Barrett's oesophagus is defined as columnar-lined oesophagus of any length containing specialised intestinal metaplasia. Diagnosis depends on close corroboration between the endoscopist and histopathologist. It occurs in 10% of patients presenting endoscopically with reflux symptoms and has an adenocarcinoma incidence of 0.4% to 2%. Surveillance is performed to detect precancerous change (dysplasia) and early stage disease has a good surgical prognosis. Computer models suggest cost efficacy comparable to other health measures. However most patients with Barrett's do not die of oesophageal cancer and elective oesophagectomy has an appreciable mortality. Endoscopic ablation techniques and improved definition of high risk subgroups will help shape future surveillance programmes.
In 1950 Norman Barrett described the columnar-lined oesophagus, which he considered to be a congenital abnormality. (1) It is now accepted that Barrett's oesophagus represents the metaplastic adaptation of the distal oesophageal squamous epithelium to a columnar lining containing specialised intestinal metaplasia in response to chronic duodenogastro-oesophageal reflux. (2) Most authorities define "traditional" Barrett's oesophagus as the presence of three or more centimetres of columnar-lined oesophagus above the gastro-oesophageal junction. (3) This is an arbitrary figure used by earlier investigators to help overcome the technical and practical problems in endoscopic identification of the gastro-oesophageal junction (4 5) and does not address the issues associated with short segment Barrett's oesophagus (< 3 cm). Specialised intestinal metaplasia is the most significant histological finding and is a form of incomplete intestinal metaplasia containing certain histological and immunohistological features of b oth small intestinal, colonic and gastric epithelium. (6) Its importance is as a marker of an unstable epithelium with a predisposition to neoplastic change. (7 8) It may appear at a normal appearing gastro-oesophageal junction in 9%-36% of unselected patients undergoing endoscopic examination. (9-11)
Histology reports can be interpreted in several ways. They can be diagnostic when juxtaposition of native oesophageal structures to glandular mucosa is seen (occurs in only 10% of biopsies (12), or corroborative if glandular mucosa with intestinal metaplasia is found, or "in keeping with" if gastric type mucosa alone is described. These latter two reports may represent biopsies mistakenly taken from the gastro-oesophageal junction or a hiatus hernia. Hence biopsy of the most proximal end of Barrett's changes may provide the most accurate histological assessment.
A combination of careful endoscopic examination, accurate biopsy technique, and appropriately stained histological sections provide the best diagnostic approach: many experts now recommend that the segment length is not a requirement for diagnosis (2 13 14): an alternative more descriptive classification using the term columnar-lined oesophagus plus intestinal metaplasia is more practical.(2) However, the significance of specialised interstitial metaplasia at a normal appearing gastro-oesophageal junction is unknown and this finding on its own (sometimes referred to as an "ultra short Barrett's oesophagus") should not presently be regarded as Barrett's oesophagus, certainly not in terms of recommendations for surveillance. (15 16) Malignant transformation is well described in short segment Barrett's, (17 18) although there is evidence to suggest that longer segment Barrett's carries an increased risk of cancer development. (19 20)
It is important to note that most published epidemiological data about Barrett's oesophagus have been based on the outdated definition requiring a [greater than or equal to]3 cm segment. (21)
SIZE OF THE PROBLEM
The prevalence of Barrett's oesophagus in endoscopic series for any indication is 1%. (21) If endoscopy is performed for reflux symptoms alone the prevalence rises to 10%-15%. (22 23) The majority of patients with Barrett's oesophagus do not seek medical attention for reflux symptoms or have silent reflux. From necropsy and endoscopic series, Cameron et al estimated that for every known patient with Barrett's oesophagus there might be 20 more unrecognised in the general population. (24) This raises significant public health issues when viewed against an observed background of a rapidly increasing incidence of oesophageal adenocarcinoma in the western hemisphere. (25-27) The average annual age adjusted incidence in white males has risen from 0.8/100 000 in 1976-78 to 2.5/100 000 in l988-90. (28) There is no accurate information on the effect of Barrett's oesophagus on life expectancy which may be normal overall; a few cohort studies have reported an excess of mortality in patients with Barrett's but no compari sons with control populations were included. (29 30 31).
The incidence of oesophageal adenocarcinoma from endoscopic surveillance studies varies from 1:46 to 1:441 patient years of follow up, representing a 30 to 125-fold increase compared with the general population. (32 33) The reasons for this wide variation include the small number of cases in most published series and short length of follow up. (34) Retrospective study design, potential referral bias in reports from tertiary centres, (35) population bias, and presence of advanced preneoplastic change at entry into surveillance programmes may also contribute. From prospective studies an average risk of about 1% per annum (range 0.4%-2%) is generally accepted, (36) but more recent studies suggest the cancer risk is lower at around 1:200 patient years. (13 37) There is a strong inverse correlation between study size and malignant risk; the bigger studies giving a lower cancer incidence.
WHY CARRY OUT SURVEILLANCE?
The objective of Barrett's surveillance is to detect oesophageal adenocarcinoma at an early treatable stage. It is proposed that cancer develops progressively through sequential change from metaplasia to dysplasia to invasive adenocarcinoma.(38-40) The restriction of dysplasia into only two grades (high and low) using the recently proposed Vienna classification may enable clearer and more reproducible histological assessment of patients. (41) In patients presenting de novo the prognosis of oesophageal cancer is poor with overall five year survival rates of about 5%. (27) Currently only surgery offers the chance of cure, but even in tertiary referral centres oesophagectomy for high grade dysplasia/early cancer carries an appreciable morbidity and mortality between 5% and 10%.(42-44) Operative mortality for palliative resection is at least double this. Cancer survival after oesophagectomy is dependent on the stage of disease with 90% five year survival for stage 1 disease (confined to the mucosa …