ESOPHAGITIS following subtotal or total gastrectomy, as in patients who have little or no acid in their gastric juice, is a well-established clinical entity.1,2 The reflux of alkaline secretions originating in the pancreas and liver have been incriminated as the principal etiological agents.
Palmer3 has suggested, however, that in some people a primary subepithelial disease of the esophagus exists. Others have implied infectious, vascular aberrations, vitamin deficiencies, and inherent susceptibility of the lower esophagus to the trauma of ingested food as causative factors leading to the pathological and clinical pictures of esophagitis.2
In contrast to the esophagitis of acid or peptic reflux, investigative experiments have been minimal and the role of various possible agents, one of which is bile, very controversial. Cross and Wangensteen4 produced esophagitis in dogs with bile, pancreatic juices, and a mixture of the two. However, Redo5,6 was unable to produce such