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Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology
Author(s) -
Harris P.K.,
Hussey D.J.,
Watson D.I.,
Mayne G.C.,
Bradshaw A.,
Joniau S.,
Tan L.W.,
Wormald P.J.,
Carney A.S.
Publication year - 2009
Publication title -
clinical otolaryngology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.914
H-Index - 68
eISSN - 1749-4486
pISSN - 1749-4478
DOI - 10.1111/j.1749-4486.2008.01852.x
Subject(s) - medicine , adenoid , immunohistochemistry , gastroenterology , western blot , pepsin , adenoid hypertrophy , prospective cohort study , etiology , reflux , gerd , hyperplasia , pathology , adenoidectomy , disease , enzyme , biology , biochemistry , tonsillectomy , gene
Objectives: To compare pepsin, carbonic anhydrase III (CAIII), cyclooxygenase‐2 (COX‐2) and mucin 5AC (MUC5AC) expression in children with adenoid hypertrophy and normal controls. Design: A non‐randomised, controlled prospective study. Setting: Two paediatric hospitals in Adelaide, South Australia. Participants: Children aged 2–10 years, 21 undergoing adenoidectomy and 12 controls undergoing routine dental surgery. Main outcome measures: We measured expression of pepsin, CAIII, COX‐2 and MUC5AC levels by real‐time RT‐PCR, immunohistochemistry, and Western blot to determine any difference between children with hyperplastic adenoids and controls. Results: Pepsin was not detected in any study or control adenoid by immunohistochemistry or Western blot. Real‐time RT‐PCR analysis showed a statistically significant difference between groups with respect to COX‐2 ( P = 0.027) and MUC5AC ( P = 0.02) but no difference in CAIII expression ( P = 0.414). A significant correlation was also found between COX‐2 and MUC5AC expression (Kendall Tau = 0.4, P = 0.005). Conclusion: Our results suggest that the biochemical changes seen in adenoid hypertrophy are different to those seen in reflux‐affected tissues. The decreased COX‐2 and MUC5AC expression may be due to squamous metaplasia and other inflammatory changes associated with adenoid hypertrophy. Our findings infer there is little evidence of reflux being a major contributory factor in the pathophysiology of adenoidal hypertrophy.