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Contents | Director | One | Two | Three | Four | Topic | EKG 1 | EKG 2 | Rad Albany Medical Review - August 2001 |
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Controversies in Barrett's Esophagus |
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Georgios I. Papachristou, MD
Consider this senario: CC: Heart burn. A 45-year-old
white male presents with worsening episodes of reflux symptoms.
He reports that over the last several years he has an intense burning
sensation one-half to one hour after large or spicy meals, and after
his nighttime snack. Furthermore, he sometimes wakes up in the middle
of the night with a sour taste in his mouth. He had achieved partial
relief with over the counter antacids, but his symptoms were completely
abated when his PMD gave him a proton pump inhibitor eight weeks
ago. However, when he stopped the medication last week his symptoms
returned.
What is the work up? EGD? UGI series? The patient reports long-standing, frequent symptoms of heartburn, and regurgitation. These symptoms occur also at night, and they are severe enough to wake him up. The diagnosis is gastro-esophageal reflux disease (GERD). GERD is an extremely common, chronic, relapsing gastrointestinal disorder, which has been associated with the development of Barrett’s esophagus and subsequently esophageal adenocarcinoma. Upper endoscopy (EGD) is the procedure usually preferred, because biopsies can be done at the same time, if there are any abnormal findings detected during the procedure. EGD findings Erosive esophagitis, Barrett’s esophagus without dysplasia, gastritis. Esophagitis secondary to gastro-esophageal reflux disease is a very common medical condition in western countries with 30% of adults complaining of heartburn at least once per month, a third of whom will have endoscopic evidence of esophagitis. Forty percent of patients with esophagitis improve spontaneously, 50% have persistent esophagitis, and 10% progress to Barrett’s esophagus.[1] Between 0.5 and 2% of adults in the western world have Barrett’s esophagus (BE). The term of BE is variably defined, and may hamper our understanding of the condition to which it is applied. It represents the replacement of the normal stratified squamous mucosa that lines the distal esophagus with specialized columnar epithelium. This transformation occurs in response to injury of the esophageal mucosa by acid and bile reflux in genetically susceptible individuals. The label BE traditionally was applied to columnar epithelium that extended 3 cm or more above the gastroesophageal junction. However, the definition of BE has been appropriately broadened to include specialized columnar epithelium containing goblet cells regardless of the extent.[2] The importance of this specialized intestinal metaplasia lies in its potential for malignant transformation into adenocarcinoma. What treatment should be given, if any? Pt has erosive esophagitis, therefore, high dose proton pump inhibitors is the recommended treatment. PPIs are highly effective and more efficacious than H2-receptor antagonists in the management of erosive esophagitis, but they don’t convincingly reverse or halt the progression of Barrett’s. PPIs
are potent acid-suppressive medications, but they cannot inhibit
the refluxate in general, which contains other highly important
constituents in the pathogenesis of BE, such as bile acids.[1] Scenario 1 Pt has been placed back on a PPI twice a day. It was also emphasized the importance of antireflux measures, the need to stop smoking, and cessation of alcohol. He returns for a three-month follow up, having stopped smoking and now only has an occasional drink on the weekends. His reflux symptoms have resolved now and the only finding on physical examination is that he is fifteen pounds heavier. How often should he return for follow up exams and upper endoscopies? BE does not regress. Furthermore, 40% of patients with Barrett’s have few or no reflux symptoms. Specialized intestinal metaplasia is thought to give rise to most, if not all, esophageal and gastro-esophageal junction adenocarcinomas with the rate of neoplastic change each year about 1%. The risk factors for the development of Barrett’s adenocarcinoma are: male sex, age >45 years, white race, family history of gastric cancer, obesity, heavy smoking, severe and frequent (more than three times per week) gastro-esophageal reflux, duration >10 years, length of metaplasia >8 cm, ulceration or stricture in Barrett’s metaplasia, absent H. pylori, and the use of nitrates, benzodiazepines, anticholinergics, theophyllines. The above conventional risk factors are neither sensitive nor specific enough.[1] BE
is a common condition found in up to 5%-15% of patients undergoing
upper endoscopy for reflux symptoms. For every known individual
with BE there may be additional 20 unrecognized cases in the general
population.[5] Because BE is the strongest risk factor
for esophageal adenocarcinoma and esophageal cancers have a long,
asymptomatic growth phase, there is a logical appeal to surveillance.
Although lifelong endoscopic and histologic surveillance for the
detection of dysplasia and cancer is widely recommended, there are
no controlled data showing that this practice actually improves
survival. Furthermore, regular surveillance is very expensive and
the cost effectiveness of this approach has been questioned. The
current recommendations for repeating the endoscopy for BE without
dysplasia are 2 years.[4]
Scenario 3 Pt returns for the repeat endoscopy at a specified period of time, and repeat esophageal biopsies indicate Barrett esophagus with foci of low-grade dysplasia. What do you recommend? The endoscopic surveillance for low-grade dysplasia is most commonly performed at 6-month intervals. There is considerable variation in techniques and intervals of surveillance for BE in the United States. Clearly, one universal guideline cannot fit all patient groups. Additional risk stratification can be based on the length of Barrett’s epithelium, presence of ulceration or stricture, and tumor markers. Tailoring surveillance in this fashion will be critical to optimizing the benefits while containing costs.[5] The
majority of the gastroenterologists does not utilize ablation therapy,
nor recommend esophagectomy for low-grade dysplasia.
Special
thanks to Dr Prabhjot Kaur, and the Department of Pathology, Albany
Medical Center for providing the slides.
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