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Serum ECP and MPO, but not urinary LTE4, are associated with bronchial hyper-responsiveness
J Hedman1, E Moilanen, T Poussa
1Department of Respiratory Medicine, Tampere University Hospital, Finland. jouni.hedman@pp.inet.fi
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 E4 (LTE4) in predicting bronchial hyper-responsiveness 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. (PD20) < or = 6900 micrograms] than in non-hyper-reactive subjects (22.3 vs. 13.2 micrograms l-1, P < 0.001 and 377 vs. 278 micrograms l-1, P = 0.001, respectively). This was also seen in current smokers vs. never smokers (17.2 vs. 12.9 micrograms l-1, P = 0.03 and 372 vs. 286 micrograms l-1, P = 0.04, respectively). There were no differences in baseline urinary excretion of LTE4 between hyper-reactive and non-hyper-reactive subjects. During the 2 h after methacholine challenge, urinary LTE4 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 LTE4 (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.