Primary Motility  Disorders of the  Esophagus
 The Esophageal
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 Esophagogastric  Junction
 Barrett's
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OESO©2015
 
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.

References

1. Spechler SJ, Goyal RK. Barrett's esophagus. N Engl J Med 1986:315:312-371.

2. Winters C, Spurling TJ, Chobanian SJ, Curtis DJ, Esposito RL, Hacker JF 3d, et al. Barrett's esophagus. A prevalent, occult complication of gastroesophageal reflux disease. Gastroenterology 1987;92:118-124.

3. Spechler SJ, Zeroogian JM, Antonioli DA, Wang HH, Goyal RK. Prevalence of metaplasia at the gastro-esophageal junction. Lancet 1994;344:1533-1536.

4. Blot WJ, Devesa SS, Fraumeni JF. Continuing climb in rates of esophageal adenocarcinoma: an update. JAMA 1993;270:1320.

5. Schnell TG, Sontag SJ, Chejfec G. Adenocarcinomas arising in tongues or short segments of Barrett's epithelium. Dig Dis Sci 1992;37:137-143.

6. Weston AP, Krmpotich PT, Cherian R, Dixon A, Topalosvki M. Prospective long-term endoscopic and histological follow-up of short segment Barrett's esophagus: comparison with traditional long segment Barrett's esophagus. Am J Gastroenterol 1997;92:407-413.

7. Sharma, P, Morales TG, Bhattacharyya A, Garewal HS, Sampliner RE. Dysplasia in short segment Barrett's esophagus: a prospective 3-year follow-up. Am J Gastroenterol 1997;92:2012-2016.

8. Cameron AJ, Kamath PS, Carpenter HC. Barrett's esophagus, the prevalence of short and long segments in reflux patients. Gastroenterology 1995;108(4):A65.

9. Reynolds JC, Parkman HP. Achalasia. GI Clinics N Am 1989;18(2):223-255.

10. Shoenut JP, Duerksen D, Yaffe CS. A prospective assessment of gastroesophageal reflux before and after treatment of achalasia patients: pneumatic dilation versus transthoracic limited myotomy. Am J Gastroenterol 1997;92(7):1109-1112.

11. Jara FM, Toledo-Pereyra LH, Lewis JW, Magilligan DJ Jr. Long-term results of esophagomyotomy for achalasia of esophagus. Arch Surg 1979;114(8):935-936.

12. Andreollo NA, Earlam RJ. Heller's myotomy for achalasia:Is an added antireflux procedure necessary? Br J Surg 1987;74:765-769.

13. Jaakkola A, Reinikainen P, Ovaska J, Isolauri J. Barrett's esophagus after cardiomyotomy for esophageal achalasia. Am J Gastroenterol 1994;89(2):165-169.

14. Feczko PJ, Ma CK, Halpert RD, Batra SK. Barrett's metaplasia and dysplasia in postmyotomy achalasia patients. Am J Gastroenterol 1983;78(5):265-268.

15. Ellis FH, Gibb SP, Balogh K, Schwaber JR. Esophageal achalasia and adenocarcinoma in Barrett's esophagus: a report of two cases and a review of the literature. Dis Esophagus1997;10(1):55-60.

16. Szyjkowski RD, Shaffer RT, Kadakia S. Frequency of endoscopic and histologic short segment Barrett's epithelium in patients with treated achalasia. GI Endoscopy 1997;45:AB85.

17. Streitz JM Jr, Ellis FH Jr, Williamson WA, Glick ME, Aas JA, Tilden RL. Objective assessment of gastroesophageal reflux after short esophagomyotomy for achalasia with the use of manometry and pH monitoring. J Thorac Cardiovasc Surg 1996;111(1):112-113.

18. Shoenut JP, Trenholm BG, Micflikier AB, Teskey JM. Reflux patterns in patients with achalasia without operation. Ann Thorac Surg 1988;45:303-305.

19. Li H, Walsh TN, O'Dowd G, Gillen P, Byrne PJ, Hennessy TP. Mechanisms of columnar metaplasia and squamous regeneration in experimental Barrett's esophagus. Surgery 1994;115:176-181.


Publication date: August 2003 OESO©2015