The purpose of this study was to determine the value of serum measurements of eosinophil cationic protein (ECP) and eosinophil protein X (EPX) in diagnosing asthma in children, and to investigate the influence of concomitant allergic diseases and atopic sensitization, assessed by skin prick tests (SPT), on these markers. ECP and EPX were determined in 36 children with asthma, in 33 children with other symptoms from lower airways disease (OSLA), and in 166 control children.
Sixteen children with asthma but no anti‐inflammatory therapy had significantly higher concentrations of ECP and EPX (ECP: 27.5 μg/L, P < 0.001; EPX: 59.9 μg/L, P < 0.001) than the control children (ECP: 11.2 μg/L; EPX: 26.2 μg/L). In the 20 children on anti‐inflammatory therapy, ECP values were similar to those of controls. The children with OSLA (ECP: 13.6 μg/L, P < 0.01; EPX: 47.2 μg/L, P < 0.001) differed significantly from controls. When using the value of 24.7 μg/L (97.5 percentile in the 68 non‐atopic controls) as a pathologic upper limit for ECP, 10 (63%) of the 16 asthmatic children on no maintenance medication, two (10%) of the 20 asthmatics on maintenance therapy, and 11 (33%) of the 33 children with OSLA had high ECP; the same figure was only 18 (11%) in the 166 control children. Both ECP and EPX had a significant association with allergic disorders and with SPT reactivity. In multivariate logistic regression analysis, an elevated ECP was significantly associated with asthma (OR 2.3, 95%Cl 1.1–4.9) and atopic dermatitis (2.9, 1.2–6.9), and an elevated EPX was significantly associated with asthma (2.61, 1.19–5.74) and allergic rhinoconjunctivitis (5.23, 1.46–18.73). We conclude that serum concentrations of both ECP and EPX are higher in asthmatic than in healthy children. However, other allergic diseases, such as allergic rhinoconjunctivitis, atopic dermatitis, and allergic skin sensitization also raise the concentrations of these markers. This limits their usefulness in the diagnosis of childhood asthma. Pediatr. Pulmonol. 1998; 25:167–174. © 1998 Wiley‐Liss, Inc.