : Eosinophil is one of the important inflammatory cell involved in the airway inflammation in childhood asthma. It has been demonstrated that markers of eosinophil activation, including eosinophil cationic protein or eosinophil protein X(EPX), are increased in childhood asthma. Furthermore, they are related to disease activity and are assumed to be helpful in monitoring the treatment effect as urinary EPX(U-EPX) can be obtained easily and in a noninvasive way in children of all ages. Methods : Twenty-five children(22 male and three female) aged $11.87{\pm}3.82$ years with stable asthma were challenged with methacholine and urine was collected from each child during the following periods; before methacholine challenge test(MCT); 0-3 hr after the end of MCT; 4-7 hr after the end of MCT; and 8-24 hr after the end of MCT. Bronchial reactivity was determined by using Dosimeter( Jeager, Germany) with serially diluted methacholine from 0.05 to 25.0 mg. The $FEV_1$ less than 80% of baseline value were classified into positive MCT. U-EPX was measured with a sensitive and specific radioimmunoassay(Pharmacia & Upjohn AB, Uppsala, Sweden). Results were expressed as ${\mu}gEPX/mmol$ creatinine. Results : An early airway response after MCT was associated with an increase of U-EPX excretion for 0-3 hr after methacholine inhalation in comparison with beseline values. Most subjects showed a small increase in U-EPX excretion during late asthmatic response for 4-7 hr, which then decreased to normal level in 8-24 hr. Also, a tendency for a higher increase of U-EPX was associated with a lower threshold of methacholine challenge and a longer duration of asthma. Conclusion : Measurement of EPX in urine is a noninvasive and easy method to assess the severity of airway inflammation in asthmatic children. It may be a helpful index of the events underlying the airway inflammatory responses during nonspecific bronchial challenge, and in monitoring asthma management.

• Journal of Preventive Medicine and Public Health
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• v.27 no.2 s.46
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• pp.274-285
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• 1994

The effects of resin on the respiratory health have been investigated in 309 workers from four iron and steel foundries and the results compared with those from 122 workers who were not significantly exposed to resin gas and silica dust at the same industries. Phenol-formaldehyde resin was used in the core making and molding processes and workers were exposed to their decomposition products as well as to silica dust containing particulates. The subjects were grouped according to formaldehyde, dust and other gas exposures, and smoking habits were considered also in thi analysis. Standardized respiratory symptom questionnaire was administered by trained interviewers. Chest radiograph, pulmonary funtion tests, and methacholine challenge tests were done. Environmental measurements at the breathing zone were carried out to determine levels of formaldehyde, respiable dust and total dust. Foundry workers had a higher prevalence of symptoms of chronic bronchitis with chronic phlegm and chronic cough when exposed to dust. Exposure to gas was significantly associated with lowered $FEV_1$ and obstructive pulmonary function changes. Exposure to formaldehyde and phenol gas was associated with wheezing symptom among workers, but $FEV_1$ changes after methacholine challenge were not significantly different among different exposure groups. When asthma was defined as the presence of bronchial hyperreactivity with more than 20% decrease in $FEV_1$ after methacholine challenge, 17 workers out of 222 tested had asthma. Fewer asthmatic welters were found among groups exposed to formaldehyde, gas and dust, which indicates a healthy worker effects ill a cross-sectional study. The concentration of formaldehyde gas ranged from 0.24 to 0.43 ppm among studied foundries. The authors conclude that formaldehyde and phenol gas from combusted resin is probably the cause of asthmatic symptoms and also a selection force of those with higher bronchial reactivity away from exposures.

• Clinical and Experimental Pediatrics
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• v.49 no.9
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• pp.977-982
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• 2006

Purpose : There has been an increasing amount of literature concerning the association between Mycoplasma pneumoniae and asthma pathogenesis. Interleukin(IL)-6 stimulates the differentiation of monocytes, and can promote Th2 differentiation and simultaneously inhibit Th1 polarization. IL-8 is a potent chemoattractant and, it has been suggested, has a role in asthma pathogenesis. Nitric oxide (NO) synthesized by airway epithelium may be important in the regulation of airway inflammation and reactivity. Vascular endothelial growth factor(VEGF) has been reported to be a mediator of airway remodeling in asthma. We investigated the effects of M. pneumoniae on IL-6, IL-8, NO and VEGF production in human respiratory epithelial cells. Methods : A549 cells were cultured and inoculated with M. pneumoniae at a dose of 20 cfu/cell. After infection, the presence of M. pneumoniae in epithelial cell cultures was monitored by immunofluorescence and confirmed by polymerase chain reaction(PCR) detection. IL-6, IL-8 and VEGF were determined by an enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction. NO was measured using the standard Griess reaction. Results : In A549 cells, M. pneumoniaeinduced IL-6, IL-8, NO and VEGF release in time-dependent manners. It also induced mRNA expression of IL-6, IL-8 and VEGF in similar manners. Conclusion : These observations suggest that M. pneumoniae might have a role in the pathogenesis of the allergic inflammation of bronchial asthma.