Background Measuring inflammation (inflammometry) may assist decisions regarding preventative anti-inflammatory therapies in asthma.1 Prostaglandin metabolites, which reflect airway inflammation, may be measured in urine samples.2 We sought to prospectively assess associations between urine prostaglandins and subsequent asthma exacerbations in children, and to compare these markers to current markers that aim to predict future risk.
Methods Children with asthma aged 7–15 underwent spirometry, sputum inductions, completed the childhood asthma control test (C-ACT) and provided urine samples at baseline. Urine was also provided by healthy (non-atopic) controls. Urine PGD, PGE and PGJ metabolites were measured using HPLC-MS. At 3 months, sampling was repeated, data was collected on exacerbations (unscheduled medical attendance or day missed from school due to asthma symptoms) and the receiver operator characteristic was calculated for the baseline assessment.
Results 73 children (asthma n = 25, controls n = 48) were included. Urine PGD2, PGE2 and PGJ2 metabolites were increased in asthma in comparison to controls, and 15-dPGJ2 predicted subsequent asthma exacerbation (PPV=75%, NPV=90%, ROC AUC 0.858, p = 0.005). Sputum eosinophils, spirometry and C-ACT did not predict subsequent exacerbations after correction for multiple comparisons, and sputum phenotypes were unstable. Change in C-ACT score was associated with interim control (p = 0.04).
Conclusions Urinary prostaglandin metabolites are increased in children with asthma in comparison to controls. Urine 15-dPGJ2 is a biologically plausible, non-invasive marker for inflammometry in childhood asthma, and is superior to assessment of sputum eosinophils, C-ACT, or spirometry.