title: Sinus and adenoid inflammation in children with chronic rhinosinusitis and asthma.
abstract: BACKGROUND
  Chronic rhinosinusitis (CRS) and asthma frequently coexist in children and adults. However, the precise pathophysiologic mechanism of this interaction is still poorly understood, especially in children, owing to the lack of direct measurements of mucosal inflammation in the upper airways.
  
  
  OBJECTIVE
  To determine the pathophysiologic mechanism by analyzing the expression of a large array of inflammatory cytokines and chemokines in the sinus and adenoid tissues surgically removed from pediatric patients with CRS refractory to medical management.
  
  
  METHODS
  Twenty-eight children 2 to 12 years old diagnosed with CRS with or without asthma and 10 controls were included in this prospective, nonrandomized study. Mucosal expression of 40 inflammatory cytokines was measured with a multiplex assay and was normalized to total tissue protein.
  
  
  RESULTS
  Compared with children with CRS and without asthma, children with CRS and asthma had significantly higher sinus levels of tumor necrosis factor-α and adenoid levels of epidermal growth factor, eotaxin, fibroblast growth factor-2, growth-related oncogene, and platelet-derived growth factor-AA.
  
  
  CONCLUSIONS
  The inflammatory response in the upper airway mucosa of children with asthma and CRS was similar, but more severe, compared with children with CRS without asthma. This observation is consistent with the hypothesis that asthma in these patients is caused or exacerbated by severe upper airway disease and supports the concept that treating sinus disease is paramount in the management of chronic asthma in children using, for the first time, direct measurements of airway inflammation in children.
authors.affiliation: Department of Otolaryngology, West Virginia University, Morgantown, West Virginia.
authors.forename: Antony
authors.initials: A
authors.lastname: Anfuso
authors.affiliation: Department of Otolaryngology, West Virginia University, Morgantown, West Virginia.
authors.forename: Hassan
authors.initials: H
authors.lastname: Ramadan
authors.affiliation: Department of Otolaryngology, West Virginia University, Morgantown, West Virginia.
authors.forename: Andrew
authors.initials: A
authors.lastname: Terrell
authors.affiliation: Department of Pediatrics, West Virginia University, Morgantown, West Virginia.
authors.forename: Yesim
authors.initials: Y
authors.lastname: Demirdag
authors.affiliation: Department of Pediatrics, West Virginia University, Morgantown, West Virginia.
authors.forename: Cheryl
authors.initials: C
authors.lastname: Walton
authors.affiliation: Department of Pediatrics, West Virginia University, Morgantown, West Virginia; Allegheny Health Network, Pittsburgh, Pennsylvania.
authors.forename: David P
authors.initials: DP
authors.lastname: Skoner
authors.affiliation: Pediatric Institute and Children's Hospital, Cleveland Clinic, Cleveland, Ohio. Electronic address: PIEDIMG@ccf.org.
authors.forename: Giovanni
authors.initials: G
authors.lastname: Piedimonte
mesh_terms: D000233:Adenoidectomy; D000234:Adenoids / Q000276:immunology / Q000601:surgery; D001249:Asthma / Q000276:immunology / Q000503:physiopathology*; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008297:Male; D009297:Nasal Mucosa / Q000276:immunology*; D014066:Palatine Tonsil / Q000276:immunology / Q000601:surgery; D010256:Paranasal Sinuses / Q000276:immunology*; D011446:Prospective Studies; D012220:Rhinitis / Q000276:immunology / Q000503:physiopathology*; D012852:Sinusitis / Q000276:immunology / Q000503:physiopathology*; D011795:Surveys and Questionnaires; D014068:Tonsillectomy
chemical_list: D016207:Cytokines