title: Longitudinal changes in airflow limitation and airway hyperresponsiveness in patients with stable asthma.
abstract: BACKGROUND
  There are few long-term studies of the effects of treatment on the natural course of asthma.
  
  
  OBJECTIVE
  To investigate the longitudinal changes in airflow limitation and airway hyperresponsiveness (AHR) in asthma.
  
  
  METHODS
  We recruited 81 outpatients (never smokers) with stable asthma from the Kyoto University Hospital. They were evaluated for pulmonary function and AHR, expressed by forced expiratory volume in 1 second (FEV1) and the provocation dose that caused a 20% fall in FEV1 (PD20-FEV1), respectively, at entry and every 6 months over 3 years. We used random effects models to estimate the slopes of these changes, and then evaluated the relationship between these changes and their predictive factors.
  
  
  RESULTS
  Using random effects models, the percentage of the predicted FEV1 (%FEV1) declined significantly but slightly at a mean rate of 0.5%/year (P = 0.002; 95% confidence interval, 0.3 to 0.8). The mean decline rate of FEV1 was 34 mL/year. However, Log(PD20-FEV1) showed significant improvement at a mean rate of 0.088 cumulative units/year (P < 0.001; 95% confidence interval, 0.053 to 0.122). Multiple regression analysis showed that the baseline values of %FEV1 and Log(PD20-FEV1) were the most significant predictive factors for their subsequent changes, respectively.
  
  
  CONCLUSIONS
  In stable asthmatic patients treated according to international guidelines, airflow limitation progressed at a nearly normal rate over 3 years. However, AHR continued to improve despite its ceiling effects. Multiple regression analysis revealed a significant negative relationship between the initial values and the subsequent changes in airflow limitation and AHR, respectively.
authors.affiliation: Respiratory Division, Kyoto-Katsura Hospital, Kyoto, Japan. ogat@df7.so-net.ne.jp
authors.forename: Toru
authors.initials: T
authors.lastname: Oga
authors.forename: Koichi
authors.initials: K
authors.lastname: Nishimura
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Tsukino
authors.forename: Takashi
authors.initials: T
authors.lastname: Hajiro
authors.forename: Susumu
authors.initials: S
authors.lastname: Sato
authors.forename: Akihiko
authors.initials: A
authors.lastname: Ikeda
authors.forename: Chikuma
authors.initials: C
authors.lastname: Hamada
authors.forename: Michiaki
authors.initials: M
authors.lastname: Mishima
mesh_terms: D000328:Adult; D000402:Airway Obstruction / Q000209:etiology*; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use; D001249:Asthma / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000503:physiopathology*; D001985:Bronchial Provocation Tests; D002648:Child; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007564:Japan; D008137:Longitudinal Studies; D008297:Male; D016210:Methacholine Chloride; D008875:Middle Aged; D008954:Models, Biological; D012044:Regression Analysis; D013147:Spirometry
chemical_list: D018927:Anti-Asthmatic Agents; D016210:Methacholine Chloride; D007073:Immunoglobulin E