Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology

Abstract

<h4>Objectives</h4>To compare pepsin, carbonic anhydrase III (CAIII), cyclooxygenase-2 (COX-2) and mucin 5AC (MUC5AC) expression in children with adenoid hypertrophy and normal controls.<h4>Design</h4>A non-randomised, controlled prospective study.<h4>Setting</h4>Two paediatric hospitals in Adelaide, South Australia.<h4>Participants</h4>Children aged 2-10 years, 21 undergoing adenoidectomy and 12 controls undergoing routine dental surgery.<h4>Main outcome measures</h4>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.<h4>Results</h4>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).<h4>Conclusion</h4>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.