Upper airway hyperresponsiveness To methacholine in patients with suspected asthma / 천식및알레르기

BACKGROUND: Upper airway diseases, such as vocal cord dysfunction (VCD), masquerade as asthma. Bronchial hyperresponsiveness (BHR) to methacholine (MCh) has been demonstrated in only part of suspected asthma patients. Investigators have shown upper airway hyperresponsi- veness (UHR) in patients with VCD. OBJECTIVE: To determine the clinical importance of UHR and to evaluate the usefulness of UHR test in patients with suspected asthma. METHODS: Thirty-six consecutive patients with suspected asthma underwent a MCh inhalation challenge. BHR was determined with PC20 25% from the baseline, and upper airway obstruction (UAO) with MEF50/MIF50 > 1. RESULTS: Only 17 patients (47.2%) showed BHR. Also, the same proportion of subjects showed UHR, and the each combination of BHR/UHR was nearly equal in distribution (9 BHR+/UHR-, 8 BHR+/UHR+, 9 BHR-/UHR+, and 10 BHR-/UHR-). Patients with BHR-/UHR+ had significantly lower serum total IgE level than those with BHR-/UHR-. Eight patients with UHR and UAO showed significantly shorter duration of disease (p < 0.05), smaller numbers of atopy family history (p < 0.05), and lower serum total IgE level than the others (p < 0.05). CONCLUSION: Many patients with suspected asthma showed UHR, and about half of patients with negative MCh-BHR showed UHR that might be related to non-asthmatic diseases including VCD. Therefore, a routine UHR test may be warranted in detecting upper airway diseases in suspected asthma.

A clinical comparison between early-onset and late-onset asthma in the elderly / 대한내과학회지

BACKGROUND: The asthma mortality has risen during last decades, especially in the elderly. This study was performed to investigate whether newly-developed asthma in the elderly has any difference in clinical features relating to asthma severity compared to early-onset asthma (EOA). METHODS: Thirty-three asthma patients (> or = 60 years-old) hospitalized due to severe attack were classified to late-onset (LOA) when their asthma developed after the age of 60 and the remaining to EOA. Data obtained from their medical records were analyzed retrospectively. RESULTS: Ten out of the 33 patients (30.3%) were LOA. Duration of asthma was significantly longer in EOA (21.6+/-14.8 years vs. 2.9+/-2.4 years, p<0.001). There were no significant differences between both groups in age, sex, atopy history (personal and familial), sinusitis, and peripheral blood eosinophils. However, EOA showed more smoking history and frequent exacerbations following URI-like symptoms (p<0.05, respectively), and higher serum total IgE level (geographic mean: 228 vs. 20 IU/mL, p<0.001). Life-threatening asthma attack was developed more frequently (89.5% vs. 40%, p<0.05), and the lung function measurements obtained just before discharge were significantly lower (FEV1/FVC: 54.8+/-10.1% vs. 64.6+/-11.7%, p<0.05) in EOA. Severity of chronic asthma was significantly more severe in EOA (moderate to severe persistent asthma: 95.6% vs. 60.0%, p<0.05). CONCLUSION: Many elderly asthmatics develop asthma newly in their old age. EOA is more related to atopic allergy, and seems to have more severe and long-standing asthma leading to chronic persistent airflow obstruction.

Clinical usefulness of checking wheezing and flow volume loop in methacholine bronchoprovocation test / 천식및알레르기

BACKGROUND: In methacholine bronchoprovocation test, lung function is traditionally measured by using forced vital capacity maneuver which depends on patient's effort. And insufficient breath may result in a false positive test. OBJECTIVE: To evaluate the additional indices of airflow obstruction in the interpretation of methacholine bronchoprovocation test. METHOD: FEV1/FVC, configuration index of flow-volume loop (Slope-Ratio), modified Borg dyspnea score, and wheezing in addition to FEV1 were measured before and after methacholine challenge. RESULTS: The changes of the measurements after methacholine challenge were significantly greater in patients with airway hyperresponsiveness (AHR). However, only 9 out of 29 (31.0%) patients with AHR developed all of indices and 6.9% did not show any evidence of obstruction except dyspnea. On the contrary, 40% of patients without AHR showed positive in two or more indices and 2 of them were hyperresponsive to histamine. Among patients with AHR, those without dyspnea and wheezing on challenge showed significantly lower baseline Borg score, FEV1, FEV1/FVC, and PC20, and were older than those with them (p<0.05). CONCLUSION: Methacholine-induced deltaFEV1 is related to, but not concordant with other indices of airflow obstruction. Development of dyspnea and wheezing depends on age, etc. For an accurate interpretation of methacholine bronchoprovocation test, it maybe necessary to consider these variables.

BCG infection during pre-sensitization or even post-sensitization inhibits airway sensitivity in an animal model of allergic asthma

The objective of this study is to investigate whether BCG infection before, during or after sensitization suppresses allergen-induced airway hyperresponsiveness and eosinophilic inflammation in allergic asthma rats, and to determine the required dose of BCG to induce such an inhibition. Eighty-seven Sprague-Dawley (SD) rats were sensitized and provoked with ovalbumin (OA). A pretreatment of 6 x 10(4) or 6 x 10(5) colony forming units (CFUs) of BCG or saline was done at four different times: 3 days before sensitization, at sensitization, 3 days before provocation, or at provocation. The assessment of tracheal smooth muscle (TSM) responsiveness to electrical field stimulation or acetylcholine (ACh) and bronchoalveolar lavage (BAL) were performed 1 day after OA provocation. Doses of 6 x 10(4) CFUs inhibited TSM sensitivity of rats infected 3 days before sensitization or at sensitization, but not 3 days before provocation or at provocation. However, doses of 6 x 10(5) CFUs significantly inhibited not only the airway eosinophilia of rats infected 3 days before sensitization or at sensitization, but also the TSM sensitivity of rats infected 3 days before provocation or at provocation. In conclusion, BCG infection suppresses the development of sensitivity of airway smooth muscle and airway eosinophilic inflammation in allergic asthma rats. Furthermore, a relatively high dose of BCG infection inhibits airway sensitivity, even after allergen sensitization.

BCG infection during pre-sensitization or even post-sensitization inhibits airway sensitivity in an animal model of allergic asthma

The objective of this study is to investigate whether BCG infection before, during or after sensitization suppresses allergen-induced airway hyperresponsiveness and eosinophilic inflammation in allergic asthma rats, and to determine the required dose of BCG to induce such an inhibition. Eighty-seven Sprague-Dawley (SD) rats were sensitized and provoked with ovalbumin (OA). A pretreatment of 6 x 10(4) or 6 x 10(5) colony forming units (CFUs) of BCG or saline was done at four different times: 3 days before sensitization, at sensitization, 3 days before provocation, or at provocation. The assessment of tracheal smooth muscle (TSM) responsiveness to electrical field stimulation or acetylcholine (ACh) and bronchoalveolar lavage (BAL) were performed 1 day after OA provocation. Doses of 6 x 10(4) CFUs inhibited TSM sensitivity of rats infected 3 days before sensitization or at sensitization, but not 3 days before provocation or at provocation. However, doses of 6 x 10(5) CFUs significantly inhibited not only the airway eosinophilia of rats infected 3 days before sensitization or at sensitization, but also the TSM sensitivity of rats infected 3 days before provocation or at provocation. In conclusion, BCG infection suppresses the development of sensitivity of airway smooth muscle and airway eosinophilic inflammation in allergic asthma rats. Furthermore, a relatively high dose of BCG infection inhibits airway sensitivity, even after allergen sensitization.

Risk factors of near - fatal asthma / 대한내과학회지

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.

Ozon-induced airway hyperresponsiveness of rat tracheal smooth muscle / 천식및알레르기

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.

Clinical usefulness of morphine skin prick test in diagnosis of allergic diseases / 천식및알레르기

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.

B lunted dyspnea perception in severe asthmatics / 천식및알레르기

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.

A Case of Hepatopulmonary Syndrome / 대한내과학회지

Hepatopulmonary syndrome consists of a triad of liver dysfunction, intrapulmonary vascular dilatation, and hypoxemia. This is one of the main causes of arterial hypoxemia in patients with chronic liver disease. The vascular abnormalities are precapillary dilatation, direct arterial-venous communication, and dilated pleural vessels. In this article, we report a case of hepatopulmonary syndrome in a 62-year-old woman who had complained progressively worsening dyspnea, platypnea, and orthodeoxia. She had huge splenomegaly, clubbing fingers and cyanosis of lip and fingers. Arterial blood gas analysis showed refractory arterial hypoxemia and orthodeoxia suggesting right-to-left "shunting". Chest X-ray showed increased interstitial markings on the lower part of right lung, In 99mTc-labeled macroaggregated albumin (MAA) lung perfusion scan, there was no perfusion defect in the lung, but labeled radionuclide were taken up in the intraabdominal organs, kidney, liver and spleen. The amount of shunted radionuclide were about 58 percent. In contrast echocardiography, microbubbles which were injected via cephalic vein were visualized in the left atrium at 4 cardiac cycles after leaving the right ventricle indicating intrapulmonary right-to-left "shunting" rather than intracardiac shunt. Pulmonary angiographic finding revealed diffuse blotchy arterial dilatation on both lung fields, especially lower lobes of both lungs. Current modalities of treatment of hepatopulmonary syndrome are the therapeutic embolization of direct arterial-venous communication for focal vascular dilatations, and TIPSS (Transjugular intrahepatic porto-systemic shunt) or liver transplantation for diffuse intrapulmonary vascular dilatations. Despite our recommendation of TIPSS, she refused the procedure and is under home oxygen therapy.

Diagnostic Significance of TNF-alpha in Tuberculous and Non-Tuberculous Pleural Effusion / 결핵

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.