Alterations in Airway Inflammation and Lung Function During Corticosteroid Therapy for Atopic Asthma: Discussion
Correlations Between Changes in Lung Function and Airway Inflammation
With regard to associations between changes in airway inflammation and changes in lung function, changes in EG1 were associated with changes in bronchodilator response (r = 0.77, p = 0.016) only after a period of 8 weeks (Fig 4). There was no association between the rates of change of inflammatory cells and measures of airway pathophysiology after a 2-week interval (data not shown).
This study examines associations between repeat measures of bronchial immunopathology and airway physiology during corticosteroid therapy for atopic asthma. Changes in bronchial lymphocytes and changes in macrophages are highly correlated over both short-term (2 weeks) and longer-term (8 weeks) intervals. Changes in total (EG1) eosinophils and changes in EG2+ eosinophils are highly correlated over an 8-week interval. www.canadian-familypharmacy.com read Changes in airway eosinophils and changes in bronchodilator responsiveness are correlated after 8 weeks of therapy, but not after 2 weeks of therapy. Therefore, while changes in many of the cellular components of bronchial inflammation appear to be interdependent, only changes in eosinophils appear to be closely related to alterations in lung function. Changes in airway eosinophils and changes in lung function do not occur simultaneously. This dissociation has two important implications. First, when repeat measures are obtained from the same set of subjects, relative changes in bronchial inflammation and changes in lung function are dependent on sampling interval. Second, changes in bronchial inflammation and lung function are closely associated but they do not occur simultaneously.
There are at least five alternative hypotheses to explain the coexistence of bronchial inflammation and asthmatic-type physiology: (1) there is no relation between airway inflammation and asthma (ie, their coexistence in bronchial asthma is a coincidence); (2) bronchial inflammation and airway pathophysiology are causally related; (3) a common factor causes both bronchial inflammation and pathophysiology; (4) bronchial inflammation indirectly causes abnormal physiology (by an intermediate factor); and (5) changes in airway physiology precede and cause airway inflammation.
Figure 4. XY plot of changes in number of EG1+ cells in bronchial biopsy samples and bronchodilator responsiveness (BDR) in subjects with atopic asthma (n = 9) after 8 weeks of therapy with high-dose inhaled FP, 2,000 ^g/d (r = 0.77, p = 0.016).