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Benign tumors of the esophagus constitute only about 20% of all esophageal neoplasms. Most are small, asymptomatic lesions, but these tumors may occasionally cause dysphagia or other symptoms, necessitating endoscopic or surgical removal. Depending on their site of origin in the wall, benign esophageal neoplasms may be classified as mucosal or submucosal lesions.
Squamous papillomas are uncommon, accounting for less than 5% of all esophageal neoplasms. These lesions appear as coral-like excrescences containing a fibrovascular core with multiple finger-like projections covered by hyperplastic squamous epithelium. Although the etiology of esophageal papillomas is uncertain, the human papillomavirus has been implicated in their pathogenesis.
While esophageal papillomas are benign tumors, they can be mistaken histopathologically for verrucous carcinomas. Some investigators therefore believe all papillomas in the esophagus should be resected because of potential confusion with verrucous carcinoma.
Esophageal papillomas are usually solitary lesions, ranging from 0.5 to 1.5cm in size. Most patients are asymptomatic, but dysphagia is an occasional finding. , Some patients can have multiple papillomas, a rare condition known as esophageal papillomatosis. ,
Squamous papillomas may be manifested on double-contrast esophagrams by small (<1cm), smooth or slightly lobulated polyps ( Fig. 11.1 ). Because early esophageal cancers may also appear as small polypoid lesions, endoscopy is required for a definitive diagnosis. Rarely, papillomas may have a bubbly appearance due to trapping of barium between the papillary fronds of the lesion. Despite its rarity, esophageal papillomatosis should be suspected when barium studies reveal multiple, small, lobulated protrusions on the mucosa ( Fig. 11.2 ). ,
Adenomas account for less than 1% of all benign esophageal neoplasms. Because adenomatous polyps arise from columnar epithelium, they only occur in the esophagus in patients with Barrett’s (columnar epithelial-lined) mucosa (see Chapter 8). , Esophageal adenomas are important because they can undergo malignant degeneration via an adenoma-carcinoma sequence similar to that in the colon. , Endoscopic or surgical resection is therefore warranted.
Esophageal adenomas may appear on barium studies as sessile or pedunculated polyps ( Fig. 11.3 ). Larger, more lobulated lesions are more likely to harbor adenocarcinoma. Because adenomas arise in Barrett’s mucosa, they are almost always located in the distal esophagus and can be mistaken for inflammatory esophagogastric polyps (see next section), though adenomatous polyps tend to be larger and more lobulated. When an adenoma is suspected, endoscopy is required for a definitive diagnosis.
An inflammatory esophagogastric polyp represents the bulbous tip of a thickened gastric fold protruding into the distal esophagus. These lesions consist histologically of inflammatory and granulation tissue (so they are not actual neoplasms) and are thought to develop as a sequela of reflux esophagitis (see Chapter 8). As a result, affected patients often have chronic reflux symptoms. Because these polyps have no malignant potential, endoscopic resection is not usually warranted.
Inflammatory esophagogastric polyps are usually manifested on barium studies by a single prominent fold that arises in the gastric fundus and extends into the distal esophagus as a smooth, ovoid or club-shaped protuberance ( Fig. 11.4 ). , , The lesions frequently straddle a hiatal hernia and can be associated with reflux esophagitis. When characteristic features are present on barium studies, endoscopy is unnecessary. Occasionally, however, endoscopy may be required to exclude malignant tumor when the lesions are larger or more lobulated.
Since its original description in 1970, glycogenic acanthosis has been recognized as a benign condition of unknown etiology characterized histologically by hyperplastic squamous epithelial cells containing increased cytoplasmic glycogen. , It is a common condition with a prevalence of 3% to 15% at endoscopy. The lesions appear endoscopically as small, white mucosal plaques. , A definitive diagnosis is made on biopsy specimens showing the glycogen-rich epithelial cells.
Glycogenic acanthosis is a degenerative condition that markedly increases in prevalence in patients over 60 years of age. Nevertheless, it rarely causes esophageal symptoms, and there is no risk of malignant degeneration. Glycogenic acanthosis therefore represents an incidental finding of little or no clinical importance.
Glycogenic acanthosis is characterized on double-contrast esophagrams by a variable number of small (2 to 4 mm in size), discrete, rounded nodules or plaques in the mid or, less commonly, distal esophagus ( Fig. 11.5 ). Occasionally, individual plaques can be as large as 1 cm.
Glycogenic acanthosis should be differentiated on barium studies from other causes of mucosal nodularity, such as superficial spreading carcinoma and reflux or Candida esophagitis. However, superficial spreading carcinoma is characterized by confluent nodules and plaques (see Chapter 12), and reflux esophagitis is characterized by innumerable tiny nodules in the distal esophagus, producing a granular appearance (see Chapter 8), whereas glycogenic acanthosis is characterized by discrete nodules that are most prominent in the midesophagus. Candida esophagitis may produce similar findings (see Chapter 9), but candidiasis usually occurs in immunocompromised patients with odynophagia, whereas glycogenic acanthosis occurs in immunocompetent patients who have no esophageal symptoms.
Oral leukoplakia is a common condition characterized by tiny mucosal plaques that exhibit hyperkeratosis, epithelial dysplasia, or even frank carcinoma on histologic examination. Leukoplakia rarely involves the esophagus, , and its malignant potential in the esophagus is unknown. Endoscopy may reveal small white plaques that are occasionally recognized on double-contrast esophagrams as tiny nodules. ,
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