Barrett’s Esophagus

An Article by Dr. William D. Lyday

Barrett’s esophagus is a common condition affecting the esophagus and its management remains controversial in the medical community. Barrett’s is considered a pre-cancer and clearly elevates the risk of esophageal adenocarcinoma in carriers of this condition. In this post, we will attempt to summarize the risk factors associated with Barrett’s esophagus, who should undergo screening, and how is Barrett’s treated. Most importantly, who is at most risk for developing esophageal cancer and what can we do to prevent that from happening.

A brief history on Norman Rupert Barrett…

Barrett’s esophagus is a condition named for the late Norman Rupert Barrett, an influential esophageal surgeon who was born in Adelaide, Australia in 1903. Barrett worked for most of his career as a consultant surgeon at St. Thomas’ Hospital in London. He was a pioneer in the field of thoracic surgery and a charismatic academic leader who served for more than 25 years as editor of Thorax. By all accounts, Norman Barrett was an outstanding surgeon, scholar, and teacher. However, Norman Barrett was not the first to describe the condition that now bears his name; in fact, his original contentions about the nature and pathogenesis of the condition were incorrect.

Credit for describing the columnar-lined esophagus probably should go to Wilder Tileston, a pathologist who, while working in Boston in 1906, described 3 cases of “peptic ulcer of the oesophagus,” and noted “the close resemblance of the mucous membrane about the ulcer to that normally found in the stomach.” Tileston wrote that “the first requisite for the formation of the peptic ulcer of the esophagus is an insufficiency of the cardia” (i.e. gastroesophageal reflux). Thus, almost a half-century before Barrett, Tileston described the columnar-lined esophagus and correctly attributed the pathogenesis of the associated ulceration to gastroesophageal refluxReference: Gastroenterology. 2010 Mar; 138(3): 854–869

What causes Barrett’s esophagus?

Barrett’s is caused by injury to the esophageal lining due to acid, bile, and other stomach contents that have refluxed into the esophagus. The lining of the lower esophagus bears the brunt of this injury and not surprisingly, this is where Barrett’s esophagus get started. It is believed that several years of uncontrolled acid reflux causes small mutations in cell DNA. Over time, these DNA mutations lead to the formation of Barrett’s esophagus and in some cases, esophageal cancer.

Who Gets Barrett’s esophagus?

Barrett’s esophagus is a silent disease, there are no warning signs. The individual most likely to acquire this condition is anyone with a long history of heartburn.

High risk groups include:Heartburn Article - Dr William Lyday at Gastroenterology Atlanta GI Specialist in Heartburn, IBS, Colonoscopy, Cancer Prevention & Wellness, Nutrition, Optifast & Weight Loss Balloon

  • Males over 50
  • Caucasians
  • Tobacco use
  • Nocturnal reflux symptoms
  • Obese
  • Elevated body mass index
  • Patients with an intra-abdominal distribution of body fat
  • Hiatal hernia
  • Barrett’s esophagus appears to be uncommon in African Americans.
  • Data on the prevalence in Hispanics are contradictory.
  • Barrett’s esophagus is also prevalent in Asian countries.
  • Individuals with family history of esophageal cancer, Barrett’s or GERD. Some studies have suggested that patients with a peptic stricture have a higher prevalence of Barrett’s esophagus than those without strictures. This relationship is not surprising since both peptic stricture and Barrett’s esophagus are associated with more severe GERD.

How is it detected?

Barrett’s esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years [1]. Although Barrett’s esophagus can affect children, it rarely occurs before the age of five [2]. This observation supports the contention that Barrett’s esophagus is an acquired condition, not a congenital one.

Barrett’s can be detected using a lighted fiber optic scope to directly view the esophageal lining. Barrett’s can be seen easily as an area of salmon colored mucosa rather than the usual light pink coloration. Biopsies of the esophageal lining can confirm the presence of Barrett’s. These biopsies, taken at the time of endoscopy reveal that the esophageal lining has developed an unusual cell shape – rather than the normal squamous cell which is flat, the cell has become tall and columnar with evidence of mucus production. A special stain called Alcian blue is useful for detecting the presence of this mucus,  also called goblet cells. Barrett’s is also called intestinal metaplasia. This is a laboratory term used to describe an occurrence when cells transform to a new shape.

Studies on Barrett’s…

Estimates of the prevalence of Barrett’s esophagus in the general population have varied widely ranging from 0.4 to more than 20 percent depending in part upon the population studied and the definitions used [3-7]. The male to female ratio is approximately 2:1 [8]. The following studies illustrate the range of findings:

  • A study from Sweden estimated that Barrett’s esophagus was present in 1.6 percent of the general population [9]. Applying these prevalence estimates to the United States would translate into about 3.3 million individuals with Barrett’s esophagus [10].
  • 44 percent of patients lacked “troublesome heartburn and/or acid regurgitation during the past three months,” suggesting that screening programs based upon reflux symptoms alone may be inadequate to identify patients with Barrett’s esophagus.
  • In a study conducted in the United States, the prevalence of Barrett’s esophagus was 6.8 percent among 961 patients undergoing a colonoscopy [11].
  • Among 556 patients who had never had heartburn, the prevalence was 5.6 percent.
  • Among 384 subjects with a history of heartburn, the prevalence was 8.3 percent.
  • Most cases were “short-segment.”
  • Long-segment Barrett’s was especially uncommon in those without a history of heartburn.
  • Among patients who have endoscopic examinations because of chronic GERD symptoms, long-segment Barrett’s esophagus can be found in 3 to 5 percent.
  • Whereas 10 to 15 percent have short-segment Barrett’s esophagus.
  • In a meta-analysis of 51 studies that included 453,157 individuals, the pooled prevalence of histologically confirmed Barrett’s esophagus was 1.3 percent, of which 82 percent was short-segment Barrett’s esophagus [17].
  • Obesity is a risk factor for gastroesophageal reflux disease (GERD) and may be a risk factor for Barrett’s esophagus [18,19]. A 2009 meta-analysis that included 11 observational studies demonstrated a small increase in the risk of Barrett’s esophagus in patients with a body mass index (BMI) >30 kg/m2 as compared with patients with a BMI <30 kg/m2 (OR 1.4, 95% CI 1.1-1.6) [18]. However, other studies have suggested that rather than BMI, abdominal obesity as measured by a high waist to hip ratio (≥0.9 in males and ≥0.85 in females) is associated with an increase in risk of Barrett’s esophagus [19-22].
  • A study of 40 patients who had subtotal esophagectomy with esophagogastrostomy, an operation frequently complicated by severe reflux esophagitis in the esophageal remnant, supports the notion that cardiac-type epithelium is metaplastic [45]. Endoscopic examinations performed at a median of 36 months postoperatively showed that 19 of the 40 patients had developed columnar metaplasia in the esophageal remnant (10 cardiac-type epithelium, 9 intestinal metaplasia).
  • Seven patients who had serial endoscopic examinations showed progression from cardiac-type epithelium on the initial postoperative endoscopy to specialized intestinal metaplasia on subsequent studies. The median time to the development of cardiac-type epithelium was 14 months, whereas specialized intestinal metaplasia was found at a median of 27 months postoperatively. These findings suggest that cardiac epithelium is not only metaplastic, but also the precursor of intestinal metaplasia in the esophagus.

Differences between long- and short-segment Barrett’s

As discussed above, the prevalence of short-segment Barrett’s esophagus is substantially higher than long-segment Barrett’s esophagus. Both conditions are diagnosed most frequently in patients age 55 years and older, and are predominantly seen in male Caucasians.

Studies have shown that patients with long and short-segment Barrett’s were predominantly male and white. Patients with short-segment Barrett’s had a shorter history of heartburn and many had no GERD symptoms at all. In contrast, those with intestinal metaplasia of the GEJ had a similar gender distribution and were more likely to be infected by Helicobacter pylori.

The degree and mechanism of acid exposure in patients with short- and long-segment Barrett’s esophagus suggest that patients who develop long-segment Barrett’s were predisposed to more severe reflux [48]:

Patients with long-segment Barrett’s tend to have:

  • Upright and supine reflux in contrast to those with short-segment Barrett’s who have predominantly upright reflux.
  • Proximal esophageal acid exposure is more common in patients with long-segment Barrett’s.
  • The risk of adenocarcinoma has been estimated to be 2 to 15 times higher in patients with long-segment Barrett’s.

Patients with short-segment Barrett’s tend to have:

  • Higher LES pressures
  • Higher distal esophageal peristaltic amplitudes
  • A lower incidence of dysplasia since less mucosa is involved [3,49,50].

Heartburn Article - Dr William Lyday at Gastroenterology Atlanta GI Specialist in Heartburn, IBS, Colonoscopy, Cancer Prevention & Wellness, Nutrition, Optifast & Weight Loss Balloon

Endoscopic Screenings Showing the Findings of Barrett’s Esophagus

The Importance of Screening Patients with GERD

More than 40 percent of patients with esophageal adenocarcinoma have no history of heartburn [54,56]. Thus, any screening program that targets only patients with heartburn can have only limited impact on cancer mortality rates and there is little evidence that these programs have prevented deaths from esophageal adenocarcinoma. In published series of patients found to have these tumors, fewer than 5 percent were known to have had Barrett’s esophagus before they presented with symptoms of esophageal cancer [57].

The impact of the incidence of esophageal adenocarcinoma on screening was evaluated using a Markov model based upon age- and sex-specific incidences of esophageal adenocarcinoma in American non-Hispanic whites with GERD symptoms [55]. The study noted that the overall incidence of esophageal adenocarcinoma is low, but increases with age:

  • For men between the ages of 30 and 80 years, the incidence ranged from 0.1 to 15.4/100,000 for those without GERD or with GERD less than once per week, and from 0.4 to 75.9/100,000 for those with GERD at least once per week.
  • For women between the ages of 30 and 80 years, the rates were lower, ranging from 0 to 2.3/100,000 for those without GERD or with GERD less than once per week, and from 0 to 11.2/100,000 for those with GERD at least once per week.
  • The incidence of esophageal adenocarcinoma for men without GERD was higher than the incidence for women with GERD at any given age (eg, at age 60 years the incidence in men without GERD was 7.0/100,000 and the incidence in women with GERD was 3.9/100,000).

In Summary

Barrett’s esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years. The specialized intestinal columnar metaplasia typical of Barrett’s esophagus causes no symptoms. Most patients are seen initially for symptoms of associated gastroesophageal reflux disease (GERD), such as heartburn, regurgitation, and dysphagia.

Two criteria must be fulfilled to make a diagnosis of Barrett’s esophagus:

  • The endoscopist must document that columnar epithelium lines the distal esophagus.
  • Histologic examination of biopsy specimens from that columnar epithelium must reveal specialized intestinal metaplasia. Some data suggests that gastric cardiac-type epithelium in the esophagus also might predispose to cancer and thus might be considered “Barrett’s esophagus,” but most authorities still require the presence of specialized intestinal metaplasia for an unequivocal diagnosis.
If you have any questions about Barrett’s esophagus or a concerned that you may be experiencing some the of the symptoms discussed in this article. Call our office at 404-257-0000 or click here to schedule your virtual appointment or office visit.

REFERENCES

    1. Spechler SJ. Barrett’s esophagus. Semin Gastrointest Dis 1996; 7:51.
    2. Hassall E. Columnar-lined esophagus in children. Gastroenterol Clin North Am 1997; 26:533.
    3. Hirota WK, Loughney TM, Lazas DJ, et al. Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophagogastric junction: prevalence and clinical data. Gastroenterology 1999; 116:277.
    4. Cameron AJ, Zinsmeister AR, Ballard DJ, Carney JA. Prevalence of columnar-lined (Barrett’s) esophagus. Comparison of population-based clinical and autopsy findings. Gastroenterology 1990; 99:918.
    5. Ormsby AH, Kilgore SP, Goldblum JR, et al. The location and frequency of intestinal metaplasia at the esophagogastric junction in 223 consecutive autopsies: implications for patient treatment and preventive strategies in Barrett’s esophagus. Mod Pathol 2000; 13:614.
    6. Gerson LB, Shetler K, Triadafilopoulos G. Prevalence of Barrett’s esophagus in asymptomatic individuals. Gastroenterology 2002; 123:461.
    7. Ward EM, Wolfsen HC, Achem SR, et al. Barrett’s esophagus is common in older men and women undergoing screening colonoscopy regardless of reflux symptoms. Am J Gastroenterol 2006; 101:12.
    8. Cook MB, Wild CP, Forman D. A systematic review and meta-analysis of the sex ratio for Barrett’s esophagus, erosive reflux disease, and nonerosive reflux disease. Am J Epidemiol 2005; 162:1050.
    9. Ronkainen J, Aro P, Storskrubb T, et al. Prevalence of Barrett’s esophagus in the general population: an endoscopic study. Gastroenterology 2005; 129:1825.
    10. Sampliner RE. A population prevalence of Barrett’s esophagus–finally. Gastroenterology 2005; 129:2101.
    11. Rex DK, Cummings OW, Shaw M, et al. Screening for Barrett’s esophagus in colonoscopy patients with and without heartburn. Gastroenterology 2003; 125:1670.
    12. Winters C Jr, Spurling TJ, Chobanian SJ, et al. Barrett’s esophagus. A prevalent, occult complication of gastroesophageal reflux disease. Gastroenterology 1987; 92:118.
    13. Spechler SJ. Clinical practice. Barrett’s Esophagus. N Engl J Med 2002; 346:836.
    14. Bersentes K, Fass R, Padda S, et al. Prevalence of Barrett’s esophagus in Hispanics is similar to Caucasians. Dig Dis Sci 1998; 43:1038.
    15. Abrams JA, Fields S, Lightdale CJ, Neugut AI. Racial and ethnic disparities in the prevalence of Barrett’s esophagus among patients who undergo upper endoscopy. Clin Gastroenterol Hepatol 2008; 6:30.
    16. Corley DA, Kubo A, Levin TR, et al. Race, ethnicity, sex and temporal differences in Barrett’s oesophagus diagnosis: a large community-based study, 1994-2006. Gut 2009; 58:182.
    17. Shiota S, Singh S, Anshasi A, El-Serag HB. Prevalence of Barrett’s Esophagus in Asian Countries: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol 2015; 13:1907.
    18. Kamat P, Wen S, Morris J, Anandasabapathy S. Exploring the association between elevated body mass index and Barrett’s esophagus: a systematic review and meta-analysis. Ann Thorac Surg 2009; 87:655.
    19. Jacobson BC, Chan AT, Giovannucci EL, Fuchs CS. Body mass index and Barrett’s oesophagus in women. Gut 2009; 58:1460.
    20. Corley DA, Kubo A, Levin TR, et al. Abdominal obesity and body mass index as risk factors for Barrett’s esophagus. Gastroenterology 2007; 133:34.
    21. Edelstein ZR, Farrow DC, Bronner MP, et al. Central adiposity and risk of Barrett’s esophagus. Gastroenterology 2007; 133:403.
    22. Kramer JR, Fischbach LA, Richardson P, et al. Waist-to-hip ratio, but not body mass index, is associated with an increased risk of Barrett’s esophagus in white men. Clin Gastroenterol Hepatol 2013; 11:373.
    23. Omer ZB, Ananthakrishnan AN, Nattinger KJ, et al. Aspirin protects against Barrett’s esophagus in a multivariate logistic regression analysis. Clin Gastroenterol Hepatol 2012; 10:722.
    24. Thrift AP, Pandeya N, Smith KJ, et al. The use of nonsteroidal anti-inflammatory drugs and the risk of Barrett’s oesophagus. Aliment Pharmacol Ther 2011; 34:1235.
    25. Khalaf N, Nguyen T, Ramsey D, El-Serag HB. Nonsteroidal anti-inflammatory drugs and the risk of Barrett’s esophagus. Clin Gastroenterol Hepatol 2014; 12:1832.
    26. Chak A, Lee T, Kinnard MF, et al. Familial aggregation of Barrett’s oesophagus, oesophageal adenocarcinoma, and oesophagogastric junctional adenocarcinoma in Caucasian adults. Gut 2002; 51:323.
    27. Verbeek RE, Spittuler LF, Peute A, et al. Familial clustering of Barrett’s esophagus and esophageal adenocarcinoma in a European cohort. Clin Gastroenterol Hepatol 2014; 12:1656.
    28. Orloff M, Peterson C, He X, et al. Germline mutations in MSR1, ASCC1, and CTHRC1 in patients with Barrett esophagus and esophageal adenocarcinoma. JAMA 2011; 306:410.
    29. Eloubeidi MA, Provenzale D. Does this patient have Barrett’s esophagus? The utility of predicting Barrett’s esophagus at the index endoscopy. Am J Gastroenterol 1999; 94:937.
    30. Kim SL, Waring JP, Spechler SJ, et al. Diagnostic inconsistencies in Barrett’s esophagus. Department of Veterans Affairs Gastroesophageal Reflux Study Group. Gastroenterology 1994; 107:945.
    31. Ronkainen J, Talley NJ, Storskrubb T, et al. Erosive esophagitis is a risk factor for Barrett’s esophagus: a community-based endoscopic follow-up study. Am J Gastroenterol 2011; 106:1946.
    32. Kim SL, Wo JM, Hunter JG, et al. The prevalence of intestinal metaplasia in patients with and without peptic strictures. Am J Gastroenterol 1998; 93:53.
    33. Riddell RH, Odze RD. Definition of Barrett’s esophagus: time for a rethink–is intestinal metaplasia dead? Am J Gastroenterol 2009; 104:2588.
    34. American Gastroenterological Association, Spechler SJ, Sharma P, et al. American Gastroenterological Association medical position statement on the management of Barrett’s esophagus. Gastroenterology 2011; 140:1084.
    35. Spechler SJ. The role of gastric carditis in metaplasia and neoplasia at the gastroesophageal junction. Gastroenterology 1999; 117:218.
    36. Sharma P, Morales TG, Sampliner RE. Short segment Barrett’s esophagus–the need for standardization of the definition and of endoscopic criteria. Am J Gastroenterol 1998; 93:1033.
    37. Spechler SJ. Intestinal metaplasia at the gastroesophageal junction. Gastroenterology 2004; 126:567.
  1. Fawcett DW. The esophagus and stomach. In: A Textbook of Histology, 11th ed, Bloom W, Fawcett DW (Eds), Saunders Company, Philadelphia 1986. p.619.
  2. Amano Y, Ishimura N, Furuta K, et al. Which landmark results in a more consistent diagnosis of Barrett’s esophagus, the gastric folds or the palisade vessels? Gastrointest Endosc 2006; 64:206.
  3. Sharma P, Dent J, Armstrong D, et al. The development and validation of an endoscopic grading system for Barrett’s esophagus: the Prague C & M criteria. Gastroenterology 2006; 131:1392.
  4. Alvarez Herrero L, Curvers WL, van Vilsteren FG, et al. Validation of the Prague C&M classification of Barrett’s esophagus in clinical practice. Endoscopy 2013; 45:876.
  5. HAYWARD J. The lower end of the oesophagus. Thorax 1961; 16:36.
  6. Chandrasoma P. Pathophysiology of Barrett’s esophagus. Semin Thorac Cardiovasc Surg 1997; 9:270.
  7. Oberg S, Peters JH, DeMeester TR, et al. Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg 1997; 226:522.
  8. Dresner SM, Griffin SM, Wayman J, et al. Human model of duodenogastro-oesophageal reflux in the development of Barrett’s metaplasia. Br J Surg 2003; 90:1120.
  9. Sharma P, Weston AP, Morales T, et al. Relative risk of dysplasia for patients with intestinal metaplasia in the distal oesophagus and in the gastric cardia. Gut 2000; 46:9.
  10. Jung KW, Talley NJ, Romero Y, et al. Epidemiology and natural history of intestinal metaplasia of the gastroesophageal junction and Barrett’s esophagus: a population-based study. Am J Gastroenterol 2011; 106:1447.
  11. 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.
  12. Sharma P, Morales TG, Bhattacharyya A, et al. Dysplasia in short-segment Barrett’s esophagus: a prospective 3-year follow-up. Am J Gastroenterol 1997; 92:2012.
  13. Weston AP, Krmpotich PT, Cherian R, et al. 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.
  14. Rudolph RE, Vaughan TL, Storer BE, et al. Effect of segment length on risk for neoplastic progression in patients with Barrett esophagus. Ann Intern Med 2000; 132:612.
  15. Inadomi JM, Sampliner R, Lagergren J, et al. Screening and surveillance for Barrett esophagus in high-risk groups: a cost-utility analysis. Ann Intern Med 2003; 138:176.
  16. DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol 1999; 94:1434.
  17. Rubenstein JH, Taylor JB. Meta-analysis: the association of oesophageal adenocarcinoma with symptoms of gastro-oesophageal reflux. Aliment Pharmacol Ther 2010; 32:1222.
  18. Rubenstein JH, Scheiman JM, Sadeghi S, et al. Esophageal adenocarcinoma incidence in individuals with gastroesophageal reflux: synthesis and estimates from population studies. Am J Gastroenterol 2011; 106:254.
  19. Lagergren J, Bergström R, Lindgren A, Nyrén O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999; 340:825.
  20. Dulai GS, Guha S, Kahn KL, et al. Preoperative prevalence of Barrett’s esophagus in esophageal adenocarcinoma: a systematic review. Gastroenterology 2002; 122:26.
  21. Shaheen NJ, Dulai GS, Ascher B, et al. Effect of a new diagnosis of Barrett’s esophagus on insurance status. Am J Gastroenterol 2005; 100:577.
  22. Shaheen NJ, Weinberg DS, Denberg TD, et al. Upper endoscopy for gastroesophageal reflux disease: best practice advice from the clinical guidelines committee of the American College of Physicians. Ann Intern Med 2012; 157:808.
  23. ASGE Standards of Practice Committee, Evans JA, Early DS, et al. The role of endoscopy in Barrett’s esophagus and other premalignant conditions of the esophagus. Gastrointest Endosc 2012; 76:1087.
  24. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol 2013; 108:308.
  25. Kadri SR, Lao-Sirieix P, O’Donovan M, et al. Acceptability and accuracy of a non-endoscopic screening test for Barrett’s oesophagus in primary care: cohort study. BMJ 2010; 341:c4372.

Barrett’s Esophagus

An Article by Dr. William D. Lyday

Barrett’s esophagus is a common condition affecting the esophagus and its management remains controversial in the medical community. Barrett’s is considered a pre-cancer and clearly elevates the risk of esophageal adenocarcinoma in carriers of this condition. In this post, we will attempt to summarize the risk factors associated with Barrett’s esophagus, who should undergo screening, and how is Barrett’s treated. Most importantly, who is at most risk for developing esophageal cancer and what can we do to prevent that from happening.

A brief history on Norman Rupert Barrett…

Barrett’s esophagus is a condition named for the late Norman Rupert Barrett, an influential esophageal surgeon who was born in Adelaide, Australia in 1903. Barrett worked for most of his career as a consultant surgeon at St. Thomas’ Hospital in London. He was a pioneer in the field of thoracic surgery and a charismatic academic leader who served for more than 25 years as editor of Thorax. By all accounts, Norman Barrett was an outstanding surgeon, scholar, and teacher. However, Norman Barrett was not the first to describe the condition that now bears his name; in fact, his original contentions about the nature and pathogenesis of the condition were incorrect.

Credit for describing the columnar-lined esophagus probably should go to Wilder Tileston, a pathologist who, while working in Boston in 1906, described 3 cases of “peptic ulcer of the oesophagus,” and noted “the close resemblance of the mucous membrane about the ulcer to that normally found in the stomach.” Tileston wrote that “the first requisite for the formation of the peptic ulcer of the esophagus is an insufficiency of the cardia” (i.e. gastroesophageal reflux). Thus, almost a half-century before Barrett, Tileston described the columnar-lined esophagus and correctly attributed the pathogenesis of the associated ulceration to gastroesophageal refluxReference: Gastroenterology. 2010 Mar; 138(3): 854–869

What causes Barrett’s esophagus?

Barrett’s is caused by injury to the esophageal lining due to acid, bile, and other stomach contents that have refluxed into the esophagus. The lining of the lower esophagus bears the brunt of this injury and not surprisingly, this is where Barrett’s esophagus get started. It is believed that several years of uncontrolled acid reflux causes small mutations in cell DNA. Over time, these DNA mutations lead to the formation of Barrett’s esophagus and in some cases, esophageal cancer.

Who Gets Barrett’s esophagus?

Barrett’s esophagus is a silent disease, there are no warning signs. The individual most likely to acquire this condition is anyone with a long history of heartburn.

High risk groups include:

  • Males over 50
  • Caucasians
  • Tobacco use
  • Nocturnal reflux symptoms
  • Obese
  • Elevated body mass index
  • Patients with an intra-abdominal distribution of body fat
  • Hiatal hernia
  • Barrett’s esophagus appears to be uncommon in African Americans.
  • Data on the prevalence in Hispanics are contradictory.
  • Barrett’s esophagus is also prevalent in Asian countries.
  • Individuals with family history of esophageal cancer, Barrett’s or GERD. Some studies have suggested that patients with a peptic stricture have a higher prevalence of Barrett’s esophagus than those without strictures. This relationship is not surprising since both peptic stricture and Barrett’s esophagus are associated with more severe GERD.

Heartburn Article - Dr William Lyday at Gastroenterology Atlanta GI Specialist in Heartburn, IBS, Colonoscopy, Cancer Prevention & Wellness, Nutrition, Optifast & Weight Loss Balloon

How is it detected?

Barrett’s esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years [1]. Although Barrett’s esophagus can affect children, it rarely occurs before the age of five [2]. This observation supports the contention that Barrett’s esophagus is an acquired condition, not a congenital one.

Barrett’s can be detected using a lighted fiber optic scope to directly view the esophageal lining. Barrett’s can be seen easily as an area of salmon colored mucosa rather than the usual light pink coloration. Biopsies of the esophageal lining can confirm the presence of Barrett’s. These biopsies, taken at the time of endoscopy reveal that the esophageal lining has developed an unusual cell shape – rather than the normal squamous cell which is flat, the cell has become tall and columnar with evidence of mucus production. A special stain called Alcian blue is useful for detecting the presence of this mucus,  also called goblet cells. Barrett’s is also called intestinal metaplasia. This is a laboratory term used to describe an occurrence when cells transform to a new shape.

Studies on Barrett’s…

Estimates of the prevalence of Barrett’s esophagus in the general population have varied widely ranging from 0.4 to more than 20 percent depending in part upon the population studied and the definitions used [3-7]. The male to female ratio is approximately 2:1 [8]. The following studies illustrate the range of findings:

  • A study from Sweden estimated that Barrett’s esophagus was present in 1.6 percent of the general population [9]. Applying these prevalence estimates to the United States would translate into about 3.3 million individuals with Barrett’s esophagus [10].
  • 44 percent of patients lacked “troublesome heartburn and/or acid regurgitation during the past three months,” suggesting that screening programs based upon reflux symptoms alone may be inadequate to identify patients with Barrett’s esophagus.
  • In a study conducted in the United States, the prevalence of Barrett’s esophagus was 6.8 percent among 961 patients undergoing a colonoscopy [11].
  • Among 556 patients who had never had heartburn, the prevalence was 5.6 percent.
  • Among 384 subjects with a history of heartburn, the prevalence was 8.3 percent.
  • Most cases were “short-segment.”
  • Long-segment Barrett’s was especially uncommon in those without a history of heartburn.
  • Among patients who have endoscopic examinations because of chronic GERD symptoms, long-segment Barrett’s esophagus can be found in 3 to 5 percent.
  • Whereas 10 to 15 percent have short-segment Barrett’s esophagus.
  • In a meta-analysis of 51 studies that included 453,157 individuals, the pooled prevalence of histologically confirmed Barrett’s esophagus was 1.3 percent, of which 82 percent was short-segment Barrett’s esophagus [17].
  • Obesity is a risk factor for gastroesophageal reflux disease (GERD) and may be a risk factor for Barrett’s esophagus [18,19]. A 2009 meta-analysis that included 11 observational studies demonstrated a small increase in the risk of Barrett’s esophagus in patients with a body mass index (BMI) >30 kg/m2 as compared with patients with a BMI <30 kg/m2 (OR 1.4, 95% CI 1.1-1.6) [18]. However, other studies have suggested that rather than BMI, abdominal obesity as measured by a high waist to hip ratio (≥0.9 in males and ≥0.85 in females) is associated with an increase in risk of Barrett’s esophagus [19-22].
  • A study of 40 patients who had subtotal esophagectomy with esophagogastrostomy, an operation frequently complicated by severe reflux esophagitis in the esophageal remnant, supports the notion that cardiac-type epithelium is metaplastic [45]. Endoscopic examinations performed at a median of 36 months postoperatively showed that 19 of the 40 patients had developed columnar metaplasia in the esophageal remnant (10 cardiac-type epithelium, 9 intestinal metaplasia).
  • Seven patients who had serial endoscopic examinations showed progression from cardiac-type epithelium on the initial postoperative endoscopy to specialized intestinal metaplasia on subsequent studies. The median time to the development of cardiac-type epithelium was 14 months, whereas specialized intestinal metaplasia was found at a median of 27 months postoperatively. These findings suggest that cardiac epithelium is not only metaplastic, but also the precursor of intestinal metaplasia in the esophagus.

Differences between long- and short-segment Barrett’s

As discussed above, the prevalence of short-segment Barrett’s esophagus is substantially higher than long-segment Barrett’s esophagus. Both conditions are diagnosed most frequently in patients age 55 years and older, and are predominantly seen in male Caucasians.

Studies have shown that patients with long and short-segment Barrett’s were predominantly male and white. Patients with short-segment Barrett’s had a shorter history of heartburn and many had no GERD symptoms at all. In contrast, those with intestinal metaplasia of the GEJ had a similar gender distribution and were more likely to be infected by Helicobacter pylori.

The degree and mechanism of acid exposure in patients with short- and long-segment Barrett’s esophagus suggest that patients who develop long-segment Barrett’s were predisposed to more severe reflux [48]:

Patients with long-segment Barrett’s tend to have:

  • Upright and supine reflux in contrast to those with short-segment Barrett’s who have predominantly upright reflux.
  • Proximal esophageal acid exposure is more common in patients with long-segment Barrett’s.
  • The risk of adenocarcinoma has been estimated to be 2 to 15 times higher in patients with long-segment Barrett’s.

Patients with short-segment Barrett’s tend to have:

  • Higher LES pressures
  • Higher distal esophageal peristaltic amplitudes
  • A lower incidence of dysplasia since less mucosa is involved [3,49,50].

Heartburn Article - Dr William Lyday at Gastroenterology Atlanta GI Specialist in Heartburn, IBS, Colonoscopy, Cancer Prevention & Wellness, Nutrition, Optifast & Weight Loss Balloon

Endoscopic Screenings Showing the Findings of Barrett’s Esophagus

The Importance of Screening Patients with GERD

More than 40 percent of patients with esophageal adenocarcinoma have no history of heartburn [54,56]. Thus, any screening program that targets only patients with heartburn can have only limited impact on cancer mortality rates and there is little evidence that these programs have prevented deaths from esophageal adenocarcinoma. In published series of patients found to have these tumors, fewer than 5 percent were known to have had Barrett’s esophagus before they presented with symptoms of esophageal cancer [57].

The impact of the incidence of esophageal adenocarcinoma on screening was evaluated using a Markov model based upon age- and sex-specific incidences of esophageal adenocarcinoma in American non-Hispanic whites with GERD symptoms [55]. The study noted that the overall incidence of esophageal adenocarcinoma is low, but increases with age:

  • For men between the ages of 30 and 80 years, the incidence ranged from 0.1 to 15.4/100,000 for those without GERD or with GERD less than once per week, and from 0.4 to 75.9/100,000 for those with GERD at least once per week.
  • For women between the ages of 30 and 80 years, the rates were lower, ranging from 0 to 2.3/100,000 for those without GERD or with GERD less than once per week, and from 0 to 11.2/100,000 for those with GERD at least once per week.
  • The incidence of esophageal adenocarcinoma for men without GERD was higher than the incidence for women with GERD at any given age (eg, at age 60 years the incidence in men without GERD was 7.0/100,000 and the incidence in women with GERD was 3.9/100,000).

In Summary

Barrett’s esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years. The specialized intestinal columnar metaplasia typical of Barrett’s esophagus causes no symptoms. Most patients are seen initially for symptoms of associated gastroesophageal reflux disease (GERD), such as heartburn, regurgitation, and dysphagia.

Two criteria must be fulfilled to make a diagnosis of Barrett’s esophagus:

  • The endoscopist must document that columnar epithelium lines the distal esophagus.
  • Histologic examination of biopsy specimens from that columnar epithelium must reveal specialized intestinal metaplasia. Some data suggests that gastric cardiac-type epithelium in the esophagus also might predispose to cancer and thus might be considered “Barrett’s esophagus,” but most authorities still require the presence of specialized intestinal metaplasia for an unequivocal diagnosis.
If you have any questions about Barrett’s esophagus or a concerned that you may be experiencing some the of the symptoms discussed in this article. Call our office at 404-257-0000 or click here to schedule your virtual appointment or office visit.

REFERENCES

    1. Spechler SJ. Barrett’s esophagus. Semin Gastrointest Dis 1996; 7:51.
    2. Hassall E. Columnar-lined esophagus in children. Gastroenterol Clin North Am 1997; 26:533.
    3. Hirota WK, Loughney TM, Lazas DJ, et al. Specialized intestinal metaplasia, dysplasia, and cancer of the esophagus and esophagogastric junction: prevalence and clinical data. Gastroenterology 1999; 116:277.
    4. Cameron AJ, Zinsmeister AR, Ballard DJ, Carney JA. Prevalence of columnar-lined (Barrett’s) esophagus. Comparison of population-based clinical and autopsy findings. Gastroenterology 1990; 99:918.
    5. Ormsby AH, Kilgore SP, Goldblum JR, et al. The location and frequency of intestinal metaplasia at the esophagogastric junction in 223 consecutive autopsies: implications for patient treatment and preventive strategies in Barrett’s esophagus. Mod Pathol 2000; 13:614.
    6. Gerson LB, Shetler K, Triadafilopoulos G. Prevalence of Barrett’s esophagus in asymptomatic individuals. Gastroenterology 2002; 123:461.
    7. Ward EM, Wolfsen HC, Achem SR, et al. Barrett’s esophagus is common in older men and women undergoing screening colonoscopy regardless of reflux symptoms. Am J Gastroenterol 2006; 101:12.
    8. Cook MB, Wild CP, Forman D. A systematic review and meta-analysis of the sex ratio for Barrett’s esophagus, erosive reflux disease, and nonerosive reflux disease. Am J Epidemiol 2005; 162:1050.
    9. Ronkainen J, Aro P, Storskrubb T, et al. Prevalence of Barrett’s esophagus in the general population: an endoscopic study. Gastroenterology 2005; 129:1825.
    10. Sampliner RE. A population prevalence of Barrett’s esophagus–finally. Gastroenterology 2005; 129:2101.
    11. Rex DK, Cummings OW, Shaw M, et al. Screening for Barrett’s esophagus in colonoscopy patients with and without heartburn. Gastroenterology 2003; 125:1670.
    12. Winters C Jr, Spurling TJ, Chobanian SJ, et al. Barrett’s esophagus. A prevalent, occult complication of gastroesophageal reflux disease. Gastroenterology 1987; 92:118.
    13. Spechler SJ. Clinical practice. Barrett’s Esophagus. N Engl J Med 2002; 346:836.
    14. Bersentes K, Fass R, Padda S, et al. Prevalence of Barrett’s esophagus in Hispanics is similar to Caucasians. Dig Dis Sci 1998; 43:1038.
    15. Abrams JA, Fields S, Lightdale CJ, Neugut AI. Racial and ethnic disparities in the prevalence of Barrett’s esophagus among patients who undergo upper endoscopy. Clin Gastroenterol Hepatol 2008; 6:30.
    16. Corley DA, Kubo A, Levin TR, et al. Race, ethnicity, sex and temporal differences in Barrett’s oesophagus diagnosis: a large community-based study, 1994-2006. Gut 2009; 58:182.
    17. Shiota S, Singh S, Anshasi A, El-Serag HB. Prevalence of Barrett’s Esophagus in Asian Countries: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol 2015; 13:1907.
    18. Kamat P, Wen S, Morris J, Anandasabapathy S. Exploring the association between elevated body mass index and Barrett’s esophagus: a systematic review and meta-analysis. Ann Thorac Surg 2009; 87:655.
    19. Jacobson BC, Chan AT, Giovannucci EL, Fuchs CS. Body mass index and Barrett’s oesophagus in women. Gut 2009; 58:1460.
    20. Corley DA, Kubo A, Levin TR, et al. Abdominal obesity and body mass index as risk factors for Barrett’s esophagus. Gastroenterology 2007; 133:34.
    21. Edelstein ZR, Farrow DC, Bronner MP, et al. Central adiposity and risk of Barrett’s esophagus. Gastroenterology 2007; 133:403.
    22. Kramer JR, Fischbach LA, Richardson P, et al. Waist-to-hip ratio, but not body mass index, is associated with an increased risk of Barrett’s esophagus in white men. Clin Gastroenterol Hepatol 2013; 11:373.
    23. Omer ZB, Ananthakrishnan AN, Nattinger KJ, et al. Aspirin protects against Barrett’s esophagus in a multivariate logistic regression analysis. Clin Gastroenterol Hepatol 2012; 10:722.
    24. Thrift AP, Pandeya N, Smith KJ, et al. The use of nonsteroidal anti-inflammatory drugs and the risk of Barrett’s oesophagus. Aliment Pharmacol Ther 2011; 34:1235.
    25. Khalaf N, Nguyen T, Ramsey D, El-Serag HB. Nonsteroidal anti-inflammatory drugs and the risk of Barrett’s esophagus. Clin Gastroenterol Hepatol 2014; 12:1832.
    26. Chak A, Lee T, Kinnard MF, et al. Familial aggregation of Barrett’s oesophagus, oesophageal adenocarcinoma, and oesophagogastric junctional adenocarcinoma in Caucasian adults. Gut 2002; 51:323.
    27. Verbeek RE, Spittuler LF, Peute A, et al. Familial clustering of Barrett’s esophagus and esophageal adenocarcinoma in a European cohort. Clin Gastroenterol Hepatol 2014; 12:1656.
    28. Orloff M, Peterson C, He X, et al. Germline mutations in MSR1, ASCC1, and CTHRC1 in patients with Barrett esophagus and esophageal adenocarcinoma. JAMA 2011; 306:410.
    29. Eloubeidi MA, Provenzale D. Does this patient have Barrett’s esophagus? The utility of predicting Barrett’s esophagus at the index endoscopy. Am J Gastroenterol 1999; 94:937.
    30. Kim SL, Waring JP, Spechler SJ, et al. Diagnostic inconsistencies in Barrett’s esophagus. Department of Veterans Affairs Gastroesophageal Reflux Study Group. Gastroenterology 1994; 107:945.
    31. Ronkainen J, Talley NJ, Storskrubb T, et al. Erosive esophagitis is a risk factor for Barrett’s esophagus: a community-based endoscopic follow-up study. Am J Gastroenterol 2011; 106:1946.
    32. Kim SL, Wo JM, Hunter JG, et al. The prevalence of intestinal metaplasia in patients with and without peptic strictures. Am J Gastroenterol 1998; 93:53.
    33. Riddell RH, Odze RD. Definition of Barrett’s esophagus: time for a rethink–is intestinal metaplasia dead? Am J Gastroenterol 2009; 104:2588.
    34. American Gastroenterological Association, Spechler SJ, Sharma P, et al. American Gastroenterological Association medical position statement on the management of Barrett’s esophagus. Gastroenterology 2011; 140:1084.
    35. Spechler SJ. The role of gastric carditis in metaplasia and neoplasia at the gastroesophageal junction. Gastroenterology 1999; 117:218.
    36. Sharma P, Morales TG, Sampliner RE. Short segment Barrett’s esophagus–the need for standardization of the definition and of endoscopic criteria. Am J Gastroenterol 1998; 93:1033.
    37. Spechler SJ. Intestinal metaplasia at the gastroesophageal junction. Gastroenterology 2004; 126:567.
  1. Fawcett DW. The esophagus and stomach. In: A Textbook of Histology, 11th ed, Bloom W, Fawcett DW (Eds), Saunders Company, Philadelphia 1986. p.619.
  2. Amano Y, Ishimura N, Furuta K, et al. Which landmark results in a more consistent diagnosis of Barrett’s esophagus, the gastric folds or the palisade vessels? Gastrointest Endosc 2006; 64:206.
  3. Sharma P, Dent J, Armstrong D, et al. The development and validation of an endoscopic grading system for Barrett’s esophagus: the Prague C & M criteria. Gastroenterology 2006; 131:1392.
  4. Alvarez Herrero L, Curvers WL, van Vilsteren FG, et al. Validation of the Prague C&M classification of Barrett’s esophagus in clinical practice. Endoscopy 2013; 45:876.
  5. HAYWARD J. The lower end of the oesophagus. Thorax 1961; 16:36.
  6. Chandrasoma P. Pathophysiology of Barrett’s esophagus. Semin Thorac Cardiovasc Surg 1997; 9:270.
  7. Oberg S, Peters JH, DeMeester TR, et al. Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg 1997; 226:522.
  8. Dresner SM, Griffin SM, Wayman J, et al. Human model of duodenogastro-oesophageal reflux in the development of Barrett’s metaplasia. Br J Surg 2003; 90:1120.
  9. Sharma P, Weston AP, Morales T, et al. Relative risk of dysplasia for patients with intestinal metaplasia in the distal oesophagus and in the gastric cardia. Gut 2000; 46:9.
  10. Jung KW, Talley NJ, Romero Y, et al. Epidemiology and natural history of intestinal metaplasia of the gastroesophageal junction and Barrett’s esophagus: a population-based study. Am J Gastroenterol 2011; 106:1447.
  11. 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.
  12. Sharma P, Morales TG, Bhattacharyya A, et al. Dysplasia in short-segment Barrett’s esophagus: a prospective 3-year follow-up. Am J Gastroenterol 1997; 92:2012.
  13. Weston AP, Krmpotich PT, Cherian R, et al. 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.
  14. Rudolph RE, Vaughan TL, Storer BE, et al. Effect of segment length on risk for neoplastic progression in patients with Barrett esophagus. Ann Intern Med 2000; 132:612.
  15. Inadomi JM, Sampliner R, Lagergren J, et al. Screening and surveillance for Barrett esophagus in high-risk groups: a cost-utility analysis. Ann Intern Med 2003; 138:176.
  16. DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol 1999; 94:1434.
  17. Rubenstein JH, Taylor JB. Meta-analysis: the association of oesophageal adenocarcinoma with symptoms of gastro-oesophageal reflux. Aliment Pharmacol Ther 2010; 32:1222.
  18. Rubenstein JH, Scheiman JM, Sadeghi S, et al. Esophageal adenocarcinoma incidence in individuals with gastroesophageal reflux: synthesis and estimates from population studies. Am J Gastroenterol 2011; 106:254.
  19. Lagergren J, Bergström R, Lindgren A, Nyrén O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999; 340:825.
  20. Dulai GS, Guha S, Kahn KL, et al. Preoperative prevalence of Barrett’s esophagus in esophageal adenocarcinoma: a systematic review. Gastroenterology 2002; 122:26.
  21. Shaheen NJ, Dulai GS, Ascher B, et al. Effect of a new diagnosis of Barrett’s esophagus on insurance status. Am J Gastroenterol 2005; 100:577.
  22. Shaheen NJ, Weinberg DS, Denberg TD, et al. Upper endoscopy for gastroesophageal reflux disease: best practice advice from the clinical guidelines committee of the American College of Physicians. Ann Intern Med 2012; 157:808.
  23. ASGE Standards of Practice Committee, Evans JA, Early DS, et al. The role of endoscopy in Barrett’s esophagus and other premalignant conditions of the esophagus. Gastrointest Endosc 2012; 76:1087.
  24. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol 2013; 108:308.
  25. Kadri SR, Lao-Sirieix P, O’Donovan M, et al. Acceptability and accuracy of a non-endoscopic screening test for Barrett’s oesophagus in primary care: cohort study. BMJ 2010; 341:c4372.
dr william lyday

Dr William D. Lyday, Gastroenterologist

Gastroenterology Atlanta
Our Specialty Services:

Heartburn – IBS – Weight Management Nutritional CounselingColonoscopy Cancer Screening – Genomic DNA Testing

Call us today to request an online virtual consultation or checkup with Dr. Lyday. We offer comprehensive medical evaluations from the comfort of your own home, including complete examinations, ordering of all tests, X-Rays & labs and prescriptions.

Call us at 404-257-0000 or click here to schedule your virtual appointment or office visit.

dr william lyday

Dr William D. Lyday, Gastroenterologist

Gastroenterology Atlanta

Our Specialty Services:

IBS Heartburn Colonoscopy Cancer Prevention Weight Management Nutritional Counseling Genomic DNA Testing

Call us today to request an online virtual consultation or checkup with Dr. Lyday. We offer comprehensive medical evaluations from the comfort of your own home, including complete examinations, ordering of all tests, X-Rays & labs and prescriptions.

Call us at 404-257-0000 or click here to schedule your virtual appointment or office visit.