THE PATIENT with peptic esophagitis has long been neglected, allowing progression of the disease to chronic ulceration, fibrosis, and stricture. This neglect has been due to a failure of appreciation of the pathogenesis and clinical course of the disease and an ineffective therapeutic program.
Peptic esophagitis is an inflammatory process of the esophagus which occurs when there is a persistent association of gastric or intestinal secretions with the nonresistant squamous mucosa of the esophagus.1 The reflux of these secretions into the esophagus is due to nonfunction or failure of the cardiac sphincter mechanism. This is usually caused by an associated sliding hiatus hernia, persistent vomiting, or the surgical excision or disruption of the cardiac sphincter (Table 1).
The major factors involved in the prevention of regurgitation into the esophagus by the cardiac sphincter can be identified. The inferior constrictor muscle of the esophagus and the oblique gastric muscles about