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However, recent studies about cough variant asthma (CVA) revealed normal baseline pulmonary function and mild bronchial hyperresponsiveness [ 13, 14].
HRV, baseline pulmonary function, and medication data were collected for each participant on 7 days in fall 1999 and/or spring 2000.
Some authors have suggested that patients with difficult-to-treat severe asthma show better baseline pulmonary function and lower fractional exhaled nitric oxide (FeNO) than do those with treatment-resistant severe asthma [ 4].
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Our findings of effect modification by medication use and baseline pulmonary function, COPD, and a recent MI, however, were consistent with our findings of differential susceptibility for individuals with COPD and a recent MI.
Strengths of the current study include a consecutive patient sample with complete data on smoking, baseline pulmonary function tests, and the novel study context of an outpatient-based program that allowed for examination of hospitalization as a study outcome.
No difference could be found in the baseline pulmonary function between etodolac and placebo treatments.
Because the baseline pulmonary function was normal and narrowly distributed for individuals with recent MI, the observed impact of baseline pulmonary function on the PM2.5 SDNN response largely reflects variation in baseline pulmonary function among individuals with COPD.
Similar effect modification by medication use and baseline pulmonary function was also found for EC but with smaller effect sizes.
No difference could be found in the baseline pulmonary function, peripheral blood eosinophil counts and IgE production between cilostazol and placebo treatments.
All baseline pulmonary function tests (FEV1, FVC, FEV1/FVC, and PEF) were similar between smokers and non-smokers (P ≥ 0.157,Two-way ANOVA).
Subject characteristics and baseline pulmonary function measurements are shown in Table 1.
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