What is acid reflux?

Gastroesophageal reflux is a physiologic process that refers to the effortless movement of stomach contents from the stomach to the esophagus. It occurs in everyone, multiple times every day, usually without producing symptoms or signs of damage. Reflux can also be pathologic and produce symptoms and signs of injury to the esophagus, oropharynx, larynx, and respiratory tract. Reflux damage to the esophagus (reflux esophagitis) is the most common form of Acid Reflux Disease and is most often recognized by recurrent heartburn. In almost all patients with heartburn, esophageal mucosal pathology is identifiable, although only about 40% have endoscopically detectable erosions. The remaining 60% of patients with heartburn have endoscopically undetectable (microscopic) pathology—termed nonerosive reflux disease (NERD).

Acid Reflux Disease is one of the most common diseases in the Western world based on the prevalence of heartburn. In the United States, about 45% of adults have heartburn at least once a month, about 20% once a week, and about 10% daily. Heartburn affects men two- to threefold more often than it affects women and is more common in whites than blacks. Although Acid Reflux Disease rarely causes death, it reduces quality of life and has a morbidity rate of 10 to 15% secondary to ulceration, bleeding, stricture, Barrett's esophagus, and adenocarcinoma. The overall risk for esophageal adenocarcinoma in patients with heartburn is very low, with estimates of 1 in 2500 cases per year for those with daily heartburn to 1 in 10,000 cases per year for those with monthly heartburn.

Acid Reflux Disease develops when acidic stomach contents reflux into the esophagus and remain there long enough to overcome the resistance of the esophageal epithelium. Based on 24-hour esophageal pH monitoring, Acid Reflux Disease develops in at least two fundamentally different ways: (1) under conditions in which there is prolonged contact of the esophageal epithelium with refluxed stomach acid and (2) under conditions in which the esophageal epithelium is damaged despite a normal duration of contact with refluxed stomach acid. Prolonged acid contact results from defects in the antireflux barriers or luminal clearance mechanisms (or both), with transient LES relaxations accounting for more than 50% of acid reflux events in NERD. These relaxations are non–swallow-induced, reflex relaxations of the LES caused by stomach fundic distention. They are associated with acid reflux because they are twice as long as relaxations with swallowing and, unlike swallow-induced LES relaxations, are accompanied by inhibition of diaphragmatic contraction and unaccompanied by lumen-obliterating esophageal peristalsis. The cause of the increase in the frequency of acid reflux episodes associated with transient relaxations in patients with Acid Reflux Disease is unclear but is unrelated to delayed stomach emptying or infection with Helicobacter pylori. A diet rich in nonabsorbable carbohydrates may be one possible provocateur. In erosive esophagitis, transient LES relaxations account for less than 50% of acid reflux events, with most occurring across a mechanically weak LES. Whether LES weakness causes erosive esophagitis or is a consequence of it remains unclear because products released during inflammation can impair LES contractility. Similarly, hiatal hernias and impaired peristalsis are common in erosive esophagitis, but whether they are cause or consequence is also unclear because esophagitis can result in both esophageal shortening (by sustained contraction of the longitudinal muscle) and peristaltic dysfunction (by weakening circular muscle contractility). Patients with heartburn despite normal acid contact time presumably have primary defects in tissue resistance, with these defects probably being acquired by dietary indiscretions such as excess exposure to alcoholic, hypertonic, or hot-temperature products.