Gastroesophageal reflux disease, pH monitoring, and treatment

Research into the causes of gastroesophageal reflux disease continues to cover a broad base. It ranges from the roles of transient relaxations of the lower esophageal sphincter, neural control mechanisms, nitric oxide, and impairment of the crural diaphragm in the production of reflux, to the roles of mucosal bicarbonate secretion, mucosal blood flow, and epithelial cell acid handling in the protection of the esophageal mucosa. Impaired esophageal acid clearance is also likely to be a major factor, although current manometric techniques have not been able to identify a clear abnormality in mild to moderate reflux disease. It is still unclear whether episodes of esophageal alkalinization signal the reflux of noxious pancreaticobiliary secretions or whether they indicate the presence of esophageal mucosal and salivary bicarbonate. There is increasing interest in the central and peripheral mechanisms responsible for the genesis of esophageal symptoms and also in the relationship between reflux and respiratory tract symptoms. Esophageal pH monitoring is used widely but there is continuing debate regarding its clinical utility; concomitant monitoring of other modalities, including esophageal motility and electrocardiography, remains a research tool. It is clear that the proton pump inhibitors, omeprazole and lansoprazole, are highly effective therapy for reflux esophagitis but the comparison of healing rates achieved by different medical modalities and by surgery remains thwarted by the absence of a generally accepted classification system for reflux esophagitis. Controlled studies comparing the latest treatment options, including laparoscopic fundoplication and proton pump inhibitors, are needed urgently.