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Richard E Sampliner

Publications and source records attributed to Richard E Sampliner.

24 records · Page 2Linked to original sources
PubMed2002

Appearance and prognosis of dysplasia in Barrett's esophagus.

Dysplasia in a patient who has Barrett's esophagus (BE) is the first step in the neoplastic process. The grade of dysplasia correlates with the likelihood of developing adenocarcinoma of the esophagus during follow-up surveillance endoscopy and biopsy. Surveillance intervals are proposed based on the existing data of the likelihood of developing adenocarcinoma. In the future these intervals will be refined as a result of better definition of the risk factors the development of adenocarcinoma of the esophagus. Risk stratification of the individual patients by age, gender, grade of dysplasia, length of BE, length of hiatal hernia, and presence of genetic mutations will be possible.

Adenocarcinoma↗
PubMed2002

Barrett esophagus.

A number of publications have provided valuable insight into and data on the epidemiology, pathogenesis, diagnosis, risk factor evaluation, and treatment of patients with Barrett esophagus. Although the incidence of esophageal adenocarcinoma has rapidly increased over the past two decades, it is not clear whether there has been a parallel increase in the frequency of Barrett esophagus. The issue of surveillance endoscopy in patients with Barrett esophagus remains controversial; prospective data are still lacking. Bile reflux plays an important role in the pathogenesis of Barrett esophagus; however, this usually occurs in the presence of acid. Newer technology and techniques, including chromoendoscopy, magnification endoscopy, optical coherence tomography, and spectroscopy, have opened the field by providing a more accurate and "nonbiopsy" diagnosis of intestinal metaplasia and dysplasia. The field of biomarkers remains continues to expand and is providing insight into risk stratification of patients with Barrett esophagus. The exact role of acid suppression in patients with this premalignant disease remains controversial, and endoscopic therapies appear promising.

Journal Article↗
PubMed2002

Impact of esophageal acid exposure on the endoscopic reversal of Barrett's esophagus.

OBJECTIVE: Normalization of esophageal acid exposure had been assumed to be necessary for the reversal of Barrett's esophagus with endoscopic therapy. This assumption is examined by evaluating the esophageal pH in a group of patients undergoing reversal therapy with fixed high-dose proton pump inhibitor therapy and endoscopic multipolar electrocoagulation (MPEC). METHODS: Patients with Barrett's esophagus of 2-6 cm in length were treated with omeprazole (40 mg b.i.d.). They underwent 24-h esophageal pH monitoring 5 cm above the upper margin of the lower esophageal sphincter determined by a water-perfused catheter. They then underwent MPEC therapy to an endpoint of elimination of Barrett's (reversal) by both endoscopy and biopsy 6 months after the last MPEC session or failure to achieve visual (endoscopic) reversal after six treatment sessions. RESULTS: Twenty patients had 24-h pH testing and reached a reversal endpoint. Three patients had abnormal pH tests, two total and supine and one supine only. These patients had documented reversal. The remaining 17 patients had normal pH testing but five failed reversal therapy. CONCLUSION: Barrett's esophagus can be completely reversed with endoscopic therapy despite abnormal esophageal acid exposure. Also, patients can fail reversal even with normal esophageal acid exposure. The necessary reduction of esophageal acid exposure for reversal therapy has yet to be defined.

Adult↗
PubMed2002

Relationship between rate of change in acid exposure along the esophagus and length of Barrett's epithelium.

OBJECTIVE: Gastroesophageal reflux disease (GERD) plays a major role in the development of Barrett's esophagus. Recently, we demonstrated that duration of esophageal acid exposure in the distal esophagus correlates with the length of Barrett's mucosa. The aim of this study was to determine whether there is a relationship between the rate of the change in acid exposure along the esophagus and the length of Barrett's esophagus. METHODS: A total of 17 patients (16 men and one woman; mean age 66 +/- 15 yr, range 41-83 yr) with varying lengths of biopsy-proven Barrett's esophagus were recruited prospectively into the study. Ambulatory 24-h esophageal pH monitoring was performed using a commercially available pH probe with four sensors located 5 cm apart. For each patient, a least squares regression line of the fraction of the study that the pH was <4 against the height of the sensor above the lower esophageal sphincter was fit. The slope of the regression line was used to represent the rate of change in acid exposure. Linear regression analysis was conducted to analyze the relationship between the rate of change in acid exposure and the length of Barrett's mucosa. RESULTS: The mean Barrett's length was 5 +/- 3 cm (range 1-11 cm). Linear regression demonstrated a statistically significant relationship between the rate of change in acid exposure and the length of Barrett's esophagus for the 24-h duration of the study, as well as for the fraction of the study that patients were in the upright position (p = 0.0096 and 0.0076, respectively). For the supine position, the relationship did not reach statistical significance (p = 0.095). CONCLUSIONS: We demonstrated a significant relationship between the rate of change in acid exposure and the length of Barrett's mucosa. Thus, as the rate at which recorded acid exposure values increases from the proximal to distal esophagus, the length of Barrett's esophagus significantly increases (for percent total time and upright position).

Adult↗
PubMed2002

Acid suppression therapy may not alter malignant progression in Barrett's metaplasia showing p53 protein accumulation.

OBJECTIVES: Several previous studies have shown that malignant progression in Barrett's metaplasia (BM) occurs even in patients treated with fundoplication or acid suppression therapy (AST). The aim of this study was to test the hypothesis that AST may not alter malignant progression in BM if key genes involved in DNA repair and cell cycle control, particularly p53, are defective. METHODS: Initial and follow-up biopsies from 21 patients with BM treated with AST and observed for 1-13 yr were entered in the study. All biopsies were graded for dysplasia and evaluated for p53 protein accumulation and oxidative DNA damage by immunohiostochemistry, using antibodies to p53 and to 8-hydroxydeoxyguanosine, respectively. DNA ploidy was determined using image analysis. Statistical analysis was performed using Kaplan-Meier curves, log rank test, and multivariate regression. RESULTS: Patients with p53 positive initial biopsies were more likely to have progression in dysplasia grade (p = 0.022) and DNA ploidy status (p = 0.023) than those with p53 negative biopsies. In eight patients AST resulted in significant reduction in oxidative DNA damage in the five patients with p53-negative initial biopsies, but not the three with p53 positive ones (p = 0.0007). CONCLUSIONS: We conclude that failure of AST to alter malignant progression in BM may be due, at least in part, to defects in DNA repair and cell cycle control resulting from p53 gene mutation, present before AST treatment. Although AST may be effective in preventing further DNA damage, it is unlikely to alter progression in genetically unstable cells.

Barrett Esophagus↗