Biliary Acids and Barrett’s Esophagus

Abstract

Introduction: Recent evidence reveals the actions of biliary acids as signaling molecules related to the state of anatomical and functional integrity of the compromised organism under their toxic effects, associated or not with comorbidity. In the esophagus, these actions are expressed as an inflammatory condition that worsens gradually, in direct relation to the intensity and persistence of biliary reflux or sequential cascade acute esophagitis–chronic esophagitis–Barrett's metaplasia–dysplasia–cancer.

Objective: To expose current theoretical foundations on the toxic effects of biliary acids in duodenogastroesophageal reflux that trigger this cascade.

Methods: A systematic review in PubMed, SciELO, Lilacs and Elsevier was conducted at Centro Nacional de Cirugía de Mínimo Acceso of reports between 1981-2023 on the biomolecular mechanisms that could make up the theoretical basis of esophageal carcinogenesis from its initial inflammation in the course of its interaction with biliary acids.

Development: The biomolecular mechanisms were reviewed that could support the link between the toxic effects of biliary acids and dysbiosis, Barrett's metaplasia and esophageal cancer. The sequential cascade inflammation–esophageal carcinogenesis confirms that these mechanisms may be controllable and preventable, particularly the activation of receptors overexpressed in Barrett's metaplasia associated with persistent duodenogastroesophageal reflux.

Conclusions: The described mechanisms define biliary acids contained in duodenogastroesophageal reflux as risk markers for esophageal carcinogenesis, depending on their pH, persistence, intensity and the esophageal microbiota.