title: Comparison of exhaled nitric oxide, serum eosinophilic cationic protein, and soluble interleukin-2 receptor in exacerbations of pediatric asthma.
abstract: The hypotheses tested in this study were that during acute asthma exacerbations (1) exhaled nitric oxide concentrations [eNO] are a more sensitive, noninvasive indicator of asthma disease activity than serum markers of inflammation such as eosinophil cationic protein (ECP) or soluble interleukin 2 receptor (sIL2R), and (2) elevated [eNO] are reduced after treatment with glucocorticoids (GC). Peak eNO levels were measured by chemiluminescence during slow expiration. Seven asthmatic subjects (mean age 11 yrs; mean morning FEV1 65% predicted) receiving inhaled GC, and with no radiographic evidence of acute sinusitis, were studied before and after a course of oral GC. Measurements of [eNO], ECP and sIL2R levels, and FEV1% were obtained before and after a course of GC. Six atopic nonasthmatic subjects (mean age 12 years; mean FEV1 94% predicted) and seven normal subjects (mean age 13 years; mean FEV1 100% predicted) were studied. The mean peak [eNO] level (parts per billion: ppb) for the asthma subjects before treatment (52 +/- 5 ppb SEM) was greater than the value for both nonasthmatic atopic and normal subjects (16 +/- 2 ppb and 14 +/- 2 ppb SEM, respectively; P < 0.0001). There was no significant difference in ECP or sIL2R values between asthmatic subjects and either atopic or normal subjects (P > 0.05). Baseline pre-GC treatment ECP levels in the asthmatic subjects were significantly higher (P < 0.002) than post-GC treatment values. The mean peak [eNO] level in the asthmatic subjects declined after oral GC treatment to 14 +/- 1 ppb (P < 0.0002) and was less than 2 ppb different from either control group (P > 0.75). We conclude that [eNO] is a more sensitive marker of asthma disease activity than ECP and sIL2R levels. In addition, [eNO] appears to be a more useful indicator of the beneficial response to GC therapy than these other measurements in pediatric asthma.
authors.affiliation: Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Lanz
authors.forename: D Y
authors.initials: DY
authors.lastname: Leung
authors.forename: D R
authors.initials: DR
authors.lastname: McCormick
authors.forename: R
authors.initials: R
authors.lastname: Harbeck
authors.forename: S J
authors.initials: SJ
authors.lastname: Szefler
authors.forename: C W
authors.initials: CW
authors.lastname: White
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001249:Asthma / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D015415:Biomarkers; D001798:Blood Proteins / Q000032:analysis / Q000378:metabolism*; D001944:Breath Tests; D016022:Case-Control Studies; D002648:Child; D016903:Drug Monitoring; D047091:Eosinophil Granule Proteins; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D009569:Nitric Oxide / Q000032:analysis*; D015375:Receptors, Interleukin-2 / Q000097:blood*; D012260:Ribonucleases; D012680:Sensitivity and Specificity; D013256:Steroids
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D015375:Receptors, Interleukin-2; D013256:Steroids; D009569:Nitric Oxide; D012260:Ribonucleases