Pilot study: Association between Helicobacter pylori in adenoid hyperplasia and reflux episodes detected by multiple

R Katra1, Z Kabelka1, M Jurovcik1

  • 1Department of ENT, 2nd Faculty of Medicine, University Hospital Motol, Charles University, Prague, Czech Republic.

Insights

Gastroesophageal reflux reaching the upper esophagus may transmit Helicobacter pylori, contributing to adenoid hyperplasia in children. This pilot study links reflux episodes to H. pylori presence in adenoid tissue.

Area of Science:

  • Otolaryngology
  • Pediatric Gastroenterology
  • Microbiology

Background:

  • Adenoid hyperplasia is common in children, often linked to recurrent infections.
  • Helicobacter pylori (H. pylori) has been implicated in various inflammatory conditions.
  • Gastroesophageal reflux disease (GERD) can present with extraesophageal symptoms in children.

Purpose of the Study:

  • To explore the association between laryngopharyngeal reflux (LPR) and H. pylori in children with adenoid hyperplasia.
  • To determine if LPR, detected by impedance and pH monitoring, correlates with H. pylori presence in adenoid tissue.

Main Methods:

  • A pilot study involving 30 children with adenoid hyperplasia and GERD symptoms.
  • Adenoidectomy followed by real-time polymerase chain reaction (PCR) for H. pylori DNA detection.
  • Multiple intraluminal impedance and pH monitoring to assess reflux episodes.

Main Results:

  • Children with H. pylori-positive adenoid tissue had significantly more reflux episodes (median 35) compared to H. pylori-negative (median 0).
  • Significantly more reflux episodes reached the upper esophageal sphincter in H. pylori-positive patients.
  • Absence of reflux episodes was the sole independent predictor for H. pylori negativity.

Conclusions:

  • Reflux episodes reaching the upper esophageal sphincter may facilitate H. pylori transmission to nasopharyngeal lymphoid tissue.
  • This mechanism could contribute to the development of adenoid hyperplasia in pediatric populations.
  • Findings suggest a potential link between LPR and H. pylori-mediated adenoid pathology.
Abstract

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