Alan J. Cameron

Increasing incidence of adenocarcinoma of the esophagus and esophagogastric junction

BACKGROUND The aim of this study was to determine whether the incidence of adenocarcinoma of the esophagus and esophagogastric junction in a well-defined population was higher than previously recognized. METHODS Clinical records and original histological slides from patients residing in Olmsted County, Minnesota, were reviewed and compared with a previous study in the same population. RESULTS The incidence of esophageal adenocarcinoma rose from 0.13 for 1935-1971 to 0.74 for 1974-1989, and the incidence of adenocarcinoma of the esophagogastric junction rose from 0.25 to 1.34 per 100,000 person-years. Histological review of preserved surgical specimens showed associated intestinal metaplasia (Barretts esophagus) in 2 of 2 esophageal and in 5 of 9 esophagogastric adenocarcinomas. CONCLUSIONS The incidence of adenocarcinoma in each location increased five to sixfold compared with the earlier study. This increase could not be explained by improved diagnostic methods or classification changes. The association with Barretts esophagus and the parallel increased incidence of cancer in each location is evidence that adenocarcinoma of the esophagus and of the esophagogastric junction are related disorders.

The Incidence of Adenocarcinoma in Columnar-Lined (Barrett's) Esophagus

We evaluated the risk of adenocarcinoma developing in Barretts esophagus (esophagus lined with columnar epithelium). Mayo Clinic records were reviewed, and all cases that met predefined histologic criteria for the diagnosis of Barretts esophagus in 1979 or earlier were included. In 18 of 122 such cases, adenocarcinoma of the esophagus and Barretts esophagus were diagnosed simultaneously. The status of the remaining 104 cases was determined after a mean interval of 8.5 years. During this time, adenocarcinoma of the esophagus developed in 2 patients, and 24 died from other causes. We conclude that although the incidence of esophageal adenocarcinoma is increased in patients with symptomatic Barretts esophagus, it does not occur in the majority of such patients.

Prevalence of columnar-lined (Barrett's) esophagus: Comparison of population-based clinical and autopsy findings

In this study, two different methods were used to investigate the prevalence of columnar-lined (Barretts) esophagus. First, a population-based study of clinically diagnosed cases was performed in Olmsted County, Minnesota. Twenty-five residents of this county, who had undergone endoscopy and biopsy between 1969 and 1986, were diagnosed as having Barretts esophagus. On January 1, 1987, 17 of these patients were still living in the county, representing an age- and sex-adjusted prevalence rate of 22.6 cases per 100,000 population (95% confidence interval, 11.7-33.6 cases). A prospective search of Mayo Clinic autopsy material for Barretts esophagus was conducted using the same diagnostic criteria as in the clinical study. Over an 18-month period ending in September 1987, 7 cases of Barretts esophagus were found in 733 unselected autopsies. In 5 of the 7 cases, Barretts esophagus was first detected at the time of autopsy. Using the age- and sex-specific prevalence from the clinically diagnosed study, researchers expected to find 0.19 cases of Barretts esophagus at the 226 autopsies performed on Olmsted County residents, although 4 were actually observed (P less than 0.001). This approximately 21-fold increase (95% confidence interval, 5-54 cases) corresponds to an autopsy estimated prevalence of 376 cases per 100,000 population (95% confidence interval, 95-967 cases). In conclusion, a majority of cases of Barretts esophagus, a condition that predisposes to esophageal malignancy, remains unrecognized in the general population.

Barrett's esophagus: Age, prevalence, and extent of columnar epithelium

The development of Barretts esophagus was studied using data from 51,311 patients undergoing upper gastrointestinal endoscopy between 1976 and 1989. Three hundred seventy-seven patients had greater than or equal to 3-cm columnar epithelium in the esophagus and no carcinoma. The prevalence of Barretts esophagus increased with age to reach a plateau by the seventh decade. Half of the maximum prevalence was reached by age 40 years, the estimated median age of development of the disorder. Unlike prevalence, the mean length of columnar epithelium did not increase with age. No significant change in length was found in 21 patients followed up for a mean of 7.3 years (mean initial length, 8.29 +/- 0.85 cm; mean final length, 8.33 +/- 0.77 cm). The length of columnar epithelium did not increase in the presence of esophagitis or decrease when esophagitis was absent. Mean age at diagnosis of Barretts esophagus was 63 years without carcinoma and 64 years in a separate group of patients with adenocarcinoma. The data are consistent with a fairly rapid evolution of Barretts esophagus to its full length with little subsequent change. Barretts esophagus may develop more than 20 years before the mean age of clinical recognition or the development of esophageal adenocarcinoma.

Adenocarcinoma of the esophagogastric junction and Barrett's esophagus.

BACKGROUND & AIMS Barretts esophagus is associated with adenocarcinoma of the esophagus. The aim of this study was to find the prevalence of Barretts esophagus in patients with adenocarcinoma of the esophagogastric junction. METHODS Consecutive, freshly resected surgical esophagogastrectomy specimens were examined, and multiple histological sections were made around the tumor periphery. Barretts esophagus was defined as specialized columnar epithelium above the esophagogastric junction. Tumors centered < or = 2 cm from the junction were defined as junction cancers. RESULTS Barretts esophagus was found in 9 of 9 (100%) esophageal adenocarcinomas compared with 0 of 8 (0%) squamous carcinoma controls (P < 0.001). Ten of 24 (42%) junction adenocarcinomas had a Barretts esophagus. A Barretts esophagus was found in 8 of 12 (67%) junction cancers < or = 6 cm in length but only 2 of 12 (17%) larger tumors (P < 0.05). Barretts esophagus was significantly associated with junction tumors < 6 cm compared with squamous carcinoma controls (P < 0.02). In 5 specimens with junction cancer, the length of Barretts esophagus was < 3 cm, and in 5 specimens it was > or = 3 cm. Specialized epithelium was often found below the esophagogastric junction in controls. CONCLUSIONS Adenocarcinomas of the esophagogastric junction are associated with short and long segments of Barretts esophagus. Larger cancers probably overgrow and conceal the underlying specialized columnar epithelium from which they arise.

Secular trends in the epidemiology and outcome of Barrett's oesophagus in Olmsted County, Minnesota

BACKGROUND The incidence of oesophageal adenocarcinoma has increased greatly. Barretts oesophagus is a known risk factor. AIMS To identify changes in the incidence, prevalence, and outcome of Barretts oesophagus in a defined population. SUBJECTS Residents of Olmsted County, Minnesota, with clinically diagnosed Barretts oesophagus, or oesophageal or oesophagogastric junction adenocarcinoma. METHODS Cases were identified using the Rochester Epidemiology Project medical records linkage system. Records were reviewed with follow up to 1 January 1998. RESULTS The incidence of clinically diagnosed Barretts oesophagus (>3 cm) increased 28-fold from 0.37/100 000 person years in 1965–69 to 10.5/100 000 in 1995–97. Of note, gastroscopic examinations increased 22-fold in this same time period. The prevalence of diagnosed Barretts oesophagus increased from 22.6 (95% confidence interval (CI) 11.7–33.6) per 100 000 in 1987 to 82.6/100 000 in 1998. The prevalence of short segment Barretts oesophagus (<3 cm) in 1998 was 33.4/ 100 000. Patients with Barretts oesophagus had shorter than expected survival but only one patient with Barretts oesophagus died from adenocarcinoma. Only four of 64 adenocarcinomas occurred in patients with previously known Barretts oesophagus. CONCLUSIONS The incidence and prevalence of clinically diagnosed Barretts oesophagus have increased in parallel with the increased use of endoscopy. We infer that the true population prevalence of Barretts oesophagus has not changed greatly, although the incidence of oesophageal adenocarcinoma increased 10-fold. Many adenocarcinomas occurred in patients without a previous diagnosis of Barretts oesophagus, suggesting that many people with this condition remain undiagnosed in the community.

Epidemiology of columnar-lined esophagus and adenocarcinoma.

Barretts esophagus is found in about 1% of the older population and in 3% to 5% of persons with gastroesophageal reflux. It is acquired more commonly by men and the prevalence increases with age. Most cases in the population remain undiagnosed. The incidence of adenocarcinoma of the esophagus and esophagogastric junction is increasing, both being related to Barretts esophagus. Small areas of intestinal metaplasia are common but of uncertain significance.

Barrett's esophagus: prevalence and size of hiatal hernia.

OBJECTIVE:Barretts esophagus is caused by gastroesophageal reflux and predisposes to adenocarcinoma. Hiatal hernia may cause reflux. The prevalence and size of hernias in patients with Barretts esophagus was investigated.METHODS:Axial hernia length and the width of the diaphragmatic hiatus were measured prospectively at endoscopy.RESULTS:A 2-cm or longer hernia was found in 96% of 46 patients with Barretts esophagus, in 42% of 103 controls (p < 0.001), and in 72% of 18 patients with short segment Barretts esophagus (p < 0.05vs controls). A hernia was found in 71% of 31 controls with esophagitis and in 29% of 72 controls without esophagitis (p < 0.001). Of 54 controls with neither esophagitis or reflux symptoms, 20% had a hernia. Mean hernia length was 3.95 cm in Barretts esophagus, and 2.81 cm in controls (p < 0.005). Mean hiatus width was 3.52 cm in patients with Barretts esophagus and hernia, and 2.24 cm in controls with hernia. Hernia length was similar in patients with and without esophagitis, and in short segment Barretts esophagus.CONCLUSIONS:Most patients with Barretts esophagus have hiatal hernia; their hernias are longer and the hiatal openings wider than in controls with or without esophagitis. Hiatal hernia likely contributes to the development of Barretts esophagus.

Relationship between body mass index, diet, exercise and gastro-oesophageal reflux symptoms in a community

Background : Body mass index (BMI) is a risk factor for gastro‐oesophageal reflux but may simply be explained by diet and lifestyle.

Linear gastric erosion: A lesion associated with large diaphragmatic hernia and chronic blood loss anemia

A prospective study was undertaken to identify mucosal lesions that might cause chronic blood loss anemia in patients with large diaphragmatic hernia. Patients with one-third or more of the stomach above the diaphragm on barium x-ray were examined by a gastroscopist who was given no clinical information. A total of 109 patients were included: 55 with anemia and 54 with a large hernia but no anemia. The incidence of esophagitis and peptic ulcer did not differ significantly in the anemic and nonanemic groups. Linear gastric erosions were found on the crests of mucosal folds at or near the level of the diaphragm in 23 anemic patients and 13 without anemia (p less than 0.05). Blood on the surface of a linear erosion was found in 14 anemic patients and 4 without anemia (p less than 0.05). We suggest that these erosions are due to trauma and can cause chronic blood loss anemia in hernia patients.