Barrett's esophagus (BE) usually develops in patients with
gastroesophageal reflux disease and therefore it has been suggested that esophageal
acid exposure plays an import role in the initiation of BE and its progression towards esophageal
adenocarcinoma (EAC). The mechanisms whereby
acid exposure causes BE are not completely revealed and the potential role of esophageal
acid exposure in
carcinogenesis is unclear as well. Since
acid exposure is thought to play an important role in the progression of BE,
therapies aimed at preventing the development of EAC have primarily focused on pharmacological and surgical
acid suppression. In clinical practice,
acid suppression is effective in relieving reflux symptoms and decreases esophageal
acid exposure in most patients. However, in some individuals, pathological
acid exposure persists and these patients continue to be at risk for developing dysplasia or EAC. To date, published trials suggest that
acid suppression is able to prevent the development and progression of dysplasia in patients with BE, but definite and compelling proof is still lacking. This article reviews the mechanisms of
acid-induced
carcinogenesis in BE and the role of
acid suppression in the prevention of neoplastic progression.