Epidemiologic studies and the development of Barrett's esophagus.
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Adenocarcinoma↗
Biomedical subjects
A J Cameron
Publications and source records attributed to A J Cameron.
Barrett's esophagus and adenocarcinoma: from the family to the gene.
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Adenocarcinoma↗
Barrett's esophagus: age, prevalence, and extent of columnar epithelium.
The development of Barrett's 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 Barrett's 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 Barrett's 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 Barrett's esophagus to its full length with little subsequent change. Barrett's esophagus may develop more than 20 years before the mean age of clinical recognition or the development of esophageal adenocarcinoma.
Adult↗
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 (Barrett's) 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 Barrett's 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 Barrett's 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 Barrett's esophagus were found in 733 unselected autopsies. In 5 of the 7 cases, Barrett's 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 Barrett's 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 Barrett's esophagus, a condition that predisposes to esophageal malignancy, remains unrecognized in the general population.
Aged↗
An unusually intractable Schatzki ring.
Most patients with Schatzki's ring have dysphagia that can be relieved by esophageal dilation. We report an unusual case in which dysphagia caused by a Schatzki ring could not be managed conservatively. The obstructing ring was excised through a gastrotomy approached by a left-sided thoracotomy. An antireflux procedure was done after elimination of the ring. Five years later, the patient remained symptom free.
Aged↗
Campylobacter pylori and Barrett's esophagus.
Campylobacter pylori is thought to be confined to gastric mucosa; when detected in the duodenum in association with duodenal ulceration, the organism infects only areas of gastric metaplasia. Barrett's esophagus is a metaplastic condition of the esophagus, in which areas or islands of "gastric-type" epithelium are found. To determine whether C. pylori colonized the esophagus of patients with Barrett's esophagus, we studied retrospectively 23 unselected patients who had endoscopic and biopsy evidence of Barrett's esophagus. Mucosal biopsy specimens were stained by the Warthin-Starry silver technique and reviewed by an experienced, "blinded" histopathologist. Of the 23 patients, 12 (52%) had C. pylori in the esophagus. Patients with and those without C. pylori were of similar age and gender, had similar scores for acute and chronic inflammation, and had similar lengths of tubular esophagus with metaplastic gastric mucosa. These observations suggest that C. pylori commonly infects Barrett's esophagus. The clinical importance of this finding is unknown.
Adult↗
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.
Aged↗
The incidence of adenocarcinoma in columnar-lined (Barrett's) esophagus.
We evaluated the risk of adenocarcinoma developing in Barrett's esophagus (esophagus lined with columnar epithelium). Mayo Clinic records were reviewed, and all cases that met predefined histologic criteria for the diagnosis of Barrett's esophagus in 1979 or earlier were included. In 18 of 122 such cases, adenocarcinoma of the esophagus and Barrett's 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 Barrett's esophagus, it does not occur in the majority of such patients.
Adenocarcinoma↗
Bacterial reduction of fensulfothion and its hydrolysis product 4-methylsulfinyl phenol.
Oxygen-limited cultures of Klebsiella pneumoniae reduced 4-methylsulfinyl phenol to 4-methylthiophenol. A study of the effect of 4-methylthiophenol on the growth of K. pneumoniae revealed that the specific growth rate was retarded by 40% in the presence of 200 micrograms of the phenol per ml. A soil bacterium, Hafnia sp., was isolated that could reduce the organophosphorus insecticide fensulfothion to fensulfothion sulfide.
Chromatography, Gas↗
Surgical management for recurrent pharyngoesophageal (Zenker's) diverticulum.
Recurrent pharyngoesophageal diverticulum is uncommon after a one-stage diverticulectomy. Among 888 operations at the Mayo Clinic, recurrence has been noted after only 32 (3.6%). The present report outlines our management during a 19-year period of 44 patients operated on previously, including management of various late complications seen in 13 patients after diverticulopexy and diverticulectomy performed at other institutions. The study then focuses on the results in 31 patients in whom reoperation for symptomatic recurrent diverticulum was performed at the Mayo Clinic during the same period. Although reoperation posed a technical challenge, there was only 1 operative death (3.2%). Surviving patients experienced highly satisfactory late results, with only two recurrences. Early surgical morbidity was considerably higher than for primary operations, but this did not interfere with most patients having excellent to good late results.
Adult↗
Abdominal angina and neurofibromatosis.
A young man with severe abdominal pain and weight loss due to intestinal ischemia was examined. At operation, the origins of the celiac and superior mesenteric arteries were found to be compressed by plexiform neurofibromatosis. Symptoms were relieved by reconstructive arterial surgery.
Abdomen↗
Physiopathology of lower esophageal diverticulum and its implications for treatment.
This study attempted to define the esophageal motor disturbances and pathogenesis of symptoms in patients with lower esophageal diverticulum. Sixty-five patients were investigated by manometry in addition to roentgenography and endoscopy. Fifty had manometric evidence of abnormal motility, most often diffuse spasm or achalasia. Of the 15 patients with normal esophageal motility, 13 had hiatal hernia, and five of these had a high grade distal esophageal stricture. Pressures in the lower esophagus and lower esophageal sphincter in patients with lower esophageal diverticulum and motor disturbance were the same as for those in matched patients with motor disturbances but no diverticulum. Dysphagia, chest pain and regurgitation were common presenting symptoms. Of 46 patients with dysphagia, only ten had mechanical obstruction to explain this symptom. Of 32 patients with chest pain, only two had ulceration in the diverticulum as a possible cause of pain. We conclude that the development of lower esophageal diverticulum and its symptoms are associated with a motor disturbance of the esophagus in the majority of patients and with an organic obstruction in the minority of patients. The diverticulum itself is usually not the sole cause of the esophageal symptoms, although diverticula can produce symptoms in the absence of other definable conditions. When surgical treatment is indicated, the diverticulum should be excised and the underlying motor or mechanical obstruction should be corrected to prevent serious postoperative complications and recurrence of the diverticulum and its symptoms.
Adult↗
Association of myocardial cell necrosis with experimental cardiac hypertrophy.
Cardiac hypertrophy was induced in rabbits by injecting thyroxine or isoprenaline, or by surgically constricting the abdominal aorta. An increase in heart weight was associated with a change in the ratios of bound to free forms of five lysosomal enzymes, a change in serum creatine phosphokinase and lactate dehydrogenase, and a change in the morphology of the myocardial cells. Isoprenaline treatment for 5 days induced a maximal change in heart weight, in the ratio of lysosomal enzymes, and in the serum enzymes. Thyroxine treatment was required for 15 days before maximal changes in heart weight, ratio, and serum enzymes were observed. In contrast, coarctation of the aorta caused a progressive change in heart weight, in the ratio of lysosomal enzymes, and in serum enzymes. These results suggest that necrosis of the myocardial cells does indeed accompany cardiac hypertrophy. It was further observed that autophagosomes, degenerating mitochondria in the myocardial cells during the induction of cardiac hypertrophy, and myofibril lysis were found, all of which confirms the suggestion of myocardial cell necrosis in the experimentally enlarged heart.
Animals↗
Metabolism of lipids in experimental hypertrophic hearts of rabbits.
Cardiac hypertrophy was induced in rabbits by subcutaneous injection of thyroxine or isoprenaline or by surgically constricting the abdominal aorta. Alterations in lipid metabolism were observed in these hypertrophic hearts. Thyroxine or isoprenaline treatment increased the fatty acids in the serum and stimulated a marked increase in total lipids, triglycerides, and fatty acids in the hypertrophied myocardium. Coarctation of the aorta, in contrast, induced a significant increase in these lipids without significantly affecting serum free fatty acids. Histochemical and morphological studies confirmed an increase in neutral lipids. It is suggested that the observed increase in fatty acids in the heart following thyroxine or isoprenaline treatment is related to the increase in serum free fatty acids, which is followed by an increase in the removal of serum fatty acids by the heart. However, the amount of serum fatty acids that is removed exceeds the amount that is oxidized, which leads to an increase in lipid stores. The increase in lipid stores in the heart following coarctation of the aorta probably corresponds to the decrease in myocardial concentrations of carnitine. Serum lipid levels following coarctation were not significantly different from those of controls.
Animals↗
The relationship between fibrosis and lactate dehydrogenase isoenzymes in the experimental hypertrophic heart of rabbits.
Cardiac hypertrophy was induced in rabbits by injecting either thyroxine or isoprenaline or by surgically constricting the abdominal aorta. An increase in heart weight was associated with a change in the lactate dehydrogenase isoenzyme pattern and an increase in fibrosis (as measured by hydroxyproline concentrations). Isoprenaline treatment led to a moderate increase in heart weight, a marked decrease in the heart/skeletal muscle subunit ratio of lactate dehydrogenase, and a marked increase in hydroxyproline. Thyroxine treatment led to a small increase in both heart weight and hydroxyproline and a small decrease in the heart/skeletal muscle subunit ration. Coarctation of the aorta, in contrast, caused a marked increase in heart weight, a moderate decrease in heart/skeletal muscle subunit ratio, and a moderate increase in hydroxyproline. These results suggest that the decrease in the heart/skeletal muscle subunit ratio of lactate dehydrogenase in the experimental hypertrophic heart reflects the extent of myocardial fibrosis, rather than changes within the hypertrophied myocardial cells.
Animals↗
Barrett's esophagus occurring as a complication of scleroderma.
Two patients had both scleroderma and a columnar epithelium-lined lower esophagus (Barrett esophagus). Features of Barrett's esophagus included high esophageal strictures in both patients and ulcer craters in the columnar area of one. Biopsy confirmed columnar epithelium in the lower esophagus of each patient. In these patients, the Barrett esophagus probably was a complication of scleroderma and resulted from long-standing gastroesophageal reflux.
Aged↗
Lactate dehydrogenase isoenzymes in the human hypertrophic heart.
Lactate dehydrogenase isoenzymes have been measured in human hearts at autopsy. As compared with normal hearts, hypertrophic hearts and ischaemic hypertrophic hearts showed a shift in the isoenzyme distribution. This shift appeared to be more closely associated with an increase in the relative proportion of fibrous tissue than with changes in the myocardial cells.
Cardiomegaly↗
The value of gastroscopy in clinical diagnosis: a computer-assisted study.
The additional information obtained by gastroscopy in patients already examined by upper gastrointestinal roentgenography was assessed. For this purpose, a data sheet for computer analysis was filled in at the time of gastroscopy and again at patient dismissal. Overall, gastroscopy resulted in an altered diagnosis in 18 percent of 1, 368 examinations, and in another 7 percent of cases there were findings of possible clinical significance. Gastroscopic findings differed significantly from x-ray findings in 7 to 35 percent of cases, depending on the indication for the procedure.
Computers↗