Although gastroesophageal reflux disease (GERD) is acommon disorder in Western countries, with a significantimpact on quality of life and healthcare costs, themechanisms involved in the pathogenesis of symptomsremain to be fully elucidated. GERD symptoms andcomplications may result from a multifactorial mechanism,in which acid and acid-pepsin are the importantnoxious factors involved. Prolonged contact of theesophageal mucosa with the refluxed content, probablycaused by a defective anti-reflux barrier and luminalclearance mechanisms, would appear to be responsiblefor macroscopically detectable injury to the esophagealsquamous epithelium. Receptors on acid-sensitivenerve endings may play a role in nociception andesophageal sensitivity, as suggested in animal modelsof chronic acid exposure. Meanwhile, specific cytokineand chemokine profiles would appear to underlie thevarious esophageal phenotypes of GERD, explaining,in part, the genesis of esophagitis in a subset of patients.Despite these findings, which show a significantproduction of inflammatory mediators and neurotransmittersin the pathogenesis of GERD, the relationshipbetween the hypersensitivity and esophageal inflammationis not clear. Moreover, the large majority of GERDpatients (up to 70%) do not develop esophageal erosions,a variant of the condition called non-erosive refluxdisease (NERD). This summary aims to explore theinflammatory pathway involved in GERD pathogenesis,to better understand the possible distinction betweenerosive and non-erosive reflux disease patients and toprovide new therapeutic approaches.

Gastroesophageal reflux disease: Update on inflammation and symptom perception

Altomare A;GUARINO M;Emerenziani S;Cicala M
2013-01-01

Abstract

Although gastroesophageal reflux disease (GERD) is acommon disorder in Western countries, with a significantimpact on quality of life and healthcare costs, themechanisms involved in the pathogenesis of symptomsremain to be fully elucidated. GERD symptoms andcomplications may result from a multifactorial mechanism,in which acid and acid-pepsin are the importantnoxious factors involved. Prolonged contact of theesophageal mucosa with the refluxed content, probablycaused by a defective anti-reflux barrier and luminalclearance mechanisms, would appear to be responsiblefor macroscopically detectable injury to the esophagealsquamous epithelium. Receptors on acid-sensitivenerve endings may play a role in nociception andesophageal sensitivity, as suggested in animal modelsof chronic acid exposure. Meanwhile, specific cytokineand chemokine profiles would appear to underlie thevarious esophageal phenotypes of GERD, explaining,in part, the genesis of esophagitis in a subset of patients.Despite these findings, which show a significantproduction of inflammatory mediators and neurotransmittersin the pathogenesis of GERD, the relationshipbetween the hypersensitivity and esophageal inflammationis not clear. Moreover, the large majority of GERDpatients (up to 70%) do not develop esophageal erosions,a variant of the condition called non-erosive refluxdisease (NERD). This summary aims to explore theinflammatory pathway involved in GERD pathogenesis,to better understand the possible distinction betweenerosive and non-erosive reflux disease patients and toprovide new therapeutic approaches.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12610/6369
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