Dysplasia can occur in metaplastic Barrett's epithelium and is a neoplas-tic change. At present, dysplasia is the best indicator of cancer risk in patients with Barrett's esophagus. The grading of dysplasia in Barrett's esophagus is based on the system used for ulcerative colitis (Riddell et al, 1983). Interobserver variability in the recognition, grading, and repro-ducibility of detection of dysplasia in Barrett's esophagus is problematic (Reid et al, 1988; Montgomery et al, 2001). The finding of dysplasia of any grade warrants repeat endoscopy with intensive biopsy of the area of dys-plasia to exclude coexisting carcinoma (Sampliner, 2002).
Dysplasia is graded as indefinite, low-grade, high-grade, or intra-mucosal carcinoma and is believed to reflect a stepwise progression that culminates in invasive adenocarcinoma. The interval between steps is extremely variable—some patients with high-grade dysplasia never develop cancer, and many patients with low-grade dysplasia never develop high-grade dysplasia. The grade of dysplasia found determines the recommended surveillance interval. Updated recommendations are shown in Table 20-1 (Sampliner, 2002). When low-grade dysplasia is detected at follow-up endoscopy with concentrated biopsies in the area of dysplasia, annual endoscopy is recommended. Once low-grade dysplasia is identified, aggressive antisecretory therapy with a proton-pump inhibitor should be started.
The finding of high-grade dysplasia necessitates repeat endoscopy with particular attention to any mucosal lesion. An intensive biopsy protocol using therapeutic endoscopy and jumbo forceps is recommended. An expert pathologist should confirm the presence of high-grade dysplasia. The extent of high-grade dysplasia is also important. High-grade dyspla-sia is defined as focal when associated cytologic or architectural changes are limited to a single focus of 5 or fewer crypts and as diffuse when more than 5 crypts are involved in a single biopsy specimen or if high-grade dysplasia involves more than 1 biopsy fragment (Sampliner, 2002). Diffuse high-grade dysplasia is associated with a 3.7-fold increase in the risk of esophageal cancer compared with the risk in patients with focal highgrade dysplasia (Buttar et al, 2001b). Patients with focal high-grade dys-plasia are less likely to have cancer during the first year after diagnosis or on subsequent follow-up than are patients with diffuse high-grade dysplasia (Buttar et al, 2001b). This observation highlights the importance of sending samples of high-grade dysplasia to experienced gastrointestinal pathologists specializing in such specimens. If uncertainty about the diagnosis cannot be resolved by expert pathology re-review, then repeat endoscopy with biopsy should be performed promptly. Updated guidelines suggest that patients with high-grade dysplasia (with 5 or fewer crypts) may be followed up with a 3-month surveillance interval. Patients with confirmed high-grade dysplasia within Barrett's esophagus have the highest risk for the development of esophageal adenocarcinoma if concurrent adenocarcinoma does not already exist. Detection of high-grade dysplasia is important because a significant proportion of patients with this condition will develop adenocarcinoma over a 5-year period. In patients with high-grade dysplasia within Barrett's esophagus referred for esophagectomy, adenocarcinoma is found in approximately 11% to 43% of cases (Heitmiller et al, 1996; Cameron and Carpenter, 1997; Tseng et al, 2003).
Available data suggest that in some patients, high-grade dysplasia actually regresses or persists and does not develop into cancer, suggesting a less aggressive approach for management (Rabinovitch et al, 2001; Schnell et al, 2001). Some cohort studies have shown that high-grade dysplasia may remain stagnant without further progression, especially if potent acid-suppression therapy is employed (Cooper et al, 1998). At the least, rigorous systematic surveillance in patients with high-grade dysplasia should involve repeat endoscopy every 3 months, with the distance between biopsies reduced to every 1 cm, as this has been shown to most consistently detect early cancers arising in high-grade dysplasia (Reid et al, 2000a). Management decisions in cases of high-grade dysplasia can be complex and challenging, particularly in patients with comorbid disease who are poor candidates for surgery. The role of endoscopic mucosal ablative therapies is discussed below. Chromoendoscopy and endoscopic fluorescence are being evaluated to improve recognition of Barrett's esophagus and, especially, to enhance detection of neoplastic lesions (Canto et al, 1996, 2000; Sharma et al, 2001a). Esophagectomy is regarded as the most definitive therapy for confirmed diffuse high-grade dysplasia and should be offered to patients deemed to be appropriate candidates for surgery (Sharma, 2001b). Outcomes of esophagectomy appear best at institutions that perform a high volume of such surgeries. Patient age and comorbid conditions also need to be weighed when deciding on the appropriate management strategy. The type of resection is based on the length of the Barrett's segment (Rusch et al, 1994).
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