Efficacy of Medical Therapy and Antireflux Surgery to Prevent Barrett’s Metaplasia in Patients With Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is a disease with multifactorial etiology. 1 The impaired lower esophageal sphincter (LES) is the basic anatomic defect that enables reflux of gastric contents into the esophagus. 2 Gastric acid may play an important role in the pathophysiology of acute reflux esophagitis. 1 However, GERD is a general motility disorder of the foregut. It may lead to deterioration of esophageal peristalsis, which impairs esophageal clearance function. 3 This prolongs the presence of the refluxate in the esophagus and may therefore enhance esophageal mucosal damage. 4 Moreover, GERD may result in alteration of gut neuropeptides that are important for the control of antroduodenal motility. 5 Weak antroduodenal motility during the fasting state impairs the clearance function of the stomach and may cause pathologic duodenogastric reflux. 6 Increased concentrations of duodenal contents have been shown in patients with GERD, especially those with Barrett’s metaplasia. 7 Duodenogastroesophageal reflux causes growth stimulation of the foregut mucosa, 8 may enhance production of oxygen-derived free radicals, 9–11 and may alter apoptosis in the esophageal mucosa. 12 These mechanisms may explain the carcinogenic potential of GERD. 13,14 Because of the wide spectrum of pathophysiologic mechanisms in GERD, medical treatment aimed at suppressing gastric acid production does not completely inhibit reflux of all gastroduodenal contents. Therefore, it may be concluded that medical therapy in GERD may not prevent the development of complications such as Barrett’s metaplasia, although patients are free of heartburn and acute esophagitis. 15 It was the aim of this prospective study to investigate whether Barrett’s metaplasia may develop despite effective medical treatment of GERD.