IMPORTANCE OF TOTAL SERUM IGE FOR IMPROVEMENT IN AIRWAYS HYPERRESPONSIVENESS WITH INHALED CORTICOSTEROIDS IN ASTHMA AND CHRONIC OBSTRUCTIVEPULMONARY-DISEASE

Airways hyperresponsiveness is a hallmark of asthma, and many patients with COPD also demonstrate hyperresponsiveness. Inhaled corticosteroi ds improve hyperresponsiveness, but the extent of improvement may vary considerably between patients. This study was designed to determine w hich patient characteristics predict these differences in response. Pa tients with mild to moderately severe obstructive airways disease (ast hma and COPD) were selected if PC20 less than or equal to 8 mg/ml and FEV(1) < 95% confidence interval of predicted normal. They were follow ed for 2.5 yr, during which one-third received inhaled corticosteroids . The independent influences of baseline FEV(1)/IVC, bronchodilator re sponse, PC20, smoking habits, allergy, age, and sex on the improvement in airways hyperresponsiveness with inhaled corticosteroids were anal yzed. Total serum IgE was taken as a parameter of allergy, next to spe cific IgE for house dust mite, skin tests, and blood eosinophils. Tota l serum IgE was found to be the most important and single independent predictor of change in PC20 with inhaled corticosteroids: patients wit h a higher IgE had a greater increase in PC20 when administered inhale d corticosteroids than those with lower IgE levels. Alternatively, pat ients with a higher IgE who did not receive corticosteroids had a decr ease in PC20 compared with patients with a lower IgE. This effect was most prominent in asthma but was inconsistent in asthmatic bronchitis and COPD. The level of IgE cannot be used to predict the response to i nhaled corticosteroids in individuals accurately. Total serum IgE is t he single most important predictor of change in PC20 with and without inhaled corticosteroids. The greater importance in this respect of tot al serum IgE relative to more specific measures of atopic status, such as skin tests, specific IgE, and blood eosinophil counts, possibly po ints to a nonspecific upregulation of IgE production as part of a chro nic inflammatory process.