Esophageal intramural pseudodiverticulosis (EIPD) is a disease of unknown pathogenesis characterized by usually systemic, cystic dilatation of the excretory ducts of esophageal submucosal glands. In this article, I review the epidemiology, clinical manifestations, endoscopic findings, esophagographic findings, and histopathology of EIPD. I also discuss the etiology and possible pathogenesis of EIPD based on my experiences with this disease and a review of the literature. EIPD usually presents with dysphagia in middle-aged individuals. It is often complicated with secondary infections, most commonly candidiasis. On esophagography, EIPD is delineated as small, multiple, flask-shaped outward projections within the esophageal wall. In recent years, EIPD has been mainly diagnosed by endoscopic findings of multiple, localized, small mucosal depressions. The orifices of the "pseudodiverticula" periodically open and close, and excrete mucus onto the mucosal surface. On histopathological examination, the luminal surface of dilated ducts in EIPD is covered by multilayered, hyperplastic epithelial cells, but myoepithelial cells in the glandular acini are well preserved. Treatment of EIPD is usually symptomatic therapy, and prevention of the infectious complications is important. The etiology and pathogenesis of EIPD are largely unknown, but functional abnormalities of autonomic nerve fibers innervating the esophageal glands likely play an important role, since the structures of the glands are basically preserved in this disease.

This report describes the first documented familial occurrence of gastric volvulus in two consecutive generations. Consideration is given to familial transmission of other foregut disorders. The report reviews the different types of gastric volvulus and considers their pathogenesis, clinical presentation, and treatment.

Twelve cases of oesophageal intramural pseudodiverticulosis are described and the findings in 85 previously reported cases are reviewed. The condition occurs in all age groups, predominantly in the sixth and seventh decades, with a slight predilection for males. The characteristic radiographic appearance is of multiple flask shaped outpouchings of 1-4 mm with narrow necks communicating with the oesophageal lumen. The source of the pseudodiverticula has been shown to be pathologically dilated excretory ducts of the submucous glands due to chronic submucosal inflammation. The distribution was segmental in 57 cases (59%) and diffuse in 40 (41%). Dysphagia is the main symptom and was found in 85 cases (88%); 88 cases out of 97 had radiological narrowing of the oesophagus; of these, 39 (44%) were in the upper oesophagus, 20 (23%) in the middle oesophagus, and 29 (33%) in the lower oesophagus. Treatment is directed towards management of the associated disorder, as the diverticula themselves rarely cause problems.

A case of intramural esophageal pseudodiverticulosis in a five-year-old with a 16-year follow up is presented.

Seven cases of esophageal intramural pseudodiverticulosis (EIPD) are presented and compared with 46 cases previously reported. EIPD is mainly a disease of older age with a 3:2 predominance of male patients. The radiologic appearance of EIPD shows great variation in localization and severity of visible changes. Radiologic examination is far more sensitive than endoscopy in diagnosing EIPD. The most effective therapy for EIPD is dilatation of strictures, leading to amelioration or disappearance of symptoms in over 90% of cases. Visible pseudodiverticula may persist after therapy, even in symptom-free patients.

Esophageal intramural pseudodiverticulosis (EIP) is a rare condition of unknown etiology. It is characterized by multiple, small, flaskshaped outpouchings in the esophageal wall. Involvement may be segmental or diffuse. Since this entity was first reported in 1960, there have been 43 cases described in the English literature. These cases are reviewed and six additional cases are reported with emphasis on clinical and radiographic parameters of this entity.

Five patients with benign oesophageal stricture are described who subsequently developed oesophageal intramural pseudodiverticulosis. Stricture was due to reflux oesophagitis in three patients and to lye ingestion in two. The minimum time between diagnosis of stricture and recognition of pseudodiverticulosis was two years. Most authors regard chronic inflammation as the initiating cause of pseudodiverticulosis. Although stricture is common, it generally occurs as part of the disease process and has not been regarded as a cause of the disorder. In our patients it is suggested that chronic inflammation due to stasis above a stricture, was the cause of pseudodiverticulosis. Out of the 36 cases of oesophageal intramural pseudodiverticulosis already reported, we could find only one patient in whom this sequence of events occurred.