Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology
| Autor: | George C. Mayne, Lorwai Tan, Peter J. Wormald, Damian J. Hussey, David I. Watson, Anthony Bradshaw, Penelope K. Harris, Andrew Carney, Sander Joniau |
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| Rok vydání: | 2009 |
| Předmět: |
Male
Pathology medicine.medical_specialty Biopsy medicine.medical_treatment Statistics as Topic Gene Expression Mucin 5AC Adenoid Gastroenterology Adenoidectomy Pepsin Risk Factors Internal medicine Humans Medicine Child Prospective cohort study Hyperplasia biology medicine.diagnostic_test Reverse Transcriptase Polymerase Chain Reaction business.industry respiratory system medicine.disease Carbonic Anhydrase III Pepsin A Squamous metaplasia stomatognathic diseases medicine.anatomical_structure Otorhinolaryngology Cyclooxygenase 2 Child Preschool Adenoids Gastroesophageal Reflux biology.protein Female business Adenoid hypertrophy |
| Zdroj: | Clinical Otolaryngology. 34:120-126 |
| ISSN: | 1749-4486 1749-4478 |
| DOI: | 10.1111/j.1749-4486.2008.01852.x |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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