Rapid method for measurement of bronchial responsiveness.

Yan, Kwok; Salome, Cheryl M.; Woolcock, Ann J.

doi:10.1136/thx.38.10.760

Cited by 714 publications

(423 citation statements)

References 4 publications

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“…There is widespread agreement in international guidelines that achievement of asthma control should be followed 16 and study completion/withdrawal (end) between subjects not using (X, ? ; n=34) and using (e, h; n=27) inhaled corticosteroids in the 3 months prior to entry in: a) airway hyperresponsiveness to histamine (geometric mean and 95% confidence interval); b) laboratory forced expiratory volume in one second (FEV1); and c) morning prebronchodilator peak expiratory flow (PEF).…”

Section: Discussionmentioning

confidence: 99%

“…The primary outcome variable for the blinded phases of the study (weeks 1±16) was change in AHR. Histamine bronchial provocation testing was performed at weeks 0, 8, 16, 24, 48 and 72 using the rapid method [16] with calculation of the provocative dose of histamine causing a 20% fall in FEV1 (PD20). Extrapolated values were calculated when the FEV1 fell by >20% with the first histamine dose, or when the FEV1 fell by <20% at the final dose of 7.8 mmol (maximum extrapolated value 15.6 mmol).…”

Section: Assessments and Outcome Variablesmentioning

confidence: 99%

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Optimal asthma control, starting with high doses of inhaled budesonide

et al. 2000

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The aim of this study was to determine whether outcomes in poorly controlled asthma can be further improved with a starting dose of inhaled budesonide higher than that recommended in international guidelines.The study had a parallel-group design and included 61 subjects with poorly controlled asthma, randomized to receive 3,200 mg or 1,600 mg budesonide daily by Turbuhaler1 for 8 weeks (double-blind), then 1,600 mg . day -1 for 8 weeks (single-blind), followed by 14 months of open-label budesonide dose down-titration using a novel algorithm, with a written asthma crisis plan based on electronic peak expiratory flow monitoring. The primary outcome variable for weeks 1±16 was change in airway hyperresponsiveness (AHR), and, for the open-label phase, mean daily budesonide dose.By week 16, there were large changes from baseline in all outcomes, with no significant differences between the 3,200-and 1,600-mg . day -1 starting dose groups (AHR increased by 3.2 versus 3.0 doubling doses, p=0.7; morning peak flow increased by 134 versus 127 L . min -1 , p=0.8). Subjects starting with 3,200 mg . day -1 were 3.8 times more likely to achieve AHR within the normal range, as defined by a provocative dose of histamine causing a 20% fall in forced expiratory volume in one second (PD20) of $3.92 mmol by week 16 (p=0.03). During dose titration, there was no significant difference in mean budesonide dose (1,327 versus 1,325 mg . day -1 , p>0.3). Optimal asthma control was achieved in the majority of subjects (at completion/withdrawal: median symptoms 0.0 days . week -1 , b 2 -agonist use 0.2 occasions . day -1 , and PD20 2.4 mmol).In subjects with poorly controlled asthma, a starting dose of 1,600 mg . day -1 budesonide was sufficient to lead to optimal control in most subjects. The high degree of control achieved, compared with previous studies, warrants further investigation. Eur Respir J 2000; 15: 226±235.

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Section: Discussionmentioning

confidence: 99%

Section: Assessments and Outcome Variablesmentioning

confidence: 99%

Optimal asthma control, starting with high doses of inhaled budesonide

et al. 2000

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“…Bronchial responsiveness was measured using the rapid method described by YAN et al [15]. Forced expiratory volume in one second (FEV1) and forced vital capacity were measured with calibrated, leak free, Vitalograph dry-wedge spirometers (Vitalograph Ltd. Buckingham, Buckinghamshire, UK).…”

Section: Bronchial Hyperresponsivenessmentioning

confidence: 99%

Risk factors for bronchial hyperresponsiveness in workers exposed to acid anhydrides

Barker¹,

Tongeren²,

Harris³

et al. 2000

Eur Respir J

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Risk factors for bronchial hyperresponsiveness have previously been established in the general community. In settings where occupational asthma is a risk, it has not been established whether occupational sensitization or measures of exposure are important.Bronchial responsiveness to histamine was measured in a cohort of 506 workers exposed to acid anhydrides. Skin-prick tests were performed with conjugates of phthalic, maleic and trimellitic anhydride with human serum albumin and with common inhalant allergens. Employment and smoking histories were recorded. Occupational exposure was measured using personal air samplers and estimates of past exposure made by retrospective exposure assessment.Three hundred and seventy workers (73%) had bronchial responsiveness measured (median age 39 yrs, range 18±77) and 46 (12%) of these were hyperresponsive (provocative dose causing a 20% fall in forced expiratory volume in one second (FEV1; PD20) #8 mmol). Twelve (3%) of these responsive workers had a skin-prick test reaction to an acid anhydride conjugate, 124 (34%) to a common inhalant allergen, and 148 (40%) were current smokers. Multivariate analysis showed that occupational sensitization, sensitization to a common inhalant allergen, age, and pack-years of smoking were independent risk factors for bronchial hyperresponsiveness. Of these only occupational sensitization was completely independent of baseline FEV1.It is concluded that sensitization to acid anhydrides is a significant risk factor for bronchial hyperresponsiveness. However, measures of personal acid anhydride exposure were not associated with bronchial hyperresponsiveness. Eur Respir J 2000; 15: 710±715.

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“…14 The FEV 1 was measured following inhalation of saline and increasing (doubling) doses of methacholine chloride delivered from calibrated hand-held nebulisers. At each dose, step one forced expiratory manoeuvre was performed unless it was thought to be technically unsatisfactory.…”

Section: Spirometry and Airway Responsivenessmentioning

confidence: 99%

Familial aggregation and heritability of asthma-associated quantitative traits in a population-based sample of nuclear families

et al. 2000

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Asthma is a common, genetically complex human disease. Elevated serum immunoglobulin E (IgE) levels, elevated blood eosinophil counts, variably reduced spirometric measures and increased airway responsiveness (AR) are physiological traits which are characteristic of asthma. We investigated the genetic and environmental components of variance of serum total and specific IgE levels, blood eosinophil counts, the forced expiratory volume in one second (FEV 1 ) and forced vital capacity (FVC), and AR in an Australian population-based sample of 232 Caucasian nuclear families. With the exception of FVC levels, all traits were closely associated with clinical asthma in this population. Log e total serum IgE levels had a narrow-sense heritability (h 2 N ) of 47.3% (SE = 10.0%). Specific serum IgE levels against house dust mite and Timothy grass, measured as a RAST Index, had a h 2 N of 33.8% (SE = 7.3%). FEV 1 levels had a h 2 N of 6.1% (SE = 11.6%), whilst FVC levels had a h 2 N of 30.6% (SE = 26.8%). AR, quantified by the log e dose-response slope to methacholine (DRS), had a h 2 N of 30.3% (SE = 12.3%). These data are consistent with the existence of important genetic determinants of the pathophysiological traits associated with asthma. Our study suggests that total and specific serum IgE levels, blood eosinophil counts and airways responsiveness to inhaled agonist are appropriate phenotypes for molecular investigations of the genetic susceptibility to asthma.

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Rapid method for measurement of bronchial responsiveness.

Cited by 714 publications

References 4 publications

Optimal asthma control, starting with high doses of inhaled budesonide

Optimal asthma control, starting with high doses of inhaled budesonide

Risk factors for bronchial hyperresponsiveness in workers exposed to acid anhydrides

Familial aggregation and heritability of asthma-associated quantitative traits in a population-based sample of nuclear families

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