Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

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Volume: Barrett's Esophagus
Chapter: Pathophysiology

Can the rate of Barrett's metaplasia in treated achalasia be evaluated?

R.D. Szyjkowski (Syracuse, New York)

Specialized columnar epithelium is essential for the histologic diagnosis of Barrett's metaplasia or Barrett's esophagus, a disease most commonly assumed to be secondary to gastroesophageal reflux disease (GERD) [1]. When 2 cm or more of specialized columnar epithelium is chosen as the diagnostic criteria for Barrett's esophagus, it is found in 12.4% of patients undergoing esophagogastroduodenoscopy for reflux symptoms [2]. Short segment Barrett's epithelium (SSBE), defined as an irregular squamocolumnar junction with specialized columnar epithelium in the distal esophagus of length less than 2 cm, has been reported in 18% of patients undergoing endoscopy for indications other than achalasia [3]. Interest in SSBE is spurred by the general increase in adenocarcinoma of the esophagus [4], the association of specialized columnar epithelium with adenocarcinoma [5], and the documentation of the presence of [6] and progression to dysplasia and adenocarcinoma [7] in SSBE. The rate of adenocarcinoma in SSBE has been reported to be as high as one per 278 patient years [8].

Achalasia is a motor disorder of the esophagus manifested by dysphagia secondary to absent peristalsis of the esophageal body. It is often associated with incomplete relaxation and hypertension of the lower esophageal sphincter (LES). Pneumatic dilation remains the medical treatment of choice. This forceful dilation results in the disruption of LES muscle fibers, weakening the LES and subsequent improvement in esophageal emptying. Symptoms attributable to GERD occur in 2% of treated patients [9] Up to 75% of treated patients however, may have abnormal pH studies and be asymptomatic [10]. Myotomy is the surgical treatment of achalasia and complications are primarily related to GERD [11].

The incidence of postoperative reflux has been reported to be as high as 13% after myotomy [12].

Jaakkola [13] reported long segment Barrett's esophagus (LSBE) in 8.7% of patients treated for achalasia with myotomy. All of these patients had symptoms of GERD, decreased LES pressure and abnormal pH studies. Severe glandular dysplasia [14] and adenocarcinoma in the setting of Barrett's esophagus have been reported less frequently than squamous cell cancers in patients with treated achalasia [15]. These cancers generally occur years to decades after primary achalasia treatment.

The prevalence of SSBE in patients treated for achalasia has also been studied [16]. Twenty one study patients had dilation as their initial therapy. Heller myotomy was ultimately performed in four. Three patients had GERD related strictures, one of whom had specialized columnar epithelium. All three of these peptic strictures required endoscopic dilation. At the time of enrollment pyrosis requiring medical therapy either with proton pump inhibitors or H2 receptor antagonists was present in six. Dysplasia and carcinoma were not seen. An irregular squamocolumnar junction suggestive of SSBE were seen in 12 of 21 patients, 11 (52%) of whom had histologic evidence of specialized columnar epithelium. SSBE in these patients was significantly correlated with male sex. Nine patients had normal appearing squamocolumnar junctions and one of these had microscopic evidence of specialized columnar epithelium but a normal squamocolumnar junction.

This study found SSBE that is much higher in treated achalasia patients than that of the general population. Barrett's esophagus is a disease most commonly assumed to be secondary to GERD [1]. Achalasia is from the Greek meaning "failure to relax", suggesting that acid reflux should not be able to occur. It is known that fermentation of retained esophageal food stuff and ingestion of acidic foods can cause esophageal acidification in achalasia and Streitz et al. suggest that esophageal acid exposure in their population is due to slow clearance of esophageal acid from relatively few reflux episodes [17]. While studies in very large populations have not been done, studies have shown that true pretreatment reflux also occurs in untreated achalasia [18].

Jaakkola [13] reported LSBE in 8.7% of patients treated for achalasia with myotomy. Development of specialized columnar epithelium may be related to injury that results in disruption of the squamous lining of the esophagus, which does not happen in myotomy. This has been suggested in a dog model where reflux is induced after an esophageal mucosal strip defect was created. Regenerating epithelium was columnar in the majority of cases and was described as villiform, but intestinal metaplasia was not seen [19]. Several recent human studies have shown that re-injury with bi-cap, laser or freezing in the face of acid suppression can result in squamous regeneration.

It is possible that disruption of the LES and subsequent acid injury may predispose to columnar and intestinal metaplasia. Unfortunately no published studies of pretreatment biopsies have been performed, therefore it is possible that these histologic changes were present prior to achalasia therapy. Unpublished data from my untreated achalasia patients shows an irregular squamocolumnar junction and specialized columnar epithelium on biopsy in 2 of 7 patients (28%). These numbers are too small to be clinically meaningful.

In summary, reports of Barrett's esophagus after myotomy are lower than the general population but SSBE in patients treated with dilation is much greater than the general population. Anecdotal data has shown SSBE in untreated achalasia patients. Given animal model studies, these data are not necessarily contradictory. Therefore, the rate of Barrett's metaplasia in achalasic patients can and should be evaluated to define the epidemiology of these findings.


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Publication date: August 2003 OESO©2015