Of the 86 patients in the study, 79 patients (91.8%) were followed up at 4 weeks. Seven asthmatic patients who were included as nonresponders had moved to the combination or add-on therapy, owing to decreases of > 12% in FEV1 or AQLQ, with symptom aggravation. A total of 79 asthmatic patients finished the study by continuing the inhaled GC therapy for 4 weeks. The mean overall compliance and accuracy rates were 83.3 ± 2.57% and 12.69 ± 0.22%, respectively. During the study period, 46 patients (53.4%) with asthma showed a ≥ 12% increase in FEV1 in response to high-dose inhaled GC therapy, and 40 patients were nonresponders (Table 1). For 17 of the nonresponders, the FEV1 values were decreased compared with the baseline levels. There was no difference in mean baseline FEV1 levels between responders and the group receiving combination or add-on therapy with symptom aggravation (60.5 ± 12.4% vs 66.5 ± 7.64%, respectively) [Table 1]. The change in FEV1 (ΔFEV1 = [FEV1 at 4 weeks − baseline FEV1]/baseline FEV1 × 100) following the inhalation of GCs varied from − 21 to 126.8% (Fig 2
). The change in FVC (ΔFVC = [FVC at 4 weeks − baseline FVC]/baseline FVC × 100) following the inhalation of GCs ranged from − 20 to 47%. The change in forced expiratory flow (FEF) [ΔFEF = (FEF at 4 weeks − baseline FEF)/baseline FEF × 100] following the inhalation of GCs ranged from −55.1 to 95%. The mean values for FEV1 percent predicted, FEF25–75%, FEV1/FVC ratio, and AQLQ score were significantly increased from baseline values after 4 weeks of GC inhalation therapy (FEV1, 63.9 ± 11.5% vs 78.2 ± 16.9% predicted, respectively; FEF25–75%, 43.7 ± 18.0% vs 68.7 ± 27.7%, respectively; FEV1/FVC ratio, 69.2 ± 11.9% vs 74.3 ± 12.1%, respectively; and AQLQ, 51.2 ± 13.8% vs 67.5 ± 12.5%, respectively; p < 0.01). The FEV1 percent predicted, FEF25–75%, FEV1/FVC ratio, and AQLQ score were also significantly increased after 4 weeks of inhaled GC therapy in patients who were classified as having moderate-to-severe asthma (Table 2
). The pretreatment values for FEV1, FVC, FEV1/FVC, and FEF25–75% were significantly lower in responder patients than in nonresponder patients (Table 1). The responder patients exhibited higher response rates to inhaled, short-acting bronchodilators than did nonresponder patients with asthma (48.3% [15 of 31 patients] vs 26.4% [9 of 34 patients], respectively; p < 0.05). The responder asthmatic patients with ΔFEV1 values of > 12% had significantly higher proportions of blood eosinophils and lower baseline FEV1 values. The ΔFEV1 values correlated negatively with the FEV1 percent predicted and FEF25–75% values (r = −0.462 and p < 0.001 vs r = −0.265 and p < 0.05, respectively) and correlated positively with the proportions of sputum eosinophils (r = 0.242; p < 0.05) prior to the inhaled GC treatment. AHR prior to the inhaled GC treatment was not associated with responsiveness to inhaled GCs. In a multiple logistic regression model that included all of the patients and that was adjusted for age, sex, atopy, AQLQ score, asthma duration, number of cigarette pack-years smoked, blood eosinophil count, and sputum eosinophil count, the FEV1 percent predicted values prior to treatment were independently associated with responsiveness to inhaled GC therapy (odds ratio, 1.126; 95% confidence interval, 1.033 to 1.228; p = 0.007).