Serum ECP and MPO, but not urinary LTE 4, are associated with bronchial hyper-responsiveness

Abstract

A random population-based sample of 131 subjects was used to assess the value of serum eosinophil cationic protein (ECP), serum myeloperioxidase (MPO), and urinary leukotriene E 4 (LTE 4) in predicting bronchial hyperresponsiveness measured by methacholine challenge. Special interest was focused on the history of aspirin intolerance and on smoking as contributing factors. The mean serum ECP and MPO were higher in hyper-reactive [provocational dose causing a 20% fall in forced expiratory volume in 1 sec. (PD 20 ≤ 6900 μg] than in non-hyper-reactive subjects (22·3 vs. 13·2 μg l −1, P<0·001) and 377 vs. 278 μg l −1, P=0·001, respectively). This was also seen in current smokers vs. never smokers (17·2 vs. 12·9 μg l −1, P=0·03 and 372 vs. 286 μg l −1, P=0·04, respectively). There were no differences in baseline urinary excretion of LTE 4 between hyper-reactive and non-hyper-reactive subjects. During the 2 h after methacholine challenge, urinary LTE 4 excretion increased from 53·8 and 69·0 ng mmol −1 creatinine in non-hyper-reactive subjects, but there was no change in hyper-reactive subjects (non-hyper-reactive vs. hyper-reactive, P=0·06). The increase was greatest in subjects with aspirin intolerance causing urticaria or angioedema but not aggravation of asthma (from 58·5 to 87·2 ng mmol −1 creatinine), probably due to extrapulmonary leukotriene production. Our results indicate that serum ECP and MPO, but not urinary LTE 4 (even in subjects with a history of aspirin intolerance), predict bronchial hyper-responsiveness to methacholine. The subject's smoking history must be taken into account when these parameters are considered.