Pulmonary alveolar proteinosis (PAP) is a rare disorder that's characterized by accumulation of surfactant components in the alveolar space. Idiopathic PAP is recognized as an autoimmune disease that's due to impaired alveolar macrophage function and this caused by autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF). We report here a case of pulmonary alveolar proteinosis that was deemed interstitial lung disease at the initial diagnosis. A 61-year-old man presented with intermittent blood tinged sputum and dyspnea on exertion. The man was a painter for 30 years and he had a 10 pack-years smoking history. Chest computerized tomography (CT) revealed multifocal ground-glass opacity with interstitial thickening at both lungs. His pulmonary function tests and methacholine test revealed non specific results. He was diagnosed with interstitial lung disease on the basis of the chest CT finding and occupational history. However, seven months later, his symptoms progressed. Follow-up chest CT was performed. Wedge resection via video-assisted thoracoscopic surgery (the anterior basal segment of the left lower lobe) was done. Microscopic examination showed large groups of alveoli with excessive amounts of surfactant and a complex mixture of protein and lipid (fat) molecules. Finally, he was diagnosed as having pulmonary alveolar proteinosis.
Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease due to bronchial colonization of Aspergillus fumigatus that occurs in susceptible patients with asthma or cystic fibrosis. A 10-year-old girl was referred to the Department of Pediatric Pulmonology for persistent consolidations on chest radiography. Pulmonary consolidations were observed in the right upper and left lower lobes and were not resolved with a 4-week prescription of broad-spectrum antibiotics. The patient had a history of atopic dermatitis and allergic rhinitis but no history of asthma. She had no fever but produced thick and greenish sputum. Her breathing sounds were clear. On laboratory testing, her total blood eosinophil count was $1,412/mm^3$ and total serum IgE level was 2,200 kU/L. Aspergillus was isolated in the sputum culture. The A. fumigatus-specific IgE level was 15.4 kU/L, and the Aspergillus antibody test was also positive. A chest computed tomography scan demonstrated bronchial wall thickening and consolidation without bronchiectasis. An antifungal agent was added but resulted in no improvement of pulmonary consolidations after 3 weeks. Pulmonary function test was normal. Methacholine provocation test was performed, revealing bronchial hyperreactivity ($PC_{20}=5.31mg/mL$). Although the patient had no history of asthma or bronchiectasis, ABPA-seropositivity was suspected. Oral prednisolone (1 mg/kg/day) combined with antifungal therapy was started. Pulmonary consolidations began decreasing after 1 week of treatment and completely resolved after 1 month. This is the first observed and treated case of seropositive ABPA in Korean children without previously documented asthma.
Kim, Yoonha;Park, Junghwan;Kwak, Jinyoung;Park, Jungmi;Ahn, Taek won
Journal of Sasang Constitutional Medicine
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v.28
no.2
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pp.147-162
/
2016
Objectives The objective of this study is to develop a taeeumin animal-experimental model induced lung fibrosis with Bleomycin and evaluate the effect on obesity in this animal-experimental model.Methods The subjects were divided into 3 groups : normal group, high fat diet(HFD) control group, and HFD group administered with bleomycin(n=10 per group). To develop taeeumin animal-experimental model with reduced respiratory metabolism, 8-week-old C57BL/6 mice were administered with 0.03ml solution of bleomycin 1U/ml dissolved in distilled water, intratracheal(IT), once. Then, the HFD control group and the experimental group were fed with high fat diet for 6 weeks. Airway hyperresponsiveness(AHR) to methacholine was measured at the 1st and 3rd week after bleomycin was administered. Food intake and body weight were measured at regular time weekly. After the final experiment, blood was gathered by cardiac puncture for bloodchemical examination and organs(liver, fatty tissue) were remoed, weighted, and mRNA was analyzed.Results and Conclusions Through the experiment, it was found that Bleomycin induced Taeeumin animal-experimental models have leptin resistace. In the experimental group administered with Bleomycin, fatty acid synthesizing gene expression increased and energy metabolizing gene expression decreased. As mRNA expression of adiponectin decreased, it was found that Taeeuim animal-experimental model is susceptible to metabolic syndrome and cardiovascular diseases.
Kwang Min Lee;Seungho Lee;Yoon-Ji Kim;Seung-eun Lee;Youngki Kim;Dongmug Kang;Se-Yeong Kim
Annals of Occupational and Environmental Medicine
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v.35
/
pp.13.1-13.12
/
2023
Background: Indoor air pollution can cause and exacerbate asthma. We report a previously undescribed case of occupational asthma related to indoor air pollution in a worker at an indoor air gun shooting range and highlight the potential risk of developing occupational asthma in this environment. Case presentation: A 31-year-old man presented with dyspnea, cough, and sputum and was diagnosed with asthma complicated by pneumonia. Objective evidence of asthma was obtained by performing a methacholine bronchial provocation test. It was suspected that the patient had occupational asthma, which began one month after changing jobs to work within the indoor air gun shooting range. The highest peak expiratory flow (PEF) diurnal variability on working days was 15%, but the highest variation was 24%, with 4 days out of 4 weeks having a variation of over 20% related to workplace exposure. Conversely, the diurnal variability on the rest days was 7%, and no day showed a variation exceeding 20%. The difference in the average PEF between working and rest days was 52 L/min. PEF deterioration during working days and improvement on rest days were noted. Conclusions: The results obtained from the in-depth analysis of the PEF were adequate to diagnose the patient with occupational asthma. Exposure to indoor air pollution and lead and the patient's atopy and allergic rhinitis may have contributed to the development of occupational asthma.
Kim, Kyung Ho;Lee, Gyu Taeg;Park, Sung Woo;Oh, Je Ho;Ki, Shin Young;Moon, Seung Hyug;Jeong, Sung Hwan;Kim, Hyun Tae;Uh, Soo Taek;Kim, Yong Hoon;Park, Choon Sik;Jin, Byung Won
Tuberculosis and Respiratory Diseases
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v.44
no.1
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pp.146-153
/
1997
Background : Chronic cough is commomly defined as a persistent or recurrent cough exceeding 3 week's duration. The prevalence of chroinc cough is reported to range from 14% to 23 % for nonsmoking adults. The post nasal drip syndrome has been determined to be the most common cause of chronic cough, followed by asthma, chronic bronchitis, gastroesophageal reflux and bronchiectasis. Cough can be the only manifestation of asthma. Bronchial provocation tests are useful in diagnosing cough variant asthma. We investigated the clinical or laboratory findings and the incidence of airway hyperresponsiveness and evaluated the etiology in patients with chronic cough. Method : We evaluated 46 patients with chronic cough. Methacholine challenge test were done. Results : The results were as follows : 1) Thirty - five percent(16/46) of the chronic cough patients and 44% of the post nasal drip syndrom(7/16) showed the positive responses to methacholine challenge test 2) The underlying causes of chronic cough were post nasal drip syndrome in 35%, bronchitis in 21.7%, cough-variant asthma in 17.4%, and unknown condition in 25.9%. 3) Airway hyperresponsiveness in chronic cough was not related to respiratory symptom, nasal symptom, post nasal drip, smoking, derangement of ventilatory function, atopy, or sinusitis. Conclusion : Airway hyperresponsivenss in patients with chronic cough increased in frequency when compaired with normal control, allergic rhinitis. Cough-variant asthma account for 17.4% of patients with chronic cough.
Background: Exercise is a very common precipitant of asthma. Bronche-constriction associated with exercise can occur in 75~90% of individuals with asthma The estimated prevalence(30~85%) of gastroesophageal reflux(GER) in patients with asthma is significantly higher than in general population. We performed pH monitoring during the exercise in order to evaluate whether exercise induced asthma(EIA) could be related to GER and acid reflux-induced esophagobronchial reflex-mediated bronchospasm might be a factor for EIA. Method: Following an overnight fast, 18 patients with a suspected EIA(6 men, 12 women) were studied. Monitoring of intraesophageal pH, ECG and spirometry was done for 1 hour before treadmill exercise. After baseline monitoring, subjects underwent symptom-limited treadmill exercise with Bruce protocol and continuous monitoring for 60 min after exercise. Spirometry was done at baseline prior to exercise, and repeated every 10 min after full exercise for 60 min. Results: Exercise-induced bronchoconstriction was noted in 15 patients, who performed MBPT and 12 patients confirmed for bronchial asthma and 3 patients were diagnosed exercise-induced astham. Five of 15 EIA patients demonstrated a pathologic degree of GER. Conclusion: We suggest that GER may be one of pathophysiologic factors of EIA and evoke further concentration on the GER in the EIA patients.
Nah, Kyu Min;Park, Yang;Kang, Eun Kyeong;Kang, Hee;Koh, Young Yull;Lee, Sun Wha;Paek, Domyung
Clinical and Experimental Pediatrics
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v.46
no.3
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pp.284-290
/
2003
Purpose : A new airway inflammatory marker, exhaled nitric oxide(ENO) has been reported to correlate with bronchial hyperresponsiveness(BHR) and atopy. The purpose of this study was to analyze the relationship of ENO with BHR or atopy in patients with asthma and with allergic rhinitis. Methods : The subjects consisted of 55 children with asthma, 17 with allergic rhinitis, and 14 healthy controls. The asthma group was subdivided into the atopic asthma group(n=37) and the nonatopic asthma group(n=18) and the allergic rhinitis group into BHR group(n=7) and non-BHR group(n=10). All were investigated with spirometry and measurements of ENO concentration. The correlations between ENO concentration and both methacholine $PC_{20}$(provocative concentration causing a 20% decrease in forced expiratory volume in one second) and the number of allergen skin test positivity were analyzed. Results : ENO concentrations of both asthma and allergic rhinitis groups were significantly greater than that of control(P<0.01). ENO concentration of atopic asthma was significantly greater than that of nonatopic asthma(P<0.01). In allergic rhinitis, ENO concentration did not differ according to the presence or absence of BHR(P=0.50). ENO concentrations correlated significantly with the number of skin test positivity(r=0.32, P=0.02) or methacholine $PC_{20}$(r=-0.38, P<0.01) in asthma group, but not in the allergic rhinitis group(r=0.42, P=0.09; r=-0.06, P=0.83). Conclusion : In asthma patients, some pathogenetic mechanisms associated with atopy and BHR seem to influence ENO concentration. In allergic rhinitis patients, some factors other than BHR may be important in determining ENO concentration.
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.
Purpose: Recently many studies show early exposure during childhood growth to endotoxin (lipopolysaccharides, LPS) and/or early exposure to allergens exhibit important role in development of allergy including bronchial asthma. The aim of this study was to evaluate the role of endotoxin and allergen exposure in early life via the airways in the pathogenesis of allergic airways inflammation and airway hyperresposiveness (AHR) in mouse model of asthma. Methods: Less than one week-old Balb/c mice was used. Groups of mice were received either a single intranasal instillation of sterile physiologic saline, 1% ovalbumin (OVA), LPS or $1.0{\mu}g$ LPS in 1% OVA. On 35th day, these animals were sensitized with 1% OVA for 10 consecutive days via the airways. Animals were challenged with ovalbumin for 3 days on 55th days, and airway inflammation, hyperresponsiveness, and cytokine expression were assessed. Measurements of airway function were obtained in unrestrained animals, using whole-body plethysmography. Airway responsiveness was expressed in terms of % enhanced pause (Penh) increase from baseline to aerosolized methacholine. Lung eosinophilia, serum OVA-IgE and bronchoalveolar lavage (BAL) fluid cytokine levels were also assessed. ANOVA was used to determine the levels of difference between all groups. Comparisons for all pairs were performed by Tukey-Kramer honest significant difference test; $P$ values for significance were set to 0.05. Results: Sensitized and challenged mice with OVA showed significant airway eosinophilia and heightened responsiveness to methacholine. Early life exposure of OVA and/or LPS via the airway prevented both development of AHR as well as bronchoalveolar lavage fluid eosinophilia. Exposure with OVA or LPS also resulted in suppression of interleukin (IL)-4, 5 production in BAL fluid and OVA specific IgE in blood. Conclusion: These results indicate that antigen and/or LPS exposure in the early life results in inhibition of allergic responses to OVA in this mouse model of astham. Our data show that early life exposure with OVA and/or LPS may have a protective role in the development of allergic airway inflammation and development of allergen-induced airway responses in mouse model of asthma.
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.
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