Evaluation of autofluorescence colonoscopy for the detection and diagnosis of colonic polyps.

BACKGROUND: Colorectal cancer is the second most common cause of death in the United Kingdom. Most cancers are believed to arise within preexisting adenomas. Although colorectal adenomas have a clear neoplastic potential, hyperplastic polyps do not. It, therefore, would be helpful to be able to differentiate between different polyps at a colonoscopy. Autofluorescence (AF) endoscopy has been developed to enhance conventional white light (WL) endoscopy in the diagnosis of GI lesions. OBJECTIVE: The aim of the present study was to evaluate whether AF colonoscopy can facilitate endoscopic detection and differentiation of colorectal polyps. DESIGN: Patients were invited to attend for colonic assessment with both AF and WL endoscopy. AF readings, pictures, and biopsy specimens were taken of any visible pathology and of any high AF areas. SETTING: Gartnavel General Hospital, Glasgow, U.K. PATIENTS: A total of 107 patients were assessed. INTERVENTION: Each patient was assessed with AF and WL colonoscopy. MAIN OUTCOME MEASUREMENTS: An AF intensity ratio (AIR) was calculated for each polyp (ratio of direct polyp AF reading/background rectal AF activity). RESULTS: A total of 75 polyps were detected: 54 adenomatous and 21 hyperplastic polyps. Colorectal adenomas had a significantly higher AIR compared with hyperplastic polyps (median, interquartile range): adenoma (3.54, 2.54-5.00] versus hyperplastic (1.60, 1.30-2.24); P = .0001). When using an AIR with the empirically cutoff value of 2.3, AF endoscopy had a sensitivity of 85% and a specificity of 81% at distinguishing adenomatous polyps from hyperplastic polyps. CONCLUSIONS: AF colonoscopy may be a valuable tool for the visual distinction between adenomatous and hyperplastic polyps.

Endoscopy has minimal impact on mortality from upper gastrointestinal cancer in patients older than 55 years with uncomplicated dyspepsia.

INTRODUCTION: The objective of the study was to determine the effectiveness of endoscopy to detect curable upper gastrointestinal malignancy in patients older than 55 years presenting with uncomplicated dyspepsia. METHODS: A cohort study was performed in North Glasgow Health Trust. One hundred and thirty-one patients older than 55 years of age, diagnosed to have upper gastrointestinal cancer within the North Glasgow Trust between January 1995 and December 1997, identified by the West of Scotland Cancer Registry were included. The main outcome measures were the proportion of upper gastrointestinal cancers that present in patients older than 55 years with uncomplicated dyspepsia, and the proportion of patients that presented with uncomplicated dyspepsia who have curable upper gastrointestinal cancer. RESULTS: Of the 131 cancer cases identified, only 30 (23%) had dyspepsia (complicated or uncomplicated) as their predominant symptom and only eight (6%) patients presented with uncomplicated dyspepsia. Of those eight patients presenting with uncomplicated dyspepsia and found to have upper gastrointestinal cancer, six were found to have lymph node metastases and/or extensive metastases at the time of diagnosis. Each of these six patients died from their cancer within 39 months of diagnosis. Of the two patients presenting with uncomplicated dyspepsia without evidence of lymph node spread, one died 55 days after diagnosis. Only one patient presenting with uncomplicated dyspepsia and found to have cancer remains alive at 5-year follow-up. CONCLUSIONS: Of the 131 patients diagnosed with upper gastrointestinal cancer, only eight presented with uncomplicated dyspepsia and only one of these was cured. Consequently a policy of endoscoping patients older than 55 years with uncomplicated dyspepsia will reduce death from upper gastrointestinal cancers by less than 1% in our population.

Gastroduodenal disease, Helicobacter pylori, and genetic polymorphisms.

Over the past 20 years, there has been marked progress in our understanding of the role of genetic and environmental factors in the etiology of gastroduodenal disease. Helicobacter pylori infection now is recognized to be the most important environmental factor for both noncardia gastric cancer and peptic ulcer disease. The likelihood of the infection resulting in significant disease depends on genetic polymorphisms influencing the virulence of the organism. However, the specific pattern of disease induced by the infection is determined to a great extent by genetic polymorphisms in the host that govern the local gastric immune response elicited. Genetic factors also are important in the treatment of gastroduodenal diseases. Polymorphisms of host CYP2C19 influence the pharmacokinetics and clinical efficacy of proton pump inhibitor therapy.

Prediction of malignant potential in reflux disease.

There is interest in noninvasive means of identifying reflux patients at increased risk of developing Barrett's esophagus and adenocarcinoma. In this issue, Gough et al. studied the prevalence of polymorphisms of cytokine genes in patients with uncomplicated esophagitis versus Barrett's/esophageal adenocarcinoma. They reported a difference between the groups with respect to the interleukin-1 receptor antagonist and interleukin-10 genes. However, the number of comparisons carried out mean that the association is not statistically significant and further studies will be required to confirm/refute the association. The genetic markers reported would unfortunately be of little value in predicting individual risk of esophageal adenocarcinoma as they are weak predictors and relatively rare within the esophagitis population. The findings of this study demonstrate the general principle that polymorphisms of individual genes are of limited value in identifying patients at risk of sporadic-types of cancer such as most cases of esophageal adenocarcinoma.

Helicobacter pylori eradication releases prolonged increased acid secretion following omeprazole treatment.

BACKGROUND & AIMS: Rebound increased acid secretion has been observed at 2 weeks after discontinuing omeprazole treatment in Helicobacter pylori -negative, but not H. pylori -positive, subjects. It is unknown whether this is a prolonged phenomenon or whether a similar phenomenon appears later in H. pylori positives or is released by eradication therapy. The aims of this study were to answer these 3 questions. METHODS: Twelve H. pylori -negative and 20 H. pylori -positive subjects were studied. Each had a basal, submaximal, and maximal pentagastrin-stimulated acid secretion study before, during, and at 7, 14, 28, 42, and 56 days after a 56-day course of omeprazole 40 mg/day. Ten of the H. pylori -positive subjects had their infection eradicated during the last week of treatment. RESULTS: In the H. pylori -negative subjects, there was rebound secretion of submaximal (P < 0.003) and maximal (P < 0.003) acid output, which persisted until at least 56 days after discontinuing omeprazole. The H. pylori -uneradicated subjects had no rebound increased secretion other than in maximal acid output at 28 (P < 0.01) and at 42 days after treatment (P < 0.02). In those eradicated of H. pylori close to the end of omeprazole, there was rebound increased secretion of submaximal acid output (P < 0.04) lasting until 56 days and of maximal acid output (P < 0.01) lasting until 28 days after treatment. CONCLUSIONS: Rebound increased acid secretion following omeprazole is a prolonged phenomenon in H. pylori -negative subjects. There is little evidence of it in H. pylori -infected subjects, but eradicating the infection releases the phenomenon. The accentuated H. pylori -related oxyntic gastritis induced by omeprazole is likely to protect against the rebound phenomenon.

Barrett's esophagus evokes a quantitatively and qualitatively altered response to both acid and hypertonic solutions.

OBJECTIVE: The stomach contents become hypertonic after a meal and provide esophageal refluxate that is both acidic and hypertonic. This study examined the symptomatic response to esophageal exposure to hypertonic and acidic solutions in patients with gastroesophageal reflux disease (GERD) and Barrett's esophagus. METHODS: Symptom intensity and character were measured in double-blind fashion during esophageal instillation of water, hypertonic saline (osmolality 1030 mOsm/kg), hydrochloric acid (pH 1 and 2.5), and acidified hypertonic saline (pH 1 and 2.5). The studies were performed in healthy controls and GERD patients with and without Barrett's esophagus. RESULTS: The GERD patients with Barrett's differed from the non-Barrett's GERD patients in being less sensitive to acid (mean intensity score, 2.3 vs 4.8, p < 0.05), more sensitive to hypertonic saline (1.3 vs 0.4, p < 0.05) and by showing an additive effect when the acid and hypertonic solutions were combined, resulting in similar scores in the two patient groups to the combination (4.4 vs 4.3). The frequency of nausea was higher in the Barrett's group compared to the other GERD patients after hypertonic saline (21% vs 0%, p < 0.05), acid (50% vs 21%, p < 0.05) and the acid hypertonic combination (71% vs 29%, p < 0.05). CONCLUSIONS: Barrett's mucosa is associated with reduced symptomatic response to acid, increased response to hypertonic solutions, and a higher incidence of nausea in response to either stimulus.