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Original Article
Oct 2011

Absence of Helicobacter pylori in Pediatric Adenoid Hyperplasia

Author Affiliations

Author Affiliations: Flinders ENT, Department of Surgery (Drs Hussey, Woods, Ooi, and Carney and Ms Harris), and Department of Histopathology (Dr Thomas), Flinders Medical Centre and Flinders University, Adelaide, Australia.

Arch Otolaryngol Head Neck Surg. 2011;137(10):998-1004. doi:10.1001/archoto.2011.136

Objectives To (1) develop a reverse transcription-polymerase chain reaction assay to determine whether Helicobacter pylori and/or other members of the Helicobacteraceae family are detected in hyperplastic adenoids of children and (2) critically analyze published polymerase chain reaction methods to ascertain whether false-positive detection of H pylori has been reported.

Design Cohort study.

Patients Adenoid biopsy specimens (78 hyperplastic and 15 normal) were collected from children aged 2 to 10 years.

Methods Total RNA was extracted before reverse transcription of bacterial RNA using Helicobacteraceae-specific primer. A nested reverse transcription–polymerase chain reaction protocol was designed to detect all species of the Helicobacteraceae family. A piece of each biopsy specimen was examined histologically.

Results Laryngopharyngeal reflux was suspected in 41% of the children (n = 23) on the basis of the Reflux Symptom Index. No evidence of H pylori was found in any adenoid sample. Candidatus Wolinella africanus was the only Helicobacteraceae family member detected in 1 hyperplastic adenoid. Histologic examination identified very few bacterial organisms. Previous polymerase chain reaction findings may be the result of false-positive H pylori detection.

Conclusions Inflammation and enlargement of the adenoids is not likely due to ongoing bacterial infection arising from laryngopharyngeal reflux. We conclude that H pylori and other Helicobacteraceae family members are not major contributors to the development of hyperplastic adenoids in children.