BACKGROUND: Few studies have demonstrated an enhanced skin responsiveness to opiates in atopic subjects. OBJECTIVE: To determine whether the skin response to morphine is increased in atopics and to assess the clinical usefulness of morphine skin prick test in diagnosis of allergic diseases. METHOD: Allergy skin prick tests were performed using 55 common allergens, histamine, and morphine in 158 patients with allergic diseases. RESULTS: Wheal and flare sizes for morphine (1mg/mL) were significantly related to and smaller than those for histamine (1mg/mL). Although the proportion of subjects with allergic rhinitis and the level of serum total IgE were not different between responders (wheal >- 2mm) and nonresponders to morphine, the positive response rate to allergens was significantly lower in nonresponders. The flare sizes for morphine were significantly higher in positive allergen test group (A/H ratio >- 0.5). Among positive allergen test group, the subjects with atopy score >- 5 showed a larger flare size for morphine than those with atopy score < 5 while the sizes for histamine were not different. CONCLUSION: Morphine skin prick test is helpful for detecting false negative responses to allergens, and morphine skin test responses are increased in highly atopic patients probably due to enhanced mast cell releasability.
Allergens ; Diagnosis* ; Histamine ; Humans ; Hypersensitivity ; Immunoglobulin E ; Mast Cells ; Morphine* ; Rhinitis ; Skin Tests ; Skin*

BACKGROUND: Blunted perception of dyspnea, which may be related to the increased mortality, has been demonstrated in patients with a history of near-fatal asthma and in the elderly. OBJECTIVE: The purpose of this study was to evaluate the relationship between the perception of dyspnea and the severity of asthma. METHOD: Baseline spirometry and Borg score change(A Borg score) during breathing through an inspiratory muscle trainer were measured in 27 consecutive asthma patients and 11 normal subjects. RESULTS: The baseline Borg score was negatively related to FEV1 A Borg score was significantly lower in asthmatics than in controls at high level of loads. A Borg score was lower in severe asthma than in mild asthma. A Borg score was positively related to the baseline FEV1. Seventy-five percent of severe asthma, 62.5% of moderate one, and 9.1% of mild one showed impaired dyspnea perception. Dyspnea perception was related to age(r, = -0.49, p<0.001). CONCLUSION: Three quarters of patients with severe asthma showed impaired dyspnea perception to inspiratory resistive load. Dyspnea perception was related to asthma severity and age.
Aged ; Asthma ; Dyspnea* ; Humans ; Mortality ; Respiration ; Spirometry

OBJECTIVES: The differentiation of tuberculous effusion from the other causes of exudative pleural effusion remained difficult even with aids of biochemical analyses and pleural biopsy. As the pathophysiology of tuberculous pleural effusion is an enhanced cell mediated immunity, Adenosine deaminase(ADA) and various cytokines including Inteferon-γ, tumor necrosis factor alpha(TNF-α) are considered as useful diagnostic tools in differentiating exudative pleural effusion The author would like to demonstrate the diagnostic usefulness of TNF-α in the differentiation of exudative pleural effusion, and compared the discriminating ability of TNF-α with ADA. METHODS: Pleural fluids obtained from 80 patients (tuberculous : 39, malignant : 31, parapneumonic : 10) with exudate pleural effusions were processed for cell counts and biochemical analysis including ADA and TNF-α RESULTS: Tuberculous pleural fluid showed higher levee of ADA and TNF-α, 48.7α 32.7U/L and 184.1±214.2pg/mL than that of non-tuberculous effusion 26.0α41.3U/L and 44.1α114.2pg/mL, respectively (ADA, TNF-α : p<0.05, p<0.01). Receiver operating characteristics(ROC) curves were generated for ADA and TNF-α, and the best cut-off value for adenosine deaminase and TNF-α were considered as 30U/L and 15pg/ml, respectively. Comparing the area under the ROC curves, there was no significant difference between ADA and TNF-α CONCLUSION: For the differential diagnosis of tuberculous pleural effusion from the other causes of exudative pleural effusions, TNF-α as well as ADA was considered as useful diagnostic method. However adding TNF-α to ADA has no further diagnotic benefit than ADA alone.
Adenosine ; Adenosine Deaminase ; Biopsy ; Cell Count ; Cytokines ; Diagnosis, Differential ; Exudates and Transudates ; Humans ; Immunity, Cellular ; Pleural Effusion* ; ROC Curve ; Tuberculosis ; Tumor Necrosis Factor-alpha*

BACKGROUND: Ozone (03) induces airway inflammation and hyperresponsiveness which are characteristic features of asthma. There have been few studies observing O3-induced increase in responsiveness of rat airway muscle. Objectives: The aims of this study were to develop an O3-induced nonallergic asthma model using rat tracheal smooth muscle (TSM) and to evaluate the role of airway epithelium on the modulation of muscle responsiveness. METHOD: Five groups of 20 male Sprague-Dawley(SD) rats were exposed to filtered air including 0.12, 0.5, 1.0, or 2.0 ppm 03 for 1 hour. Thirty minutes after the exposure, bronchoalveolar lavage (BAL) and isometric contractile responses of the isolated tracheal ring segments to KCI, acetylcholine (ACh), and electrical field stimulation (EFS) were measured. RESULTS: The percent age of neutrophils was significantly higher and that of alveolar macro-phages in BAL fluid was significantly lower in 2.0 ppm O3-exposed rats than in the control. There were no significant differences in the maximal contractile responses of TSM to KC1, ACh, EFS and in the sensitivity to ACh (ACh-EC50) and EFS (EFS-EC50) between the control group and the ozone exposed group. ACh-EC50 and EFS-EC50 were correlated positively with the percent age of neutrophils and inversely with that of macrophages. Removal of epithelium significantly increased the sensitivity to ACh in O3-exposed group, but not in the control group. CONCLUSION: These findings indicate that O3 induces neutrophilic airway inflammation, but not an increased sensitivity of TSM to ACh or EFS in SD rats. However, O3-induced epithelial damage may be associated with increased muscle response.
Acetylcholine ; Animals ; Asthma ; Bronchoalveolar Lavage ; Epithelium ; Humans ; Inflammation ; Macrophages ; Male ; Muscle, Smooth* ; Neutrophils ; Ozone ; Rats* ; Trachea

BACKGROUND: Smoking-related chronic obstructive pulmonary disease and chronic asthmatic bronchitis, which are the most important causes of chronic airflow obstruction (CAO), can occur together in a pat,ient and the prognoses of these two diseases are different each other. OBJECTIVE AND METHOD: To estimate the extent of asthmatic component in patients with CAO and to evaluate the role of atopy as a predictable index for reversibility of airflow obstruction, 89 CAO patients who were older than 40 years were examined retrospectively. RESULT: Only 15 patients (16.8%) showed an increase of >15% in FEV20 to inhaled salbutamol (short-term responder). However, 18 out of 32 patients (56.3%), who were not responded significantly to inhaled bronchodilator and performed a follow-up lung function study, showed an increase of ) 15% in FEV20 to anti-asthmatic therapy including corticosteroid for 3-4 weeks (long-term responder). Peripheral blood eosinophil count only was different between short-term responder and short-term nonresponder, and there was no difference in all of the measurements between short-term responder and long-term responder. However, there were significant differences in smoking, wheezing on auscultation, peripheral blood eosinophil counts, serum total IgE levels, and MAST atopy score between long-term responder and long-term nonresponder. The increase in FEV, following shortor long-term therapy was related to peripheral blood eosinophil counts and MAST atopy score, and it was significantly great,er in patients with high eosinophil counts or high atopy score. CONCLUSION: About 2/3 of patients with CAO who were older than 40 years had an asthmatic component ap atopy may be useful to predict good bronchodilator response to anti-asthmatic therapy.
Albuterol ; Auscultation ; Bronchitis ; Eosinophils ; Follow-Up Studies ; Humans ; Immunoglobulin E ; Lung ; Prognosis ; Pulmonary Disease, Chronic Obstructive* ; Respiratory Sounds ; Retrospective Studies ; Smoke ; Smoking

BACKGROUND: Researches on the characteristics of fatality-prone asthmatics have been performed in western countries, but there are few reports in this field in Korea. The purposes of this study were to clarify the magnitude of the problem and to identify the risk factors of near-fatal asthma(NFA). METHODS: The records of patients admitted due to asthma attack were analyzed retrospectively. RESULTS: 1) The subjects had NFA in 50.6% and PaCO2 > 45mmHg in 22.9%. Five(11.1%) among NFA patients and 3 out of 19(15.8%) subjects with PaCO2 > 45mmHg required mechanical ventilation. 2) There were no significant differences between NFA and non-NFA in age, sex, resident place, academic career, familial and personal history of atopic diseases, serum total IgE level, positive skin prick test to house dust mites, accompanying allergic rhinitis and aspirin intolerance, emphysema on chest high resolution computerized tomogram, dyspnea perception, previous asthma education, regular OPD follow-up, and use of antiinflammatory drugs. 3) However, cigarette smoking(62.2% vs 38.6%), accompanying paranasal sinusitis(66.7% vs 45.3%), chronic asthma severity(severe persistent: 55.5% vs 29.5%), hospitalization frequency(2.93 vs 1.58), and duration of recent asthma exacerbation(6.6 vs 18.8 days) in NFA were significantly different from those in non-NFA.4) The relative risk for NFA was high in patients with history of hospitalization > 3, severe persistent asthma, exacerbation period < 3 days, smoking, or sinusitis in the order of frequency. CONCLUSION: Near-fatal asthma is a prevalent problem in clinical practice and asthma admission history, severe persistent asthma, short exacerbation period < 3 days, smoking, and paranasal sinusitis are the risk factors warning near-fatal asthma attack in advance.
Aspirin ; Asthma* ; Dyspnea ; Education ; Emphysema ; Follow-Up Studies ; Hospitalization ; Humans ; Immunoglobulin E ; Korea ; Pyroglyphidae ; Respiration, Artificial ; Retrospective Studies ; Rhinitis ; Risk Factors* ; Sinusitis ; Skin ; Smoke ; Smoking ; Thorax ; Tobacco Products

BACKGROUND: It has been shown that severe asthmatic attacks are related to airway hyperresponsiveness (AHR). However, there has been no study on AHR measured just after control of acute severe asthma. OBJECTIVE: To determine the degree of AHR following acute severe asthma and to evaluate the safety of AHR measurement in patients just recovering from a severe attack. METHOD: In 23 consecutive asthma patients just recovering from a severe attack (10 severe, 13 near-fatal), all medications except inhaled or systemic steroids were withdrawn temporarily for more than each action time. Then a methacholine bronchoprovocation test was performed in patients with FEV1 > or = 75% of predicted or personal best value. RESULTS: Mean duration required to control asthma was 5.6+/-3.6 days, and methacholine provo- cation test was performed at 12.6+/-5.2 hospital days. The patients showed significantly lower methacholine-PC20 (geometric mean: 0.54 vs 1.64 mg/ml, p<0.05) and steeper slope of dose-response curve (p<0.01) compared to 62 outpatients. Initial FEV1 (r=0.470, p<0.05) and the duration required to control asthma (r=-0.623, p<0.01) were significantly related to methacholine-PC20. However, only 9 patients (39.1%) showed severe AHR, which was not significantly different from outpatients (25.8%). CONCLUSION: These results suggest that AHR is a risk factor of severe asthmatic attack and methacholine challenge just after control of acute asthma is relatively safe.
Asthma* ; Humans ; Methacholine Chloride* ; Outpatients ; Risk Factors ; Steroids