Health Questions and Answers

BARRETT’S ESOPHAGUS

What is Barrett’s esophagus?
Barrett’s esophagus is a metaplastic change in the lining of the normally squamous-lined esophagus that is recognized at endoscopy. As a result of gastroesophageal reflux disease, the esophagus is lined with intestinal metaplasia, a premalignant epithelium.

How is Barrett’s esophagus diagnosed?

The ultimate criterion for histologic diagnosis is the presence of goblet cells. Currently, two techniques are necessary: endoscopy to recognize abnormal-appearing esophageal epithelium and biopsy to detect intestinal metaplasia.

Why is Barrett’s esophagus important?
It is a premalignant lesion for adenocarcinoma of the esophagus and presumably for a proportion of adenocarcinomas of the gastric cardia. The cancer continuing to have the most rapidly rising incidence in the United States and Western Europe over the past three decades has been adenocarcinoma of the esophagus in white men.

Does short-segment Barrett’s esophagus need to be identified?
Yes. Barrett’s esophagus ranges from short tongues of intestinal metaplasia in the distal esophagus to circumferential intestinal metaplasia of nearly the entire length of the esophagus. In the mid 1970s, before the recognition of the importance of intestinal metaplasia, Barrett’s esophagus was defined as a “columnar-lined esophagus” of at least 3 cm in length. However, it is now recognized that short-segment Barrett’s esophagus can develop dysplasia and adenocarcinoma and is more common than long-segment Barrett’s.

What is the risk of cancer associated with Barrett’s esophagus?
Recent prospective series have documented a lower risk for the development of cancer than former series. Rather than a 1-2% risk per year, the risk appears to be 0.4-0.5% per year. This difference may be due to the larger, prospective series with longer follow-up. This lower incidence has been documented in higher-risk patients-predominantly Caucasian men. However, the most important question for the individual patient is his or her specific risk. An evidence-based answer has not yet been developed.

Who should be screened for Barrett’s esophagus?
People at highest risk for the development of adenocarcinoma should be screened. Clues are available from the epidemiology of adenocarcinoma: older white men, patients with long-standing reflux symptoms, smokers, and the obese. Specific criteria to select individual patients have not been defined by prospective studies. In clinical practice, however, the movement has been toward the concept of once-in-a-lifetime endoscopy for patients with chronic gastroesophageal reflux to detect Barrett’s esophagus. Focusing on patients at highest risk of developing cancer would be more effective.

What is the therapy for Barrett’s esophagus?
Standard clinical therapy is pharmacologic (proton pump inhibitor) and surgical (laparoscopic fundoplication). Both techniques are highly effective in controlling reflux symptoms and healing erosive esophagitis. For younger patients who are noncompliant or do not wish to take daily medication, surgery is an option. For patients with prominent regurgitation, inadequately controlled with proton pump inhibitors, surgery should be considered. A higher failure rate for laparoscopic fundoplication has been recognized in patients with Barrett’s esophagus compared with non-Barrett’s reflux.

Goals of therapy for Barrett’s esophagus

  • Control reflux symptoms.
  • Heal erosive esophagitis.
  • Prevent adenocarcinoma.

Does Barrett’s esophagus reverse with medical therapy?
Rarely. In published series, which typically use high doses of proton pump inhibitors, Barrett’s esophagus was eliminated in only 2% of 151 patients. Even if esophageal acid exposure is nearly eliminated, the estimated decrease in the area of Barrett’s esophagus over an interval of 2 years is only 8%.

Does Barrett’s esophagus reverse with surgical therapy?
Rarely. Barrett’s esophagus has been eliminated in <4% of 449 patients having surgery in large series in the 1990s. If the elimination of all refluxate by successful fundoplication does not reverse Barrett’s esophagus and eliminate the risk of cancer, it is unlikely that medical therapy other than chemoprevention will do so.

What is the appropriate surveillance of patients with Barrett’s esophagus?
The database for developing guidelines for surveillance of this premalignant mucosa is limited, but gastroenterologists must deal with this issue in everyday practice. Surveillance intervals are based on the detection of dysplasia with the goal of early intervention to improve the survival rates associated with adenocarcinoma. The surveillance intervals have been increasing and will probably continue to do so with improved understanding of the natural history of dysplasia. Currently, a patient with two endoscopies, with systematic biopsies showing no dysplasia, can be surveyed every 3 years. If low-grade dysplasia has no greater abnormality on follow-up endoscopy with biopsy, surveillance can be performed every year for 3 years, then every 2 years until no dysplasia is found.

Summarize the evolution of Barrett’s esophagus to adenocarcinoma.

Intestinal metaplasia → low-grade dysplasia → high-grade dysplasia → adenocarcinoma.

Describe the management of high-grade dysplasia.
Management of high-grade dysplasia is one of the most controversial issues in the treatment of Barrett’s esophagus. Current alternatives include more frequent surveillance (every 3 months) until cancer is detected, experimental endoscopic reversal therapy, and esophagectomy. The problems with conventional esophagectomy include operative mortality rate (especially in low-volume centers), the high frequency of morbidity, and the permanent impact on eating and nutrition. Many patients are elderly and are not good surgical candidates because of comorbidity. It is also not uncommon for patients to refuse surgery even after consulting with a surgeon.

Can the development of adenocarcinoma of the esophagus be prevented in patients with Barrett’s esophagus?
Prevention is not clear. It is the major challenge to clinicians. Given the lack of reversal of Barrett’s esophagus with standard medical and surgical therapy, it is not clear that we can prevent the development of adenocarcinoma. It has been argued that control of reflux into the esophagus will prevent the progression from metaplasia to dysplasia and subsequent adenocarcinoma. However, this argument is far from proven, and only retrospective data can be brought to bear upon the issue. There are exciting developments in experimental endoscopic therapy to eliminate the presence of intestinal metaplasia. Photodynamic endoscopic ablation therapy of patients with high-grade dysplasia can reduce the development of cancer over a minimum follow-up of 2 years. The overall reduction of the development of adenocarcinoma in patients with Barrett’s esophagus remains a major challenge.

What advances can we anticipate in the management of Barrett’s esophagus?
Progress in our understanding of the genetic changes involved in the progression of Barrett’s esophagus to adenocarcinoma has been dramatic. The technical advances that continue to be made in endoscopy offer the opportunity for major advances in clinical management of Barrett’s esophagus. We can look forward to unsedated endoscopy with smaller-caliber endoscopes or nonendoscopic techniques, for cheaper and easier detection of Barrett’s esophagus. Optical methods for identifying dysplasia without biopsy add the possibility of real-time recognition. Newer endoscopic techniques to remove dysplastic and metaplastic epithelium will make our current attempts look primitive. Preventing adenocarcinoma may well require validation of biomarkers that define the subgroup of patients at highest risk for developing cancer. This approach will focus surveillance on patients at highest risk, leading to cost savings and greater clinical effectiveness. Chemoprevention may offer opportunities for cancer prevention that transcend the technical advances.

References
WEBSITES
http://www.cancer.gov/
http://www.cancer.gov/cancerinfo/wyntk/esophagus

BIBLIOGRAPHY

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