A report in the October issue of Archives of Otolaryngology – Head & Neck Surgery, one of the JAMA/Archives journals shows that bacteria causing stomach inflammation and ulcers were not detectable in tissue from inflamed and enlarged adenoids in children.

Background information in the articles explains that adenoid hyperplasia is an enlargement of the lymph glands located above the back of the mouth, which causes an obstruction to the upper airway that is linked to neuro-cognitive and behavioural problems in children. Theories suggest that adenoid hyperplasia may be caused by gastroesophageal reflux disease (GERD) whereby the stomach contents is regurgitated and backed up into the esophagus, and laryngopharyngeal reflux (LPR), which is similar to GERD, and sometimes, called ‘silent reflux’.

Damian J. Hussey, Ph.D. and his team from the Flinders Medical Centre and Flinders University in Adelaide, Australia, decided to examine if Helicobacter pylori, a bacteria that cause ulcers and stomach inflammation and/or other members of the Helicobacteraceae family are detected in hyperplastic adenoids of children, and to establish whether false-positive detection of H pylori has been reported.

Researchers assessed 93 adenoid biopsy specimens from children aged between 2 and 10 years, of which 78 biopsies were hyperplastic and 15 were normal. Based on the Reflux Symptom Index, researchers suspected 41% of children to have LPR.

The researchers comment, that:

“No evidence of H pylori was found in any adenoid sample. Candidatus Wolinella africanus was the only Helicobacteraceae family member detected in one hyperplastic adenoid. Histologic examination identified very few bacterial organisms. Previous polymerase chain reaction findings may be the result of false-positive H pylori detection.”

The findings stand in contrast to claims made by other researchers, that high colonization rates of H pylori have been detected in adenoid tissue.

The authors state:

“We believe that our findings show that adenoid tissue does not serve as a reservoir for species of the Helicobacteraceae family. This suggests that colonization of the tissue by these bacteria is not a factor contributing to adenoid hyperplasia.”

They conclude saying that:

“However, the detection of Candidatus W africanus in a hyperplastic adenoid sample indicates that gastric contents can reach the adenoid, so occasional reflux episodes may form part of the pathophysiologic characteristics of this disease.”

Written by Petra Rattue