• 보건세계
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• v.43 no.12 s.484
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• pp.4-9
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• 1996

기도가 협착되어서 증상을 일으키는 질환으로 만성기관지염, 폐기종, 만성폐쇄성질환, 기관지천식 등이 있으며, 기침, 가래, 호흡곤란(숨참)등이 주요 증상인데 비의료인에게는 해소천식으로 더 잘 알려져 있다. 일반적으로 기침 가래가 나오고 숨이차면 해소천식이라고 하는데 실제로 이 만큼 오용되고 남용되는 단어는 드물 것이다. 동의보감에 의하면 해수(해소의 원명)는 기침을 말하는데 해는 가래가 없이 소리가 심한 경우이고 수는 가래를 주로하는 기침을 말하며 16가지 종류로 구분된다. 천식은 숨이 찬 증상을 말하는 것으로 8가지 종류로 구분되어 있다. 따라서 해소천식은 기침가래가 나오고 숨이 찬 증상을 말하는 것으로 특정질환을 말하는 병명이 아니다. 비의료인이 말하는 천식의 경우에는 숨이 찬 증상을 말하는 것이고 의료인이 천식이라고 할 경우에는 특정 기도질환인 기관지 천식을 말하는 것이므로 서로 오해하기가 쉽다. 실제로 일간지 건강상식란에 천식을 소개하였는데 의사는 병명으로서의 기관지천식을 설명하였고 동참한 한의사는 증상으로서의 천식을 설명하여 혼란을 일으켰던 예가 있었다. 한의학에서는 예전에 기관지천식은 효천(孝喘)이라고 부르고 천식의 증상이 심하고 위중한 상황일 때에는 천급(喘急)이라고 하여 한의학에서도 구별하였는데 도리어 현대에 와서 정확성이 없어지고 모호해진 이유는 무엇일지 궁금하다. 폐쇄성기도질환은 기도가 좁아지는 기전과 기도폐쇄의 가역성(기도가 정상으로 회복되는지)여부에 다라서 가역성폐쇄질환인 기관지천식과 비가역적인 만성폐쇄성기도질환으로 구분하고 있다.

• Journal of Acupuncture Research
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• v.24 no.5
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• pp.185-195
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• 2007

목적 : 부신피질 스테로이드약을 포함한 약물치료에도 조절되지 않았던 기관지천식 환자 6 증례에 대하여 침구치료를 행하여，연구방법의 하나인 조건반전법(N-of-1)을 이용하여 침치료의 효과를 검토하였다. 방법 : 연구디자인 : 조건반전법으로 침치료 기간(A기간)과 침치료 휴지기간(B기간)을 서로 반복하였다. A기간은 10주간으로 하고 1주간에 1회의 침치료를행하였다. 실시장소 : 메이지 침구대학부속병원 내과와 부속침구센터 대상 : 기관지천식의 표준적인 약물치료를 행하여도 천식발작이 충분히 개선되지 않았던 중등증에서 중증의 천식환자 6 증례를 대상으로 하였다. 평가 기관치천식에 대한 침치료의 효과를 아래의 항목을 이용하여 평가하였다. (1) 발작상태를 천식일지에 의해 평가 (2) 호흡곤란감을 VAS(Visual Analogue Scale)에 의해 평가 (3) 호흡기능검사 (4) 말초혈호산구수 (5) 스테로이드약의 투여량 (6) 중증도 효과 : A기간에 동시적으로 모든 예에서 천식발작과 호흡곤란감의 개선이 인정되었다. 한편 B기간에서는 6례 중 5례에서 천식발작의 재연이 확인되었다. 또한 천식발작의 개선에 수반하여 모든 예에서 중증도의 개선도 인정되었으며，6례 중 4례에서 스테로이드약의 감량이 가능하게 되었다. 결론 : 약물치료로 조절되지 않았던 기관지천식 환자에 대하여 침치료를 행한 결과, 환자의 천식발작, 자각증상, 호흡기능의 개선에 유효하였다고 생각된다.

• Tuberculosis and Respiratory Diseases
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• v.43 no.2
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• pp.182-189
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• 1996

Background : RANTES is associated with chemotaxis and activation of eosinophils. RANTES is up-regulated in allegic inflammation and play a critical role in the pathogenesis of allegic inflammation. Recently, circulating form of RANTES have been identified in the peripheral blood. Method : In the present study, we measured soluble RANTES levels in 17 patients with atopic brochial asthma (8 patients: early response to allegen challenge, 8 patients : early and late response to allergen challenge) on 30mins, 2hrs and 8 hrs after allergen challenge with house dust mite, prechallenge period. Result : RANTES levels in sera from patients with bronchial astma in prechallenge conditions were higher than in normal control subjects. But, RANTES levels in sera from patients with bronchial asthma in 30mins, 2hrs and 8hrs after challenge were no significantly higher than prechallenge conditions. Conclusion : These results suggest that RANTES plays a role in the pathogenesis of patients with atopic bronchial asthma and may be related to persistence of subclinical allergic inflammation.

• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.90-98
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• 1998

Background : The CD4+ T-helper cells comprise functionally distinct subsets of Th1 and Th2 cells that are distinguished on the basis of differential cytokines production Th1 cells secrete interferon-$\gamma$, lymphotoxin, interleukin-2. Th2 cells produce interleukin-4, interleukin-5, interleukin-10. A previous study shown that Th2 cells and their cytokines increased in patients with atopic asthma. We compared cytokines(IL-4, IFN-$\gamma$) activity and subpopulation of T-lymphocytes in peripheral blood from atopic asthmatics versus non-asthmatics. Method: Fifteen patients with atopic asthma(nine men, six women), twelve patients with chronic bronchitis(six men, six women), five healthy persons(three men, two women) were studied. Activity of IL-4, IFN-$\gamma$ and T-cell subpopulation in peripheral blood were estimated. Results: Patients had a median age of 55yr. The mean activity of IL-4 of asthmatics was significantly increased(control $0.75{\pm}1.1pmol/L$, atopic asthmatics $3.50{\pm}0.75pmol/L$, chronic bronchitis $2.01{\pm}1.2pmol/L$), but IFN-$\gamma$ was not significantly increased. In the T lymphocyte sunsets the percent of CD62L+ T-lymphoeytes of asthmatics was not significantly increased (control $16.7{\pm}16.4%$, atopic asthmatics $24.8{\pm}23.6%$, chronic bronchitis $17.0{\pm}16.9%$). Conclusion: In this study elevated production of IL-4 was observed in atopic asthmatics. CD62L+T-lymphoeytes was not increased in atopic asthma.

• Tuberculosis and Respiratory Diseases
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• v.46 no.1
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• pp.44-52
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• 1999

Background : Airway infiltration by inflammatory cells, particularly of eosinophils, is one of the characteristic features of asthma. Several mechanisms for the recruitment of eosinophil is focused on the CD4+ T lymphocyte for the preferential production of Th2-c1erived cytokines. Interleukin-10(IL-10) is identified cytokine with potent antiinflammatory activity. This molecule has been shown to inhibit the release of cytokine from inflammatory cells including Th2 cell, and also to inhibit eosinophil survival. We therefore attempted to determine whether decreased synthesis of IL-10 in the lung of bronchial asthma may contribute to inflammation that is characteristics of this dease. Method: Subjects were patients with bronchial asthma(n=23) and normal controls(n=11). IL-10 produced from peripheral mononuclear cell(PBMC) and in bronchoalveolar lavage(BAL) fluid was measured by ELISA method. Degree of bronchial inflammation was assessed by total cell counts and eosinophil percents in BAL fluid, eosinophil infiltration on bronchial biopsy tissue and $PC_{20}$ for methacholine. Results: The IL-10 level produced by PBMC and in BAL fluid from patient with bronchial asthma were not different with normal controls(respectively, $901.6\pm220.4$ pg/ml, $810.9\pm290.8$ pg/ml for PBMC, $24.5\pm9.5$ pg/mL $30.5\pm13.5$ pg/ml for BAL fluid p>0.05). There were significant negative correlation between IL-10 in BAL fluid and eosinophil percents in BAL fluid or degree of eosinophil infiltration in bronchial biopsy (respectively r=-0.522, r=-0.4486 p<0.05). However there was no difference of IL-10 level according to $PC_{20}$ for methacholine. There were no correlation between IL-10 production by PBMC and peripheral blood eosinophil counts or serum eosinophilic cationic protein levels(respectively r=0.1146, r=0.0769 p>0.05). Conclusion: These observation suggest that IL-10 may participate but not acts the crucial role in regulation of the airway inflammation in bronchial asthma.

• 건강소식
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• v.34 no.5
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• pp.16-17
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• 2010

살랑살랑 불어오는 바람마저 아름다운 이 봄이 불쾌한 이들이 있다. 바로 알레르기 질환을 앓고 있는 환자들이다. 가장 흔한 알레르기 질환에는 꽃가루병, 즉 알레르기 비염이 있으며, 이보다 흔하지는 않지만 증상이 심해 알레르기 비염보다 주목받는 기관지천식도 있다. 대표적인 만성질환 중 하나인 기관지천식에 대해서 알아본다.

• Clinical and Experimental Pediatrics
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• v.49 no.11
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• pp.1216-1222
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• 2006

Purpose : Though atopic and nonatopic asthma have different clinical manifestations, bronchial hyperresponsiveness (BHR) and airway inflammations are common characteristics of them. We investigated BHR to both methacholine and adenosine 5'-monophosphate (AMP), and their relationships with blood eosinophil markers in nonatopic asthma as well as atopic asthma. Methods : We studied 116 children (82 atopics; 34 nonatopics) with mild to moderate asthma. Methacholine and AMP challenge tests were performed and bronchial responsiveness was expressed as $PC_{20}$ (provocative concentration causing a 20 percent fall in $FEV_1$); blood eosinopil counts (ETCs) and serum eosinophil cationic protein (ECP) levels were gauged. Results : In atopics, 95.1 percent and 90.2 percent showed hyperreactivity to methacholine ($PC_{20}$<16 mg/mL) and AMP ($PC_{20}$<200 mg/mL), respectively. Meanwhile, in nonatopics, 94.1 percent and 52.9 percent displayed hyperreactivity to methacholine and AMP, respectively. The geometric mean of AMP $PC_{20}$ was lower in atopics (31.6 mg/mL) than in nonatopics (125.9 mg/mL); that of methacholine $PC_{20}$ was similar in the two groups. AMP $PC_{20}$ correlated with blood ETCs in both atopics(r=-0.30, P<0.01) and nonatopics (r=-0.57, P<0.01), and correlated with serum ECP levels (r=-0.23, P<0.01) in atopics, but not in nonatopics. Apart from AMP, methacholine $PC_{20}$ was not associated with blood eosinophil markers in either group. Conclusion : Atopics more frequently displayed BHR to AMP than nonatopics. Furthermore, BHR to AMP was associated with not only blood ETCs, but serum ECP levels in atopics but was correlated with only blood ETCs in nonatopics. Those results suggest that BHR to AMP reflects airway inflammation in asthma and is more related to atopy.

• 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.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.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.