Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology

Abstract

Our results suggest that the biochemical changes seen in adenoid hypertrophy are different to those seen in reflux-affected tissues. The decreased COX-2 and MUC5AC expression may be due to squamous metaplasia and other inflammatory changes associated with adenoid hypertrophy. Our findings infer there is little evidence of reflux being a major contributory factor in the pathophysiology of adenoidal hypertrophy.

Ribosomal therapy in patients with pharyngolaryngeal reflux

“…It is therefore conceivable that even a single reflux episode extending beyond the esophagus may be sufficient to cause pharyngeal, laryngeal, and respiratory symptoms and signs [4]. The epithelium of the upper airway has different mucosal defenses to those seen in the esophagus and this has been hypothesized to be the cause of ENT pathology in the absence of reflux symptoms [8]. Recent research has looked at the relationship between extraesophageal reflux disease and upper airway disorders.…”

“…In particular, the inflammation is characterized by edema and mononuclear cell infiltration in the mucosa and lamina propria with vascular dilation [8,10]. These studies highlight that PLRD is a result of the breakdown in the defense mechanism that protects against corrosive damage from refluxate [9]: the presence of pepsin in the upper respiratory tract tissue correlated with depleted levels of carbonic anhydrase (CA) III (which catalyzes bicarbonate production to neutralize gastric acid during reflux), suggesting that pepsin is likely to be a causal factor in CA III depletion.…”

“…This leads to an increase in the number of lymphocytes within the tonsils and adenoids without a significant response to antibiotic treatment [8,9].…”

“…Although the vast majority of the data concerning PLRD and its pathologic effects come from epidemiologic studies, recent studies have highlighted the cellular and immune mechanisms involved in this disease [8][9][10][11][12].…”

Absence of <emph type="ital">Helicobacter pylori</emph> in Pediatric Adenoid Hyperplasia

“…2 Therefore, it is hypothesized that gastroesophageal reflux and laryngopharyngeal reflux (LPR) may cause adenoid hyperplasia. 3 Recent studies by Harris et al 4 evaluated LPR biomarker expression in hyperplastic adenoids. Markers of reflux that were investigated included pepsin, carbonic anhydrase III, cyclooxygenase 2, and mucin 5AC (MUC5AC).…”