Barrett's Oesophagus: A Clinical Study of 52 Patients

Transcription

1 Quarterly Journal of Medicine, New Series 6, No. 38, pp , February 987 Barrett's Oesophagus: A Clinical Study of 5 Patients B. T. COOPER and G. O. BARBEZAT From the Gastroenterology Department, Dunedin Hospital and Department of Medicine, University of Otago Medical School, Dunedin, New Zealand Accepted September 986 SUMMARY This paper reports a series of 5 patients with Barrett's (or columnar-lined) oesophagus from one medical unit diagnosed over a six-year period. The commonest associated symptoms were heartburn, regurgitation and dysphagia but 0 patients had no oesophageal symptoms and two had no symptoms at all. Gastrointestinal bleeding (overt or occult) was observed in almost onethird of patients. At diagnosis, 6 patients had oesophagitis, 3 had oesophageal ulceration and 0 had benign oesophageal strictures. An association between oesophageal ulceration and nonsteroidal anti-inflammatory-drug ingestion was suggested by the data and patients with oesophageal ulceration were significantly older than patients with uncomplicated Barrett's oesophagus. No patient had adenocarcinoma of the oesophagus at diagnosis and neither carcinoma nor dysplasia were seen during a mean period of 6.4 months. However, 7 per cent of patients in the series had malignancies in other sites. Most patients did well on medical treatment and only two were referred for anti-reflux surgery (both for non-healing oesophageal ulcers). Barrett's oesophagus was seen in 0 per cent of patients with gastro-oesophageal reflux at endoscopy. Oesophageal ulceration in patients with Barrett's oesophagus made up per cent of oesophageal ulcers seen and benign oesophageal stricture in patients with Barrett's oesophagus constituted 3 per cent of all benign strictures seen. Barrett's oesophagus is common in our population and despite complications, it can be managed successfully, at least in the short term, by conservative means. Downloaded from by guest on May 8, 06 INTRODUCTION Barrett's oesophagus (columnar-lined oesophagus) was first described by Barrett in 950 [] and is now widely accepted to be the consequence of longstanding gastro-oesophageal reflux [, 3]. There have been only a few large series of cases reported. Burgess et al. [4] reported 7 cases in detail from a series of 85 patients seen between 950 and 969. Naef et al. [5] reported 40 cases collected from 963 to 975 but little clinical detail was recorded and the paper concentrated on the surgical aspects and the risk of malignancy. Borrie and Goldwater [6] reported 45 cases (including six children with 'congenital' Barrett's oesophagus) from Dunedin collected Address correspondence to Dr B. T. Cooper, University Department of Medicine, Bristol Royal Infirmary, Bristol BS 8HW. Oxford University Press 987

2 98 B. T. Cooper and G. O. Barbezat between 95 and 973 with emphasis on surgical treatment. Skinner etal. [7] reported 43 cases concentrating on malignant change and surgical treatment. All these series originated from surgical units and most of the cases were diagnosed after referral for consideration of surgery for gastro-oesophageal reflux and/or oesophageal stricture. Therefore it is possible that these series may have included disproportionate numbers of patients with severe symptoms. More recently, Herlihy et al. [8] reported 0 patients from a medical gastroenterology unit but there have been no other series reported from such a unit. This paper records our experience of 5 cases of Barrett's oesophagus diagnosed in one medical gastroenterology unit over a six-year period. METHODS Over the period January 980 to January 986,4448 upper gastrointestinal endoscopies were performed in the gastrointestinal unit of Dunedin Hospital. The number of patients with Barrett's oesophagus, reflux oesophagitis and/or gastro-oesophageal reflux, benign oesophageal stricture, oesophageal ulceration and adenocarcinoma of the oesophagus was determined from endoscopic records. Diagnosis of Barrett's oesophagus was made at upper gastrointestinal endoscopy with standard forward viewing fibre-optic oesophago-gastro-duodenoscopes when the squamocolumnar junction was in an obvious tubular oesophagus and was at least 3 cm proximal to the gastro-oesophageal junction. In every patient, the distance from the incisor teeth to the squamo-columnar junction (measured at endoscopy) was 3 cm or less. The diagnosis was confirmed when biopsy of the distal oesophagus cm below the squamo-columnar junction showed columnar mucosa. None of the cases was included in the previous paper on Barrett's oesophagus from Dunedin [6]. RESULTS Over the six years, 5 white Caucasian patients with Barrett's oesophagus were found. During the same period, 539 patients were found with gastro-oesophageal reflux, 77 with benign oesophageal stricture, 09 with oesophageal ulceration, and with adenocarcinoma of the TABLE. Principal symptoms and duration of symptoms Principal symptoms Heartburn and/or regurgitation 35 Dysphagia 0 Acute gastrointestinal bleed Nausea 5 Retrosternal pain 4 Epigastric pain Anorexia Duration of symptoms >0 years years -5 years 3 < year Few days No symptoms

3 Barrett's Oesophagus 99 oesophagus. The 5 patients with Barrett's oesophagus made up 0 per cent of the patients with gastro-oesophageal reflux. The series consisted of 3 males with a mean age of 6.3±5.5 (SD) years (range 33-87) and 0 females with a mean age of 66.5± 7.6 years (range 7-94). SYMPTOMS Principal symptoms at the time of diagnosis of Barrett's oesophagus are described in Table. Ten patients had no symptoms directly referrable to the oesophagus: four had an overt gastrointestinal bleed, two had symptoms of iron deficiency anaemia, two had epigastric pain and two had nausea. Two patients had no symptoms and had endoscopy during investigation of iron deficiency anaemia and two presented with only a few days history of gastrointestinal bleeding having been well before. Fifteen patients had evidence of gastrointestinal blood loss at presentation and eight of these had oesophageal ulceration. Eleven patients had overt gastrointestinal blood loss (eight haematemesis, three melaena) and four had chronic iron deficiency anaemia at presentation. OTHER FEATURES Drugs Thirty-six patients were taking regular medication at diagnosis. Of the 5 patients taking regular medication for gastro-oesophageal reflux, 0 were taking antacids, three cimetidine, two ranitidine and one metoclopramide. Sixteen patients were receiving non-steroidal antiinflammatory drugs regularly and of these were later found to have oesophageal ulceration. Only five of the 6 taking non-steroidal anti-inflammatory drugs had evidence of gastrointestinal bleeding at presentation (three haematemesis, one melaena, one iron deficiency anaemia). Smoking Twenty-three patients were non-smokers, were ex-smokers and 4 regular cigarette smokers. Smoking habits for four patients were unknown. There were no differences between the three groups with respect to the extent of Barrett's oesophagus, and to the presence or absence of reflux symptoms and of complications of Barrett's oesophagus. Other diseases A. wide variety of other diseases were present and are listed in Table. ENDOSCOPIC FEATURES Barrett's oesophagus Fifty-two patients had a columnar-lined oesophagus as proven by endoscopic biopsy. The type and extent of Barrett's oesophagus and the histology of the ephithelial mucosa in biopsies taken from cm below the squamo-columnar junction are shown in Table 3. There was no correlation between the extent of Barrett's oesophagus and either the length of history or the presence or absence of symptoms of gastro-oesophageal reflux.

4 00 B. T. Cooper and G. O. Barbezat TABLE. Other diseases in 5 patients with Barrett's oesophagus Non-malignant Ischaemic heart disease Hypertension Senile dementia Previous cerebrovascular accident Osteoarthrosis Alcoholism Benign prostatic hypertrophy Parkinson's disease Chronic obstructive airways disease Rheumatoid arthritis Ulcerative colitis Hypothyroidism Diabetes mellitus Malignant Colonic carcinoma Prostatic carcinoma Deal carcinoma Breast carcinoma Bladder carcinoma Bronchial carcinoma Laryngeal carcinoma Malignant melanoma TABLE 3. Endoscopic features in 5 patients with Barrett's oesophagus Type of Barrett's oesophagus Circumferential Island Extent of Barrett's oesophagus (distance from incisor teeth to squamo-columnar junction) Histology of Barrett's oesophagus Specialised columnar epithelium Gastric fundic epithelium Junctional epithelium Dysplastic epithelium Associated features Hiatal hernia Oesophagitis Oesophageal ulcer Benign oesophageal stricture Oesophageal carcinoma Others Gastric ulcer Duodenal ulcer Gastritis Antral erosions (mean 7) cm

5 Barrett's Oesophagus 0 TABLE 4. Clinical features in 3 patients with oesophageal ulceration Symptoms Heartburn and regurgitation 7 Dysphagia Gastrointestinal bleeding Retrosternal pain 8 4 Non steroidal anti-inflammatory drug ingestion Mean age at diagnosis (years) Endoscopic features 7 Multiple ulcers Ulcers surrounded by columnar epithelium 3 Associated with benign oesophageal stricture 3 Associated features Hiatal hernia. (Table 3) Of the four patients without a biatal hernia, three had Barrett's oesophagus alone and one had Barrett's oesophagus with a benign oesophageal stricture. Five patients with a hiatal hernia and Barrett's oesophagus had no other abnormality. Oesophageal ulcer. Twenty-three patients had oesophageal ulcers at diagnosis (Table 4). In patients, there were two or more ulcers to a maximum of six. In 0 patients, the oesophageal ulceration was at the squamo-columnar junction whereas in the remaining 3 patients, the ulceration was surrounded by columnar epithelium. These patients with Barrett's oesophagus associated with oesophageal ulceration constituted per cent of all the patients with oesophageal ulceration seen over the six-year period. Symptoms of these 3 patients with oesophageal ulceration are shown in Table 4. Eight patients had lost blood (four haematemesis, two melaena, two chronic iron deficiency anaemia). The mean age of the patients wtih oesophageal ulcer (7 ±4 (SD) years) was significantly higher than the mean age of the patients who had neither oesophageal ulcer nor benign oesophageal stricture at diagnosis (59±5, f=.84; /><0.05). The period over which histories were recorded was the same for each group. There was no correlation beween the site of the ulcer and symptoms. Downloaded from by guest on May 8, 06 Benign oesophageal stricture. Ten patients (9 per cent) had a benign oesophageal stricture and in three this was associated with oesophageal ulcer. These patients with benign oesophageal stricture made up 3 per cent of all patients with benign oesophageal stricture seen over the sixyear period. The mean age of the patients with benign oesophageal stricture at diagnosis was (59 ±9 years) which was not different from those without complications or those with oesophageal ulcer at diagnosis. Oesophagitis. Twenty-six patients (50 per cent) had oesophagitis affecting squamous epithelium adjacent to the squamo-columnar junction. Nine patients had oesophagitis in association with an oesophageal ulcer and four patients had oesophagitis associated with a benign oesophageal stricture. Other associated upper gastrointestinal abnormalities. In 0 patients upper gastrointestinal endoscopy showed other abnormalities (Table 3). Endoscopic findings in patients with dysphagia. Twenty patients had dysphagia as a presenting complaint but only nine had a benign oesophageal stricture (two had associated oesophageal

6 0 B. T. Cooper and G. O. Barbezat ulcers). The other patients had either oesophageal ulceration (0 patients), or no mucosal abnormality other than Barrett's oesophagus (one patient). One patient with a benign oesophageal stricture as well as an oesophageal ulcer did not complain of dysphagia. FURTHER OBSERVATION Details of follow up and response of symptoms during this period are shown in Table 5. There was no evidence of progression or regression of Barrett's oesophagus. Nineteen patients had not had a second endoscopy by the end of the study period. Eleven patients are still under observation and will have a second endoscopy in due course, four patients have been lost to the study and four patients will not have second endoscopies because of either severe intercurrent illness (laryngeal carcinoma) or because of extreme age and infirmity. RESPONSE TO MEDICAL TREATMENT Gastro-oesophageal reflux symptoms Twenty-three patients with symptoms of gastro-oesophageal reflux (heartburn and regurgitation) were observed. Fifteen were treated with cimetidine mg/day and seven with ranitidine 300 mg daily (Table 6). One patient was treated with antacids and improved. Oesophagitis Twenty-two patients with endoscopic oesophagitis were observed. Sixteen were treated with cimetidine mg and eight with ranitidine 300 mg daily (Table 6). Three patients treated with ranitidine had previously taken cimetidine without improvement in the oesophagitis. One patient became worse on cimetidine and developed an oesophageal ulcer. One patient with oesophagitis was successfully treated with antacids over 60 months. Oesophageal ulcer Twenty-one patients with oesophageal ulcers have been observed by endoscopy (Table 6). Fifteen patients have been treated with cimetidine mg daily. Three patients did not heal on cimetidine, two were changed to ranitidine with complete healing of the ulcer and one is to have anti-reflux surgery. One patient whose oesophageal ulcer healed with cimetidine was TABLE 5. Observation period Number observed Mean observation (months): Extent of Barrett's oesophagus (mean distance from incisor teeth to squamo-columnar junction) At diagnosis At follow up Symptoms after follow up (in 3 patients with symptoms at presentation) None Better No change Worse (-60) 6 cm 6 cm 7 0 3

7 TABLE 6. Treatment with H blockers Barrett's Oesophagus 03 Cimetidine ( mg/day) Ranitidine (300 mg/day) No. of Time on treatment No. of Time on treatment patients in months (mean) patients in months (mean) Gastro-oesophageal reflux symptoms 5-48 (4) (5) No symptoms Better No change Worse Oesophagitis 6 Healed 9 5^8(9) 3 3,7, 0 Healing 5 3 3,6, No change 5-8(5) 6, 8 Worse 5 Oesophageal ulcer 5 _- 9 Healed -35 (0) (3.5) Healing No change 3 4, 8, 43 placed on ranitidine when his ulcer relapsed after stopping cimetidine. In all, nine patients have been treated with ranitidine 300 mg daily. The patient with an unhealed ulcer after ranitidine has been recommended for surgery. Dysphagia Seventeen patients complaining of dysphagia were observed (Table 7). Five patients had endoscopic dilatation with Celestin dilators. ANTI-REFLUX SURGERY Five patients had anti-reflux surgery and repair of hiatus hernia, six to years before diagnosis of Barrett's oesophagus. Symptoms at diagnosis of Barrett's oesophagus were heartburn and regurgitation in three, dysphagia in one and iron deficiency anaemia in one. One patient had surgical treatment for gastro-oesophageal reflux with known Barrett's oesophagus and over five years there has been no evidence of regression of Barrett's oesophagus. Only two patients are being considered for anti-reflux surgery; both have non-healing oesophageal ulcers. TABLE 7. Response to treatment of dysphagia in patients with Barrett's oesophagus Cause of dysphagia Benign oesophageal Benign stricture Oesophageal stricture and oesophageal ulcer ulcer Number of patients Well on maintenance dose of H 5 0 blocker and regular dilatation Well on maintenance dose of H blocker after one initial dilatation Well on maintenance dose of H 9 blocker; no dilatation Mild dysphagia on maintenance dose - of H blocker; no dilatation yet

8 04 B. T. Cooper and G. O. Barbezat MALIGNANCY Carcinoma of the oesophagus No cases of adenocarcinoma of the oesophagus were found at diagnosis of Barrett's oesophagus or subsequently. However, only 46 patient years of observation have taken place to date. During the study period, apparent cases of adenocarcinomas of the oesophagus were diagnosed in the unit. On review, all but two appeared to be gastric adenocarcinomas which had invaded the lower oesophagus. The two cases of true adenocarcinoma of the oesophagus were both associated with hiatal hernia but only one had a history of gastro-oesophageal reflux. Barrett's oesophagus was not demonstrated in either case. No patient had dysplastic changes at diagnosis and none of the 33 patients observed by endoscopy showed either a carcinoma or dysplastic changes on oesophageal biopsy. Malignancy at other sites Nine patients (7 per cent) of the series had non-oesophageal malignancies (Table ). Only two of these patients developed malignancy during the study period; one patient developed carcinoma of the lung four years after the diagnosis of Barrett's oesophagus; one patient developed a malignant melanoma one year after the diagnosis of Barrett's oesophagus. Two patients were diagnosed as having Barrett's oesophagus during admission for treatment of carcinoma of the colon and carcinoma of the larynx respectively. In the remaining five patients carcinoma was diagnosed two to eight years before the diagnosis of Barrett's oesophagus. DISCUSSION The diagnosis of Barrett's oesophagus relies on demonstrating columnar epithelium in a tubular oesophagus. Reliable identification of the distal oesophagus can sometimes be difficult and therefore the diagnosis of Barrett's oesophagus is controversial. Many reports only include patients studied by oesophageal manometry which is used to identify the lower oesophageal sphincter. Thus Barrett's oesophagus is present when the squamo-columnar junction is 3 cm or more, proximal to the lower oesophageal sphincter [7]. However, manometry is difficult and can give misleading results [9] and patients with Barrett's oesophagus may have no demonstrable lower oesophageal sphincter [0]. An alternative means of diagnosis is to measure changes in oesophageal mucosal potential difference which allows accurate localisation of the squamo-columnar junction. While it is claimed to be specific for Barrett's oesophagus it is not sensitive [8] and has been dismissed as of little diagnostic value [3]. At endoscopy the diagnosis is usually obvious [3] and various endoscopic criteria for diagnosis have been reported [0,]. The patients in our series have been diagnosed endoscopically and no patient was included with a squamo-columnar junction greater than 3 cm from the incisor teeth. Although earlier reports suggested that Barrett's oesophagus was rare [7], it is common in certain populations. In our New Zealand population, 9.6 per cent of all cases of gastrooesophageal reflux diagnosed endoscopically showed Barrett's oesophagus. This compared with.4 per cent found in Switzerland [5] and 4 per cent in the United States [8]. Moreover approximately per cent of all endoscopies performed over the six-year period in our unit revealed the presence of Barrett's oesophagus which compared with per cent reported elsewhere [5, 8,, 3]. In our study, Barrett's oesophagus was largely a problem of the later middle aged and the elderly as indicated by a mean age of 6 in males and a mean age of 66 in females, but it may be seen in younger adults. We found Barrett's oesophagus in seven males and three females under 50 years of age. Only one possible case of 'congenital' Barrett's

9 Barrett's Oesophagus 05 oesophagus was included in the series and this was a girl who had intermittent dysphagia, heartburn and regurgitation since early childhood and was diagnosed as having Barrett's oesophagus at the age of 7. Evidence against her having true congenital Barrett's oesophagus is her later presentation and the fact that congenital Barrett's oesophagus seems to be a problem of males [3]. All but two patients had some symptoms at diagnosis. The commonest were caused by gastrooesophageal reflux (i.e. heartburn and regurgitation), seen in 67 per cent of patients, and dysphagia, seen in 38 per cent, similar findings to another medical series [8]. In contrast surgical series have much higher prevalence figures for dysphagia [6,4], which almost certainly reflects the inherent bias in these series towards patients with more severe symptoms. Fifteen of our patients (9 per cent) had evidence of gastrointestinal blood loss at presentation which is similar to other series [6]. A quarter of our patients were found to h ave B arrett's oesophagus during the investigation of non-oesophageal symptoms or anaemia. This is considerably higher than any other reported series and tends to refute the surgical view that Barrett's oesophagus is usually discovered because of symptomatic complications [6]. Our patients showed a wide variation in length of history and while more than half had symptoms for at least five years and a quarter for more than 0 years before diagnosis, other patients may be found to have Barrett's oesophagus despite a very short history of symptoms. Barrett's oesophagus itself causes no symptoms [3] and symptoms are related either to gastro-oesophageal reflux (which is the probable causative factor in Barrett's oesophagus [, 3]) or to oesophagitis or to the complications of Barrett's oesophagus (oesophageal ulceration, benign oesophageal stricture, oesophageal bleeding or adenocarcinoma). Half our patients had never smoked and there were no differences between smokers and nonsmokers with respect to the extent of Barrett's oesophagus and the presence or absence of reflux symptoms or of the complications. Other series have shown a higher proportion of smokers [8]. Our series did not support the suggestion that the malignant potential of Barrett's oesophagus was higher in patients who smoked cigarettes [7]. A feature of our series, not previously recorded, is the association with non-steroidal anti-inflammatory drugs. Sixteen patients were taking these drugs at diagnosis and were found to have oesophageal ulceration. This suggests that non-steroidal anti-inflammatory drugs should be avoided in patients with Barrett's oesophagus and that the possibility that these drugs may precipitate oesophageal ulceration should be considered. Only five patients had the island type of Barrett's oesophagus which was not associated with ulceration or stricture confirming a previous observation that this type is less prone to complication [8] and may represent Barrett's oesophagus at a much earlier stage than the classic circumferential type [8]. There was no evidence from our series that the extent of Barrett's oesophagus correlated with the length of history or with the presence or absence of symptoms of gastro-oesophageal reflux. Not all our patients had hiatal hernia confirming a previous observation that the absence of a hiatus hernia does not exclude the possibility of Barrett's oesophagus [4]- In our series all the conditions associated with Barrett's oesophagus were seen with the exception of adenocarcinoma. The commonest, oesophagitis, was seen in 50 per cent of the patients, confirming observations in other smaller studies [4,8]. Oesophagitis itself was responsible for overt gastrointestinal haemorrhage in four patients and chronic gastrointestinal blood loss in two. Twenty-three patients had oesophageal ulcers and approximately 50 per cent were true Barrett's ulcers occurring within the columnar epithelium. They made up per cent of all patients with oesophageal ulceration seen over the six-year period indicating that an oesophageal ulcer should alert the endoscopist to the possibility of Barrett's oesophagus. The proportion of oesophageal ulcers in our series was considerably higher than in other smaller

10 06 B. T. Cooper and G. O. Barbezat series where only one in 7 [4] and two in 0 [8] patients had oesophageal ulcers. None of the ulcers in our series perforated supporting an earlier suggestion that this is rare [6]. Six of the 3 patients with oesophageal ulcer presented with an acute gastrointestinal bleed, but none were serious enough to require surgery. There was no difference in the duration of symptoms between patients with uncomplicated Barrett's oesophagus and patients with Barrett's oesophagus complicated by oesophageal ulcer, but patients with oesophageal ulceration were significantly older than patients with the uncomplicated condition suggesting that oesophageal ulceration might be a complication of more longstanding gastro-oesophageal reflux and Barrett's oesophagus. Approximately 50 per cent of our patients with oesophageal ulceration had more than one ulcer which has not been stressed in previous series. Ten patients had benign oesophageal strictures making up 3 per cent of all the patients with such strictures seen over the six-year period. Our figure differs from others who reported that 44 per cent of their patients with benign oesophageal stricture also had Barrett's oesophagus [7]. The proportion of patients with stricture in this series was considerably lower than in other series [4, 6, 8, 4]. Less than 50 per cent of our patients who presented with dysphagia had a benign stricture on endoscopic examination. The most sinister complication of Barrett's oesophagus is adenocarcinoma [, 3] with a widely-quoted prevalence of 0 per cent [5] although figures as low as.5 per cent [6], and as high as 6 per cent [4] or 4 per cent [3] have been reported. These figures, all from surgical units, are likely to be inaccurate as these series will have included disproportionate numbers of patients referred for surgery because of troublesome symptoms. In our series no cases of adenocarcinoma were found either at diagnosis or during further observation. However, the observation period has been relatively short (46 patient years to date). Two cases of adenocarcinoma of the oesophagus were diagnosed over the same time but neither had Barrett's oesophagus. Therefore, Barrett's oesophagus may not be such a high risk factor for adenocarcinoma. This view is supported by two recent reports of prevalence rates of one carcinoma in 75 [5] and one in 44 [] patient observation years. This is not surprising as Barrett's oesophagus is only diagnosed when the patient complains of gastro-oesophageal reflux or of one of the complications. As patients with adenocarcinoma will always present eventually, it is likely that any series will be biased by over-representation of such cases. Epithelial dysplasia has been seen in association with adenocarcinoma in patients with Barrett's oesophagus [8,9] but we did not find it. Seventeen per cent of patients in our series had malignancy in sites other than the oesophagus. There is some evidence that patients with Barrett's oesophagus may be at increased risk of carcinoma of the colon [0] and two of our cases had this carcinoma. The apparent association with malignancy in non-oesophageal sites has not been previously reported. In a majority of patients, treatment with H blockers leads to improvement in the reflux and healing of oesophagitis and oesophageal ulceration. Previous studies have reported healing of oesophagitis with cimetidine [, ] and with ranitidine [3] and of Barrett's ulceration with cimetidine [0, 4]. Healing of Barrett's ulceration with ranitidine has not been reported before. Surgery has been widely advised as the treatment of choice for complications of Barrett's oesophagus and because it may halt progression of the columnar oesophageal mucosa [5,7,4, 5]. However, we have referred only two of our 5 patients for surgery (both for non-healing oesophageal ulceration). This probably reflects the less serious problems associated with Barrett's oesophagus in our series and we have shown that patients can be managed successfully by medical treatment. In our view, the only convincing reason for suggesting surgery for patients with Barrett's oesophagus would be if Barrett's epithelium regressed after successful

11 Barrett's Oesophagus 07 anti-reflux surgery. Most evidence suggests that regression does not occur after surgery [6-8] and in fact carcinoma has been reported after anti-reflux surgery [5, 9]. In the only study in which evidence for regression was presented, regression was only reported in four of 0 patients studied [9]. Moreover, regression may not remove any malignant potential. In our study there was no evidence of regression or progression over the relatively short observation. We conclude that patients should be treated medically and that surgery should only be advised for those with intractable symptoms or troublesome complications. However, until the true risk of malignancy is ascertained, we would agree with others [30] that regular endoscopic surveillance for dysplasia and carcinoma should be offered. REFERENCES. Barrett NR. Chronic peptic ulcer of the oesophagus and "oesophagitis". Br J Surg 950; 38: Bozymski EM, Herlihy KJ, Orlando RC. Barrett's esophagus. Ann Intern Med 98; 97: SjogTen RW, Johnson LF. Barrett's esophagus. Am J Med 983; 74: Burgess JN, Payne WS, Anderson HA, Weiland LM, Carlson HC. Barrett's esophagus: the columnar lined lower esophagus. Mayo Clin Proc 97; 46: Naef AP, Savary M, Oziello L. Columnar lined lower oesophagus: an acquired lesion with malignant predisposition. J Thorac Cardiovasc Surg 975; 70: Borne J, Goldwater L. Columnar cell lined oesophagus: assessment of aetiology and treatment. A year experience. J Thorac Cardiovasc Surg 976; 7: Skinner DB, Walther BC, Riddell RH, Schmidt H, Iascone C, DeMeester TR. Barrett's esophagus. Comparison of benign and malignant cases. Ann Surg 983; 98: Herlihy KJ, Orlando RC, Bryson JC, Bozymski EM, Carrey CN, Powell DW. Barrett's esophagus - clinical, endoscopic, histologic, manometric and electrical PD characteristics. Gastroenterology 984; 86: Edwards DAW. The oesophagus - physiology. In: Bouchier IAD, Allan RN, Hodgson HJF, Keighley MRB, eds. Textbook of gastroenterology. London: Balliere Tindall 984: Wesdorf ICE, Bartelsman J, Schipper ME, Tytgat GN. Effects of long term treatment with cimetidine and antacids in Barrett's oesophagus. Gut 98; : Cameron AJ, Ott BJ, Payne WS. The incidence of adenocarcinoma in columnar lined (Barrett's) esophagus. N Engl J Med 985; 33: Burbige EJ, Radigan J. Characteristics of the columnar lined esophagus. Gastroenterology 978; 74: Dees J, Van Blankenstein M, Frenkel M. Adenocarcinoma in Barrett's esophagus; a report of 3 cases. Gastroenterology 978; 74: Radigan LR, Glover JL, Shipley FE, Shoemaker RE. Barrett's esophagus. Arch Surg 977; : 486-^ Spechler SJ, Robbins AH, Rubins HB, et al. Adenocarcinoma and Barrett's esophagus. An over-rated risk? Gastroenterology 984; 87: Hawe A, Payne WS, Weiland LH, Fontana RS. Adenocarcinoma in the columnar epithelial lined lower (Barrett) esophagus. Thorax 973; 8: Spechler SJ, Speber H, Doos WG, Schimmel EM. The prevalence of Barrett's esophagus in patients with chronic peptic oesophageal stricture. Dig Dis Sci 983; 8: Paull A,Trier JS, DaltonMD.efa/. The histological spectrum of Barrett's esophagus. NEnglJ Med 976; 95: Smith RRL, Boitnott JK, Hamilton SR, Rogers ELC. The spectrum of carcinoma arising in Barrett's esophagus. Am J Surg Pathol 984; 8: Sonntag SJ, Schnell TG, Chejfec G, et al. Barrett's esophagus and colonic tumours. Lancet 985; : Behar HJ, Brand DL, Brown FC, et al. Cimetidine in the treatment of symptomatic esophageal reflux. Gastroenterology 978; 74: 44^47.. Wesdorp ICE, Bartelsman J, Pape K, Dekker W, Tytgat GN, Oral cimetidine in reflux esophagitis. Gastroenterology 978; 74: 8-84.

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