OBJECTIVE: Recently, it was suggested that tonsil and adenoid tissues may act as a reservoir for Helicobacter pylori (HP). A connection between chronic tubotympanal disorders and gastroesophageal reflux is well recognized, but the mechanism underlying this relationship is unclear. In this study, we investigated possible presence of HP in adenoid tissue and middle ear effusions in patients with chronic otitis media with effusion (OME) and we compared the data with the results of the children who had adenoid hypertrophy without OME. METHODS: The study was comprised of 38 consecutive children with adenoid hypertrophy and/or chronic OME. The patients were divided into two groups. The first group included 18 subjects having OME+adenoid hypertrophy and the second group included 20 subjects having solely adenoid hypertrophy. Each patient underwent the appropriate surgical procedure; myringotomy, placement of tympanostomy tubes and/or adenoidectomy. After myringotomy, the middle ear effusions were collected in a suction and collection device and a core biopsy specimen was taken from each adenoid tissue following adenoidectomy. DNA extracted from these samples was used for the amplification of 23S ribosomal RNA gene of HP by real-time polymerase chain reaction (RT-PCR). RESULTS: In the first group 34 effusion samples were obtained from ears of 18 patients (two had unilateral OME). HP was found to be positive in 12 children (67%) and 16 of 34 ears (47%) with RT-PCR. In eight children HP was positive in only one ear and in four children in both ears. No positive reaction was seen in tissue samples obtained from adenoids of these patients. In the second group a positive reaction was seen in adenoid tissue of only one patient. CONCLUSIONS: This study showed that there is HP presence in middle ears of the children with chronic OME, indicating HP having a possible role in OME pathogenesis. In addition, we demonstrated HP presence in only 1 of 38 adenoid specimens supporting the idea that adenoid tissue does not act as a reservoir for HP.
OBJECTIVE: Recently, it was suggested that tonsil and adenoid tissues may act as a reservoir for Helicobacter pylori (HP). A connection between chronic tubotympanal disorders and gastroesophageal reflux is well recognized, but the mechanism underlying this relationship is unclear. In this study, we investigated possible presence of HP in adenoid tissue and middle ear effusions in patients with chronic otitis media with effusion (OME) and we compared the data with the results of the children who had adenoid hypertrophy without OME. METHODS: The study was comprised of 38 consecutive children with adenoid hypertrophy and/or chronic OME. The patients were divided into two groups. The first group included 18 subjects having OME+adenoid hypertrophy and the second group included 20 subjects having solely adenoid hypertrophy. Each patient underwent the appropriate surgical procedure; myringotomy, placement of tympanostomy tubes and/or adenoidectomy. After myringotomy, the middle ear effusions were collected in a suction and collection device and a core biopsy specimen was taken from each adenoid tissue following adenoidectomy. DNA extracted from these samples was used for the amplification of 23S ribosomal RNA gene of HP by real-time polymerase chain reaction (RT-PCR). RESULTS: In the first group 34 effusion samples were obtained from ears of 18 patients (two had unilateral OME). HP was found to be positive in 12 children (67%) and 16 of 34 ears (47%) with RT-PCR. In eight childrenHP was positive in only one ear and in four children in both ears. No positive reaction was seen in tissue samples obtained from adenoids of these patients. In the second group a positive reaction was seen in adenoid tissue of only one patient. CONCLUSIONS: This study showed that there is HP presence in middle ears of the children with chronic OME, indicating HP having a possible role in OME pathogenesis. In addition, we demonstrated HP presence in only 1 of 38 adenoid specimens supporting the idea that adenoid tissue does not act as a reservoir for HP.
Authors: S Kariya; M Okano; K Fukushima; S Nomiya; Y Kataoka; R Nomiya; H Akagi; K Nishizaki Journal: Clin Exp Immunol Date: 2008-08-22 Impact factor: 4.330