Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

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OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Diagnosis
 

Do particular clinical factors influence development and extent of Barrett's esophagus?

G.W. Falk (Cleveland)

Barrett's esophagus is an acquired condition resulting from severe esophageal mucosal injury. However, it still remains unclear why some patients with gastroesophageal reflux disease (GERD) develop Barrett's esophagus whereas others do not. Duration and extent of acid exposure, genetic susceptibility, environmental factors and reflux of duodenogastric contents may all play a role in this regard.

Why does Barrett's esophagus develop in only some patients with gastroesophageal reflux disease?

Barrett's esophagus is predominantly a disease of middle-aged white males [1]. However, the prevalence of Barrett's esophagus in Hispanics is similar to that in Caucasians [2] and Barrett's esophagus was diagnosed in 2% of a Taiwanese population undergoing endoscopy for a variety of gastrointestinal symptoms [3]. Therefore, lifestyle changes in the Pacific Rim and other developing countries may change the epidemiology of Barrett's esophagus in the future. The prevalence of Barrett's esophagus increases until a plateau is reached between the seventh and ninth decades [1]. One population study estimated that the mean age of development of Barrett's esophagus was 40 years and the mean age at diagnosis was 63 years [1]. Hence, the disorder may be present for up to 20 years before it is clinically recognized.

When compared to GERD patients without Barrett's esophagus, Barrett's patients develop reflux symptoms at an earlier age, have an increased duration of symptoms, increased severity of nocturnal reflux symptoms, and increased complications of GERD such as stricture, ulcer and bleeding [4]. A community based study by Lieberman et al. found that compared to patients with reflux symptoms for less than one year, Barrett's esophagus was three times more common in patients with reflux symptoms for one to five years, five times more common if symptom duration was five to ten years, and 6.4 times more common if symptom duration was greater than 10 years [5]. Thus age of onset, symptom duration and presence of nocturnal symptoms or complications may be markers of increased risk for developing Barrett's esophagus. Interestingly, similar clinical risk factors were recently identified for esophageal adenocarcinoma by Lagergren et al. [6].

Barrett's esophagus is clearly associated with severe GERD. Studies consistently show that distal esophageal acid exposure, both day and night, is greater in patients with Barrett's esophagus than in patients with uncomplicated reflux disease [7, 8]. Excessive reflux of duodenogastric contents may also contribute to the development of Barrett's esophagus and its complications [8]. A variety of other motility abnormalities of the esophagus have been described in Barrett's esophagus. These include prolonged esophageal transit, low lower esophageal sphincter (LES) pressures, and peristaltic dysfunction of the esophagus [7]. Barrett's patients also have hernias that are longer and hiatal openings that are wider than controls with or without esophagitis [9]. Barrett's esophagus is not related to gastric acid hypersecretion, as studies done with appropriate controls find no difference in basal acid output, gastrin stimulated peak acid output, overnight fasting residue and pepsin output in the two groups [10].

Helicobacter pylori infection is either no more common or less common than in Barrett's esophagus patients than in control populations [11-14]. A number of studies suggest that infection with H. pylori, especially cagA+ strains, may protect against the development of Barrett's esophagus and its associated dysplasia and adenocarcinoma [12, 14, 15]. For example, Weston et al. recently reported H. pylori infection in 73 of 208 (35.1%) Barrett's patients without dysplasia compared to 17 of 47 (36.2%) with lowgrade/indefinite dysplasia, 2 of 14 (14.3%) with high-grade dysplasia and 3 of 20 (15%) with adenocarcinoma [15].

Long segment versus short segment Barrett's esophagus

Are their any clinical predictors of long versus short-segments (< 3 cm in length) of Barrett's esophagus? Patients with both long segment and short segment Barrett's esophagus are predominantly white, male, and smokers [16]. However, the duration of heartburn symptoms is greater in patients with long segment Barrett's esophagus (LSBE) compared to those with short segment Barrett's esophagus (SSBE) [16, 17].

A number of studies have examined differences in the pathophysiology of SSBE versus LSBE. Patients with SSBE may have a variety of abnormalities intermediate to those of LSBE patients and normal controls. Loughney et al. found that SSBE patients were characterized by an LES pressure lower than controls but higher than LSBE [18]. Distal acid exposure time was greater than controls but less than that in LSBE whereas the distal esophageal contraction amplitude was no different than that of controls [18]. A progressive increase in esophageal dysfunction with increased lengths of Barrett's esophagus has been confirmed by others [17]. Finally, hiatal hernias (HH) are common in both SSBE and LSBE [9, 16].

Conclusions

Clinical factors that may influence the development of Barrett's esophagus are shown in Table I. Aging, white males with chronic GERD symptoms are clearly at increased risk for

Table I. Clinical risk factors for the development of Barrett's esophagus

the development of Barrett's esophagus. These patients tend to have more severe reflux disease than do individuals without Barrett's esophagus, and the uniform presence of a HH may be a factor in this regard. Patients with SSBE have a similar demographic profile as patients with LSBE. However, it appears that the pathophysiologic abnormalities in these patients are intermediate between those of patients withuncomplicated GERD and LSBE.

References

1. Cameron AJ, Lomboy CT. Barrett's esophagus: age, prevalence, and extent of columnar epithelium. Gastroenterology 1992;103:1241-1245.

2. Bersentes K, Fass R, Padda S, Johnson C, Sampliner RE. Prevalence of Barrett's esophagus in Hispanics is similar to Caucasians. Dig Dis Sci 1998;43:1038-1041.

3. Yeh C, Hsu CT, Ho AS, Sampliner RE, Fass R. Erosive esophagitis and Barrett's esophagus in Taiwan. A higher frequency than expected. Dig Dis Sci 1997;42:702-706.

4. Eisen GM, Sandler RS, Murray S, Gottfried M. The relationship between gastroesophageal reflux disease and its complications with Barrett's esophagus. Am J Gastroenterol 1997;92:27-31.

5. Lieberman DA, Oehlke M, Helfand M. Risk factors for Barrett's esophagus in community-based practice. Am J Gastroenterol 1997;92:1293-1297.

6. Lagergren J, Bergstrom R, Lindgren A, Nyren O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999;340:825-831.

7. Singh P, Taylor RH, Colin-Jones DG. Esophageal motor dysfunction and acid exposure in reflux esophagitis are more severe if Barrett's metaplasia is present. Am J Gastroenterol 1994;89:349-356.

8. Champion G, Richter JE, Vaezi MF, Singh S, Alexander R. Duodenogastroesophageal reflux:relationship to pH and importance in Barrett's esophagus. Gastroenterology 1994;107:747-754.

9. Cameron AJ. Barrett's esophagus: prevalence and size of hiatal hernia. Am J Gastroenterol 1999;94:2054-2059.

10. Hirschowitz BI. Gastric acid and pepsin secretion in patients with Barrett's esophagus and appropriate controls. Dig Dis Sci 1996;41:1384-1391.

11. O'Connor HJ. Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management. Aliment Pharmacol Ther 1999;13:117-127.

12. Vicari JJ, Peek RM, Falk GW, Goldblum JR, Easley KA, Schnell J, Perez-Perez GI, Halter SA, Rice TW, Blaser MJ, Richter JE. The seroprevalence of cagA positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998;115:50-57.

13. Lord RV, Frommer DJ, Inder S, Tran D, Ward RL. Prevalence of Helicobacter pylori infection in 160 patients with Barrett's oesophagus or Barrett's adenocarcinoma. Aust NZ J Surg 2000;70:26-33.

14. Weston AP, Badr AS, Topalovski M, Cherian R, Dixon A, Hassanein RS. Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett's esophagus, Barrett's dysplasia, and Barrett's adenocarcinoma. Am J Gastroenterol 2000;95:387-394.

15. Chow WH, Blaser MJ, Blot WJ, Gammon MD, Vaughan TL, Risch HA, Perez-Perez GI, Schoenberg JB, Stanford JL, Rotterdam H, West AB, Fraumeni JF. An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Res 1998;58:588-590.

16. Hirota WK, Loughney TM, Lazas DJ, Maydonovitch CL, Rholl V, Wong RK. Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophagogastric junction: prevalence and clinical data. Gastroenterology 1999;116:277-285.

17. Oberg S, DeMeester TR, Peters JH, Hagen JA, Nigro JJ, DeMeester SR, Theisen J, Campos GM, Crookes P. The extent of Barrett's esophagus depends on the status of the lower esophageal sphincter and the degree of esophageal acid exposure. J Thorac Cardiovasc Surg 1999;117:572-582.

18. Loughney T, Maydonovitch CL, Wong RK. Esophageal manometry and ambulatory 24-hour pH monitoring in patients with short and long segment Barrett's esophagus. Am J Gastroenterol 1998;93:916-919.


Publication date: August 2003 OESO©2015