DOES BRONCHIAL HYPERRESPONSIVENESS PRECEDE OR FOLLOW AIRWAY-OBSTRUCTION IN ASTHMA OR COPD

Objective: The following hypothesis was tested: The degree of bronchia l hyperresponsiveness (BHR) is a risk factor for the progression of ai rway obstruction in asthma, while in chronic obstructive pulmonary dis ease (COPD) it reflects the existing airway obstruction. Methods: The relationships between the (annual change in) PC20 histamine and the (a nnual change in) FEV1 were investigated in a 2-year prospective contro lled study. The FEV1 and the PC20 histamine were assessed at 6-month i ntervals. 183 patients (74 asthma, 109 COPD) participated. The investi gated relationships were assessed by means of multiple analysis of var iance (ANOVA). Patients used bronchodilator therapy alone. No steroids were permitted during the study. Results: The results demonstrated th at the PC20 at the start of the study was related to the subsequent an nual decline of FEV1 in asthma (r = 0.32, p < 0.05) but not in COPD (r = -0.10, p = 0.89). Asthmatic patients with a PC20 value less-than-or -equal-to 2 mg/ml had an average decline of 118 ml/yr, those with a PC 20 value > 2 mg/ml of 27 ml/yr. The change in PC20 histamine during th e 2-year study period was related to the annual change in FEV1 in COPD (r = 0.45, p < 0.05), but not in asthma (r = 0.06, p = 0.90). The dis turbing influence of possible confounders was investigated and if nece ssary controlled for. Conclusions: It was concluded that BHR, assessed with PC20 histamine, is probably involved in the progression of airwa y obstruction in asthma. In COPD, however, the degree of BHR probably only reflects the degree of existing airway obstruction. This conclusi on may contribute to the ongoing debate whether it is useful to combin e the diagnosis of asthma, COPD and emphysema under the umbrella-term CARA (or CNSLD = chronic non-specific lung disease). The so-called ''D utch hypothesis'' which laid the foundation for this term, suggested t hat bronchial hyperresponsiveness plays a central role in the pathogen esis of CNSLD. The present study supports evidence that at least BHR d oes not seem to play the same role in the pathogenesis of asthma and C OPD.