Steroid-sensitive indices of airway inflammation in children with seasonal allergic rhinitis.
Previous studies involving adults have demonstrated that airway glucocorticosteroids inhibit plasma exudation and eosinophil activity in allergic rhinitis. This study explores the possibility that plasma exudation, exudative responsiveness, and the occurrence of eosinophil activity-related proteins are glucocorticosteroid-sensitive nasal mucosal indices in allergic children. Using a placebo-controlled, parallel-group design effects of nasal budesonide (64 microg per nasal cavity b.i.d) were determined in children with seasonal allergic rhinitis. Nasal lavage fluid levels of eotaxin, eosinophil cationic protein (ECP), and alpha2-macroglobulin, indicating plasma exudation, were determined, the latter with and without challenge with topical histamine. Nasal lavage fluid levels of alpha2-macroglobulin and ECP increased significantly during the pollen season, and the acute plasma exudation response to histamine was significantly greater during than outside the season. There was a trend towards a seasonal increase in nasal lavage fluid levels of eotaxin. Budesonide significantly inhibited the seasonal increase in alpha2-macroglobulin as well as the exudative hyperresponsiveness to histamine. Any tendency of increases in mucosal output of eotaxin and ECP was abolished by the glucocorticosteroid treatment. We conclude that mucosal exudation of plasma, as a global sign of active inflammatory processes, is a glucocorticosteroid-sensitive facet of allergic rhinitis in children. Exudative hyperresponsiveness, potentially caused by several weeks of mucosal inflammation, emerges as a significant feature of allergic rhinitis in children, and its development is prevented by local treatment with a glucocorticosteroid drug. The seasonal increase in ECP and the trend for an increase in eotaxin were absent in the glucocorticosteroid-treated subjects.
Meyer
Peter
P
Department of Pediatrics, University Hospital, Lund, Sweden.
Andersson
Morgan
M
Persson
Carl G A
CG
Greiff
Lennart
L
D000287:Administration, Topical; D000293:Adolescent; D000485:Allergens / Q000009:adverse effects; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D029662:Betula / Q000009:adverse effects; D001798:Blood Proteins / Q000187:drug effects / Q000378:metabolism; D001991:Bronchitis / Q000188:drug therapy*; D019819:Budesonide / Q000627:therapeutic use; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D002648:Child; D002669:Child Welfare; D004311:Double-Blind Method; D047091:Eosinophil Granule Proteins; D005260:Female; D005938:Glucocorticoids; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D017817:Nasal Lavage Fluid / Q000737:chemistry; D009297:Nasal Mucosa / Q000187:drug effects* / Q000378:metabolism*; D009299:Nasal Provocation Tests; D011058:Pollen / Q000009:adverse effects; D006255:Rhinitis, Allergic, Seasonal / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D012260:Ribonucleases; D012621:Seasons; D012720:Severity of Illness Index; D016896:Treatment Outcome; D000511:alpha-Macroglobulins / Q000187:drug effects / Q000378:metabolism
D000485:Allergens; D000893:Anti-Inflammatory Agents; D001798:Blood Proteins; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D047091:Eosinophil Granule Proteins; D005938:Glucocorticoids; D018836:Inflammation Mediators; D000511:alpha-Macroglobulins; D019819:Budesonide; D006632:Histamine; D012260:Ribonucleases