Difference between dosimeter and tidal breathing methacholine challenge: contributions of dose and deep inspiration bronchoprotection.
ABSTRACT Two bronchoprovocation methods are widely used. Compared to the tidal breathing method, the dosimeter method delivers approximately half the dose and involves five deep inhalations. Both the lower dose and the bronchoprotective deep inhalations contribute to the lesser airway response of the dosimeter.
To determine the relative role of dose and deep inspiration in the difference between the two methods.
Subjects with asthma (n = 24) underwent three methacholine challenges: a dosimeter challenge, a 2-min tidal breathing challenge (twice the dose), and a modified 2-min tidal breathing challenge (twice the dose plus five deep inhalations).
The dosimeter method produced a nonsignificantly lower response than the modified tidal breathing method (p = 0.14). Both deep inhalation methods produced significantly less response than did the standard tidal breathing method (p = 0.011). In the 12 subjects with the most mild airway hyperresponsiveness (AHR), the differences between the deep inhalation method and the tidal breathing method were greater (p = 0.007). By contrast, deep inhalations produced no effect in the 12 subjects with greater AHR; the two tidal breathing methods produced identical results, while the dosimeter produced less response than either (p = 0.033). Six current asthmatics with mild airway responsiveness (tidal breathing method) had negative dosimeter methacholine challenge results.
In subjects with moderate airway responsiveness, the difference between the methods is due to the difference in dose, whereas in subjects with mild AHR, deep inhalations had a large effect overwhelming the dose effect and producing false-negative methacholine challenge results in 25% of the subjects.
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ABSTRACT: Our study tried to find a relationship between baseline FEF25-75% and airway hyperresponsiveness (AHR) and whether a greater FEF25-75% impairment may be a marker of a more severe hyperresponsiveness in subjects with normal FEV1 and FEV1/FVC and suggestive asthma symptoms. Besides, we tried to asses a FEF25-75% cut-off value to identify hyper-reactive subjects.Allergy, asthma & immunology research 05/2014; 6(3):242-51. · 2.65 Impact Factor
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ABSTRACT: A 20% change in forced expiratory volume in 1 second (FEV(1)) during methacholine challenge testing (MCT) is a reliable marker of asthma. When the FEV(1) decrease is < 20%, there is controversy whether other changes in flows and conductance may be useful. We conducted this study to determine whether changes in sGaw, FEF(25 - 75), and FEV(1) in a negative MCT could predict future occurrence of asthma over a 3-year period. A total of 100 consecutive patients with clinical suspicion of asthma but who had a negative MCT per ATS FEV(1) criteria (< 20% FEV(1) decline at 16 mg/mL of methacholine) performed by the 5-breath dosimeter method were analyzed. Two pulmonary fellows, blinded to MCT results, reviewed the patients' medical records. Patients were classified into one of three categories: asthmatic, unclear, and not asthmatic. Decreases in sGaw, FEF(25 - 75), and FEV(1) in the five groups were then retrieved. Analysis of variance (ANOVA) was used for data analysis. Of 100 patients, 23 were excluded owing to lack of a 3-year follow-up. After complete data review, the number of patients (n) in each group was as follows: asthmatic (n = 15), unclear (n = 7), and not asthmatic (n = 55). sGaw and FEF(25 - 75) decreases from the negative MCT could not predict asthma; however, decreases in FEV(1) were associated with future asthma occurrence (sGaw p = 0.21, FEF25-75 p = 0.07, FEV(1) p = 0.0009). Forty-three percent of the patients who had a 10% to 20% decline in FEV(1) eventually developed asthma. Up to 20% of patients who have symptoms suggestive of asthma but a negative MCT can still develop asthma. Declines in sGaw and FEF(25 - 75) in a negative MCT appear to have no clinical significance. A decrease in FEV(1), especially 10% to 20%, is associated with the diagnosis of future asthma.Journal of Asthma 04/2009; 46(3):284-90. · 1.85 Impact Factor
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ABSTRACT: Airway hyperresponsiveness (AHR) to indirect agents like mannitol is thought to be dependent on concurrent airway inflammation as these stimuli exert their effects via the release of bronchoconstricting mediators from inflammatory cells. Airway inflammation correlates negatively with deep inhalation bronchoprotection against direct stimuli like methacholine. We hypothesised that deep inhalation bronchoprotection to methacholine would be absent and airway inflammation would be present in individuals with AHR to inhaled mannitol. Twenty asthmatic, otherwise healthy individuals, either gender, aged 18-65 years, with a Visit 1 (screening) methacholine two-minute tidal breathing PC20 of 16 mg/mL or less completed the study. Visits 2 and 3 consisted of either mannitol or deep inhalation methacholine challenge in random order, at least 24 h apart. All visits were completed within a period of two weeks. Eleven of the twenty participants had AHR to mannitol (PD15 ≤ 635 mg, the "responders") and nine did not (the "non-responders"). Responders did not bronchoprotect to methacholine via deep inhalation (doubling dose shift = 0.7; p = 0.13) and had high levels of exhaled nitric oxide (geometric mean 49 ppb; range 16-109 ppb). Conversely, significant deep inhalation bronchoprotection to methacholine occurred in the non-responder group (doubling dose shift = 1.6; p = 0.013). This group also had significantly lower levels of exhaled nitric oxide (geometric mean 23 ppb (range 16-45 ppb; p = 0.015). Deep inhalation bronchoprotection to methacholine and low levels of exhaled nitric oxide coincide with mannitol non-responsiveness in an asthmatic population. Clinical Trials Registration #NCT01642745 (clinicaltrials.gov).Respiratory medicine 03/2014; · 2.33 Impact Factor