Airway Responsiveness to Inhaled Aspirin is Influenced by Airway Hyperresponsiveness in Asthmatic Patients

BACKGROUND/AIMS: Many patients with aspirin-induced asthma have severe methacholine airway hyperresponsiveness (AHR), suggesting a relationship between aspirin and methacholine in airway response. This study was performed to determine whether methacholine AHR affects the response of asthmatics to inhaled aspirin. METHODS: The clinical records of 207 asthmatic patients who underwent inhalation challenges with both aspirin and methacholine were reviewed retrospectively. An oral aspirin challenge was performed in patients with a negative inhalation response. The bronchial reactivity index (BRindex) was calculated from the percent decrease in lung function divided by the last dose of the stimulus. RESULTS: Forty-one (20.9%) and 14 (7.1%) patients showed a positive response to aspirin following an inhalation and oral challenge, respectively. Only 24.3 and 14.3% of the responders had a history of aspirin intolerance, respectively. The methacholine BRindex was significantly higher in the inhalation responders (1.46 +/- 0.02) than in the oral responders (1.36 +/- 0.03, p < 0.01) and in non-responders (n = 141, 1.37 +/- 0.01, p < 0.001). The aspirin BRindex was significantly correlated with the methacholine BRindex (r = 0.270, p < 0.001). Three of four patients who received the oral challenge, despite a positive inhalation test, showed negative responses to the oral challenge. Two of these patients had severe AHR. CONCLUSIONS: A considerable number of asthmatic patients with no history of aspirin intolerance responded to the inhalation aspirin challenge. The airway response to aspirin was significantly correlated with methacholine-AHR, and a false-positive response to aspirin inhalation test seemed to occur primarily in patients with severe AHR.

Controvérsias na associação entre diabetes mellitus tipo 1 e asma / Controversies in the association between type 1 diabetes and asthma

OBJETIVO: Revisão crítica da literatura sobre a associação entre asma e diabetes mellitus tipo 1 (DM1). FONTE DOS DADOS: Pesquisa bibliográfica na base de dados MEDLINE e LILACS nos últimos vinte anos. SíNTESE DOS DADOS: Muitos estudos mostram associação inversa entre asma, atopia e o risco de desenvolver DM1. De acordo com a "Hipótese da Higiene", o risco de doenças alérgicas diminui com infecções precoces na infância no sentido de afastar-se do perfil Th2, predominante ao nascimento, em direção ao fenótipo Th1. No entanto, outros trabalhos demonstram associação positiva ou ausência de associação entre DM1 e alergias. Existe a possibilidade de fatores ambientais contribuírem para ocorrência de doenças mediadas por células Th1 e Th2 no mesmo indivíduo, por provável deficiência de mecanismos imunomodulatórios mediados pela interleucina-10 e células regulatórias. CONCLUSÃO: As informações sobre a associação inversa entre doenças mediadas por resposta Th1 (por exemplo, DM1), e aquelas mediadas por resposta Th2 (por exemplo, alergias) são conflitantes, requerendo mais estudos para esclarecer esta questão.

OBJECTIVE: Critical review of the literature to investigate the relationship between asthma and type 1 diabetes mellitus (DM1). SOURCE OF DATA: Bibliography search in MEDLINE and LILACS databases in the last twenty years. SUMMARY OF DATA: Several studies demonstrate an inverse relationship between asthma, atopic diseases and the risk to develop DM1. According to the "Hygiene Hypothesis", the risk of allergic diseases decreases with infections early in childhood, towards distance of Th2 profile, common at birth, to the Th1 phenotype. Other articles described lack of association or positive association between DM1 and allergies. There is a possibility of environmental factors interfering in the development of disorders mediated by Th1 and Th2 cells, in the same individual, due to the absence of immunomodulatory mechanisms mediated by interleukin-10 and regulatory cells. CONCLUSION: The existing information about the inverse association between Th1-mediated diseases (e.g., DM1), and those that are Th2-mediated (e.g., allergies) are conflicting requiring more investigation to explain this question.

Clinical Impact of Bronchial Reactivity and Its Relationship with Changes of Pulmonary Function After Asthmatic Attack Induced by Methacholine / 결핵

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 bronchoconstric tors 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, FEV1/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, FEV1, 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.