Does Helicobacter pylori have a role in the pathogenesis of otitis media with effusion, or is it a fallacy??
Ayse Yasemin Gunduz1,2, Mahmut Tayyar Kalcioglu3, Serdal Celik3
1Department of Otorhinolaryngology, Faculty of Medicine, Istanbul Medeniyet University, Goztepe Prof. Dr. Suleyman Yalcin City Hospital, Kadikoy, Istanbul, Türkiye. ayaseming@hotmail.com.
Purpose:
Helicobacter pylori, causing chronic systemic infection, may colonize in middle ear milieu and conduce to effusion collection. Many investigations on relationship between pathogenesis of otitis media with effusion (OME) and Helicobacter pylori yielded conflicting results. We investigated Helicobacter pylori presence in effusion and adenoid samples of children having OME and in middle ear and adenoid samples of children with healthy middle ears to elucidate its role on OME pathogenesis.
Methods:
This prospective case-control study included 300 patients aged 1-12 years. One-hundred effusion samples collected from 100 children undergoing ventilation tube insertion and adenoidectomy due to chronic OME and adenoid hypertrophy formed study group, and 100 adenoid samples collected from adenoids of these children formed Group-1. One-hundred healthy-looking middle ear irrigation solutions collected from 100 children undergoing cochlear implantation formed Group-2. One-hundred adenoid samples collected from 100 children having no effusion and only undergoing adenoidectomy formed Group-3. After DNA isolation of samples, Helicobacter pylori 16 S rRNA and 23 S rRNA gene for clarithromycin-resistance were investigated by real time-polymerase chain reaction (Rt-PCR).
Results:
The median age of 300 children was 5, and 179 were boys and 121 were girls. Helicobacter pylori was detected by Rt-PCR in none (%0) of the 400 samples (200 middle ear, 200 adenoid).
Conclusion:
In this largest sample-size study utilizing updated molecular methods to date, negative results indicate that Helicobacter pylori does not play role as an active pathogen in polymicrobiality of OME, and adenoids do not serve as a reservoir for Helicobacter pylori in this process.
Related Concept Videos
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
01:16Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
01:17Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
01:30Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
01:28Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.