PubMed Health⌕ Search

Biomedical subjects

J H Peters

Publications and source records attributed to J H Peters.

At least 55 records · Page 3Linked to original sources
PubMed2000

Fields of aberrant CpG island hypermethylation in Barrett's esophagus and associated adenocarcinoma.

Esophageal adenocarcinoma (EAC) is thought to develop through a multistage process in which Barrett's metaplasia progresses through low- and high-grade dysplasia to invasive cancer. Transcriptional silencing of tumor suppressor genes by promoter CpG island hypermethylation has been observed in many types of human cancer. Analysis of CpG island hypermethylation in EAC has thus far been limited to the CDKN2A (p16) gene. In this study, we extend the methylation analysis of EAC to include three other genes, APC, CDH1 (E-cadherin), and ESR1 (ER, estrogen receptor alpha), in addition to CDKN2A. Molecular analysis can provide insight into the complex relationships between tissues with different histologies in Barrett's esophagus and associated adenocarcinoma. Therefore, we have mapped the spatial distribution of methylation patterns in six esophagectomy cases in detail. Hypermethylation of the four CpG islands was analyzed by the MethyLight technique in 107 biopsies derived from these six patients for a total of 428 methylation analyses. Our results show that normal esophageal squamous epithelium is unmethylated at all four CpG islands. CDH1 is unmethylated in most other tissue types as well. Hypermethylation of ESR1 is seen at high frequency in inflammatory reflux esophagitis and at all subsequent stages, whereas APC and CDKN2A hypermethylation is found in Barrett's metaplasia, dysplasia, and EAC. When it occurs, hypermethylation of APC, CDKN2A, and ESR1 is usually found in a large contiguous field, suggesting either a concerted methylation change associated with metaplasia or a clonal expansion of cells with abnormal hypermethylation.

Adenocarcinoma↗
PubMed2000

Is adenocarcinoma following esophagoduodenostomy without carcinogen in the rat reflux-induced?

BACKGROUND: A widely used rat model for reflux-induced esophageal adenocarcinoma in the absence of carcinogens involves induction of duodenoesophageal reflux by performance of esophagoduodenostomy. The aim of this study was to test the hypothesis that acid reflux reduces the incidence of adenocarcinoma in this animal model. METHODS: One hundred ninety 8-week-old male Sprague-Dawley rats were studied. The animals were randomly divided into four groups with a different type of reflux established in each group. Group 1 had an esophagoduodenostomy for duodenogastroesophageal reflux (n = 59), group 2 had an esophagoduodenostomy and a total gastrectomy for duodenoesophageal reflux (n = 54), group 3 had an esophagoduodenostomy and a total gastrectomy with acid supplementation with acidified water to control for the effect of the gastrectomy (n = 50), and group 4 had a total gastrectomy with Roux-en-Y reconstruction to eliminate all reflux (n = 25). One hundred eighty-eight surviving animals were sacrificed at 36 weeks of age and the resected esophagi were examined. RESULTS: All animals except the no reflux control group had severe reflux esophagitis. The frequency of tumor development was similar in all study groups. All of the tumors were well-differentiated adenocarcinomas that were located on the external surface of the bowel either at or immediately distal to the esophagoenteric anastomosis. The tumors appeared to arise from the submucosa and did not involve the overlying mucosa. There was no definite evidence of columnar lining of the esophagus but an admixture of squamous and columnar epithelium was found microscopically in all groups. This finding was unrelated to the presence and composition of reflux. CONCLUSIONS: Adenocarcinomas in this animal model are not reflux-induced and do not arise from the mucosa. Despite previous reports to the contrary, we suggest that this model may not be valid for the study of reflux-induced esophageal adenocarcinoma.

Adenocarcinoma, Mucinous↗
PubMed2000

Determinants of intestinal metaplasia within the columnar-lined esophagus.

HYPOTHESIS: The clinical and physiological features of patients with short segments of columnar-lined esophagus (CLE) with and without intestinal metaplasia (IM) are distinct. DESIGN: Retrospective case series. SETTING: University tertiary referral center. PATIENTS: Sixty-five consecutive patients with a 2-cm or shorter length of endoscopically visible CLE. INTERVENTIONS: The type of CLE and the presence of Helicobacter pylori were determined by histopathologic examination of esophageal and gastric antrum biopsy specimens. All patients underwent esophageal manometry and simultaneous 24-hour pH and bilirubin monitoring. MAIN OUTCOME MEASURES: Clinical and physiological data were compared in patients with and without IM. RESULTS: Thirty-six patients had IM and 29 had cardiac-type mucosa without IM in biopsy specimens from the CLE. There was no significant difference in age or sex distribution, but the duration of symptoms was significantly longer in patients with IM (10 vs 5 years; P = .03). Abnormal esophageal acid exposure was found in 30 (83%) of 36 patients with IM and 23 (79%) of 29 patients without IM. The prevalence of abnormal bilirubin exposure was significantly higher in patients with IM (75% [27/36]) than in those without IM (41% [12/29]; P = .01). There was no significant difference in the prevalence of H pylori infection between the 2 groups (8% vs 10%; P >.99). CONCLUSIONS: Patients with short segments of CLE and IM have similar esophageal acid exposure but significantly higher frequency of abnormal bilirubin exposure and longer median duration of reflux symptoms than patients without IM. Therefore, CLE, regardless of histological type, is a manifestation of gastroesophageal reflux disease. The presence of duodenoesophageal reflux and the duration of reflux seem to be important in the pathogenesis of IM.

Barrett Esophagus↗
PubMed2000

Laparoscopic esophageal surgery.

In its 9-year history, laparoscopic esophageal surgery has become second only to gallbladder surgery in the frequency of minimally invasive procedures performed in routine surgical practice. Laparoscopic fundoplication has assumed a central role in the surgical treatment of gastroesophageal reflux. Laparoscopic myotomy has emerged as the optimal form of therapy for achalasia, and staging laparoscopy has been identified as an important adjunct to the preoperative evaluation of esophageal and gastroesophageal junction carcinoma. Laparoscopic paraesophageal hernia repair and remedial laparoscopic antireflux surgery currently are gaining acceptance. Laparoscopic gastroplasty, esophagectomy, and diverticulectomy are undergoing clinical trials, and their roles remain to be defined.

Diverticulum, Esophageal↗
PubMed2000

Alkaline phosphatase expression during monocyte differentiation. Overlapping markers as a link between monocytic cells, dendritic cells, osteoclasts and osteoblasts.

Human monocytes (Mo) in culture can be differentiated into macrophages (M phi), dendritic cells (DC) and osteoclasts. In addition, we have established a Mo-derived in vitro granuloma model which here was compared with ex-vivo isolated foreign body granuloma cells. In these models overlapping phenotypes developed between monocyte-derived dendritic cells (MoDC), osteoclasts, M phi, and osteoblasts. In Mo cultures granulomas were induced by immobilized particulate material. AP activity (osteoblast marker) was found to be co-expressed with cytoplasmic tartrate resistant acid phosphatase (TRAP) as a marker of osteoclasts. While proliferating, the number of AP+ cells decreased, being replaced by cells co-expressing the osteoclast markers vitronectin receptor (VNR) and TRAP. Coexpression of the Mo/M phi marker CD68 with AP or VNR confirmed the monocytic origin of the cells. When Mo were treated with interleukin-4 (IL-4), the number of AP+ cells markedly increased and remained stably expressed over 12 days. In explants from ex vivo granulomas obtained from endoprosthetic revisions the major cell type was the AP+ cell co-expressing CD68. The bone-specific alkaline phosphatase (BAP) as a marker of osteoblasts was detected by FACS analysis in the ex vivo granuloma cells. By RT-PCR the mRNA for osteocalcin, which is a highly specific marker for osteoblasts, was detected. From our results we conclude an ontogenetic relationship between macrophages, DC and osteoclasts. Furthermore, the data suggest a transdifferentiation between Mo and osteoblasts.

Alkaline Phosphatase↗
PubMed2000

Laparoscopic repair of large type III hiatal hernia: objective followup reveals high recurrence rate.

BACKGROUND: Recent studies based on symptomatic outcomes analyses have shown that laparoscopic repair of large type III hiatal hernias is safe, successful, and equivalent to open repair. These outcomes analyses were based on a relatively short followup period and lack objective confirmation that the hernia has not recurred. The aim of this study was to compare the outcomes of laparoscopic and open repair of large type III hiatal hernia using both symptomatic evaluation and barium study to assess the integrity of the repair. STUDY DESIGN: Fifty-four patients underwent repair of a large type III hiatal hernia between 1985 and 1998. The surgical approach was laparotomy in 13, thoracotomy in 14, and laparoscopy in 27. An antireflux procedure was included in all patients. Symptomatic outcomes were assessed using a structured questionnaire at a median of 24 months and was complete in 51 of 54 patients (94%). A single radiologist, without knowledge of the operative procedure, assessed the integrity of the repair using video esophagram. Videos were performed at a median of 27 months (35 months open and 17 laparoscopic) and were completed in 41 of 54 patients (75%). RESULTS: Symptomatic outcomes were similar in both groups with excellent or good outcomes in 76% of the patients after laparoscopic repair and 88% after an open repair. Reherniation was present in 12 patients and was asymptomatic in 7. A recurrent hernia was present in 12 of the 41 patients (29%) who returned for a followup video esophagram. Forty-two percent (9 of 21) of the laparoscopic group had a recurrent hernia compared with 15% (3 of 20) of the open group (p < 0.001 log-rank value on recurrence-free followup). CONCLUSIONS: Laparoscopic repair of type III hiatal hernias is associated with a disturbingly high (42%) prevalence of recurrent hernia. More than half such recurrences have few, if any, symptoms.

Adult↗
PubMed2000

Evaluation of the intestinal microflora in the rat model for esophageal adenocarcinoma.

Surgically induced duodenal reflux results in cancer development in the rat esophagus. One proposed mechanism of carcinogenesis relies on the production of carcinogens in the presence of bacterial overgrowth. Against this background, intestinal microflora in the rat jejunum was analyzed before and after reflux-inducing surgery. Total gastrectomy and esophagojejunostomy were performed on Sprague-Dawley rats to produce esophageal reflux of duodenal juice (n = 12). Three days before surgery they were randomized into three groups: animals which received tap water; animals which received acidified water at pH 1.8; and animals subjected to oral decontamination with triple antibiotics. During surgery and at autopsy after 2 weeks, intestinal juice was aspirated and analyzed immediately for bacterial content. The physiologic microflora of the rat jejunum contained Lactobacillus spp. and Bacteroides spp., both of which were resistant to the antibiotic regimen. Bacterial overgrowth with fecal bacteria was found following surgery. Acidified water did not alter the intestinal microflora. Triple antibiotics eliminated Escherichia coli and Proteus spp. and reduced the concentration of Enterococcus spp. Bacterial overgrowth by bacteria of the fecal flora occurs in the rat model of esophageal adenocarcinoma with the potential to catalyze the production of carcinogens.

Adenocarcinoma↗
PubMed2000

Minimally invasive approaches to antireflux surgery.

Gastroesophageal reflux disease is one of the most common disorders affecting western civilization. Historically, surgical antireflux therapy was reserved for patients who had failed medical therapy, typically in the presence of refractory ulcers or difficult-to-manage strictures. More recently, with improvements in acid control, these acid-pepsin-related complications of reflux have been replaced by the malignant complications of reflux disease, with emphasis now on total control of reflux. Recent developments in surgical technique and the demonstrated effectiveness of a variety of minimally invasive treatment options have changed our approach to these patients. This article summarizes the recommended diagnostic evaluation of patients with reflux symptoms and the current indications for antireflux surgery. The techniques of commonly performed minimally invasive antireflux procedures are described along with a review of the results to be expected. Future prospects for improving the management of reflux are discussed; these include recently described nonsurgical methods for restoring competency to the lower esophageal sphincter.

Cost-Benefit Analysis↗
PubMed2000

Definition of histopathologic changes in gastroesophageal reflux disease.

A series of 71 patients with multiple measured biopsies of the gastroesophageal junctional region permitting assessment of the presence and length of different glandular epithelial types is presented. All but nine of 53 patients in whom a 24-hour pH study was performed had abnormal reflux, suggesting that endoscopic recognition of an abnormal columnar mucosa at the gastroesophageal junction sufficient to precipitate multiple-level biopsies indicates a high probability of abnormal reflux. All patients had cardiac mucosa (CM) or oxyntocardiac mucosa (OCM). CM was present in 68 of 71 patients. The prevalence of intestinal metaplasia increased with increasing CM+OCM length, and was present in all 22 patients with a CM+OCM length >2 cm and in 20 of 49 patients with a CM+OCM length <2 cm. Patients with a CM+OCM length >2 cm had a markedly higher acid exposure than patients with a CM+OCM length <2 cm. The findings suggest that the presence of CM and OCM in the junctional region are predictive of abnormal acid exposure, and that increasing OCM+CM length correlates strongly with the amount of acid exposure. The histologic finding of CM and OCM represents a sensitive histologic criterion for gastroesophageal reflux rather than normal epithelia. These diagnostic criteria represent the first useful histologic definitions for assessing the presence and severity of reflux.

Gastric Mucosa↗
PubMed2000

Gastroesophageal reflux disease in asthma: effects of medical and surgical antireflux therapy on asthma control.

OBJECTIVE: To critique the English-language reports describing the effects of medical and surgical antireflux therapy on respiratory symptoms and function in patients with asthma. METHODS: The Medline computerized database (1959-1999) was searched, and all publications relating to both asthma and gastroesophageal reflux disease were retrieved. RESULTS: Seven of nine trials of histamine-receptor antagonists showed a treatment-related improvement in asthma symptoms, with half of the patients benefiting. Only one study identified a beneficial effect on objective measures of pulmonary function. Three of six trials of proton pump inhibitors documented improvement in asthma symptoms with treatment; benefit was seen in 25% of patients. Half of the studies reported improvement in pulmonary function, but the effect occurred in fewer than 15% of patients. In the one study that used optimal antisecretory therapy, asthma symptoms were improved in 67% of patients and pulmonary function was improved in 20%. Combined data from 5 pediatric and 14 adult studies of anti-reflux surgery indicated that almost 90% of children and 70% of adults had improvement in respiratory symptoms, with approximately one third experiencing improvements in objective measures of pulmonary function. CONCLUSIONS: Fundoplication has been consistently shown to ameliorate reflux-induced asthma; results are superior to the published results of antisecretory therapy. Optimal medical therapy may offer similar results, but large studies providing support for this assertion are lacking.

Adult↗
PubMed2000

Clinical significance of p53 mutations in adenocarcinoma of the esophagus and cardia.

OBJECTIVE: To compare the frequency and spectrum of p53 gene mutations in adenocarcinomas of the esophagus and cardia and to compare clinical and pathologic features in patients with p53 mutant and nonmutant cancers. SUMMARY BACKGROUND DATA: The p53 gene is commonly mutated in human cancers, and a p53 mutation is reported to be present in more than 50% of esophageal adenocarcinomas. Although many studies have investigated the frequency of p53 protein overexpression in adenocarcinomas of the esophagus or esophagogastric junction, few studies have assessed the frequency and clinical significance of p53 mutations in these tumors. In particular, the prognostic importance of p53 mutation is uncertain. Adenocarcinomas of the esophagus and cardia share many epidemiologic and pathologic features, but it is controversial whether they represent the same tumor. A comparison of the frequency and spectrum of mutations in adenocarcinomas of the esophagus and cardia would test whether these tumors are also similar at the molecular level. METHODS: DNA was isolated from microdissected paraffin-embedded tumor tissues of patients who underwent esophagogastrectomy for adenocarcinoma of the esophagus (n = 19), cardia (esophagogastric junction, n = 12), or subcardia (n = 6). Exons 5 to 8 of the p53 gene were analyzed for the presence of mutations using the polymerase chain reaction with single-strand conformation polymorphism and DNA sequencing of bands showing abnormal mobility. The presence of mutation was confirmed by selective hybridization of a mutant-specific oligonucleotide to DNA isolated from the tumor. RESULTS: p53 mutations were identified in 18 of 37 (48.6%) tumors. Patients with p53 mutant tumors were significantly younger and had a significantly poorer prognosis. There was a similar prevalence of p53 mutations in adenocarcinomas of the esophagus (53%) and cardia (58%). In contrast, mutations were relatively uncommon in subcardia adenocarcinomas (one mutant tumor [17%]). The types of mutations found in the esophageal and the cardia cancers were also similar. CONCLUSIONS: Adenocarcinomas of the esophagus and cardia have a similar frequency and spectrum of p53 gene mutations, suggesting that these tumors have a common pathogenesis. Patients with mutations are younger, have signs of more advanced disease, and have a poorer prognosis than patients without mutations.

Adenocarcinoma↗
PubMed2000

Surgery, radiotherapy, and chemotherapy in carcinoma of the esophagus.

Esophageal carcinoma remains a highly lethal disease that has shown a recent profound increase in prevalence and an equally dramatic epidemiologic shift. There is a well recognized causal association between gastroesophageal reflux disease and adenocarcinoma of the esophagus, and the molecular events underlying this progression from mucosal injury, to metaplasia, to dysplasia, to carcinoma are now becoming clear. Current diagnostic modalities and preoperative staging systems all have significant limitations. Fortunately, chemoprevention strategies and the identification of clinically useful molecular biomarkers that may be used to stage disease and select appropriate therapy are on the horizon. The extent of surgical resection for esophageal carcinoma remains an area of great controversy. Disease that is confined to the mucosa is being diagnosed more commonly, and endoscopic ablative techniques have been proposed. To date, however, preoperative discrimination of tumor depth and presence of regional nodal metastases remains inadequate in these very early lesions, and caution is urged before adopting therapies that may compromise cure. For disease penetrating the mucosa, the extent of surgical therapy must be tailored by the objectives of treatment (cure vs palliation) and preoperative stage. Surgical resection is the current standard of care, with combined-modality therapy reserved for prohibitive surgical candidates. No clear survival benefit has been documented for neoadjuvant radiotherapy or chemotherapy alone. The results of preoperative combined-modality therapy, including three prospective, randomized trials, are encouraging but to date have not shown a definite benefit.

Journal Article↗
PubMed1999

Loss of function of Trp53, but not Apc, leads to the development of esophageal adenocarcinoma in mice with jejunoesophageal reflux.

INTRODUCTION: APC and TP53 are tumor suppressor genes known to be altered frequently in human esophageal adenocarcinoma (EAC), which arises as a complication of reflux disease. To determine the functional role of these genes in the development of EAC, we have created reflux in mice gene-targeted for either Trp53 or Apc. METHODS: Wild-type (WT), p53-knockout (Trp53-/-), or Apc-mutated (ApcMin/+) mice were generated in our breeding colony. Total gastrectomy with esophagojejunostomy was performed at 6 weeks of age, creating jejunoesophageal reflux. Unoperated control mice were maintained under identical conditions. Mice were sacrificed at 30 weeks of age. Histology of the esophagus and jejunal anastamosis or gastroesophageal junction was reviewed by a single pathologist blinded to the genotype of the animal. RESULTS: The esophagus was normal in all of the unoperated mice (6 ApcMin/+, 6 WT, and 6 Trp53-/-). All operated mice (6 ApcMin/+, 12 WT, and 4 Trp53-/-) had esophagitis, with squamous hyperplasia and early focal ulceration. Barrett's metaplasia was identified in 33% of the operated ApcMin/+ (2/6) and 25% of the Trp53-/- (1/4) mice, but not in the WT mice. Of 4 operated Trp53-/- mice, all developed severe dysplasia of the squamous epithelium and 2 (50%) had EAC on histology, although no gross tumors were seen. No severe dysplasia or carcinoma was identified in any of the ApcMin/+ or WT mice. CONCLUSIONS: Loss of either Trp53 or Apc leads to the development of columnar metaplasia, whereas loss of Trp53, but not Apc, leads to development of cancer in mice with jejunoesophageal reflux.

Adenocarcinoma↗
PubMed1999

Short esophagus: analysis of predictors and clinical implications.

HYPOTHESIS: Preoperative assessment can identify the predictors of esophageal shortening in patients with gastroesophageal reflux disease. DESIGN AND SETTING: Patient comparison study in a university-based tertiary care center. PATIENTS: A total of 236 patients with gastroesophageal reflux disease underwent primary antireflux procedures. Sixty-five patients were suspected of having a short esophagus and underwent a transthoracic approach. In 37 patients, a lengthening procedure was necessary to avoid tension on the repair. The remaining 28 patients were thought-after complete esophageal mobilization-to have sufficient length for a repair without needing a gastroplasty. An abdominal approach (laparoscopic Nissen fundoplication) was performed on 171 patients judged to have normal esophageal length. MAIN OUTCOME MEASURES: Univariate and multivariate analyses of preoperative variables were performed to identify predictors of a short esophagus. RESULTS: On univariate analysis, manometric esophageal length below the fifth percentile of normal was associated with esophageal shortening. On multivariate analysis, only the presence of an esophageal stricture predicted the need for a Collis gastroplasty (odds ratio, 7.5). The presence of Barrett's esophagus of 3 cm or greater identified patients in whom the transthoracic esophageal mobilization alone was sufficient (odds ratio, 3.4). CONCLUSIONS: The presence of a stricture was associated with esophageal shortening sufficient to require a gastroplasty. Transthoracic esophageal mobilization alone was usually sufficient to perform a safe repair without tension in patients with a Barrett's esophagus of 3 cm or greater.

Adolescent↗
PubMed1999

Helicobacter pylori is not associated with the manifestations of gastroesophageal reflux disease.

HYPOTHESIS: Helicobacter pylori is not associated with gastroesophageal reflux disease and its complications, including adenocarcinoma of the esophagus and the gastroesophageal junction (GEJ). DESIGN: Retrospective analysis. SETTING: University tertiary referral center. PATIENTS: Two hundred twenty-nine patients with symptoms suggestive of foregut disease underwent esophageal manometry, 24-hour pH monitoring, and upper gastrointestinal tract endoscopy, with biopsy specimens obtained from the gastric antrum, the GEJ, and the distal esophagus. In these and in an additional 114 patients with adenocarcinoma of the esophagus and the GEJ, the presence of H. pylori was determined by Giemsa stain. The presence of gastroesophageal reflux disease, defined by abnormal esophageal acid exposure, and its manifestations (carditis, erosive esophagitis, intestinal metaplasia limited to the GEJ, Barrett esophagus, and adenocarcinoma of the esophagus and GEJ) were correlated with the presence of H. pylori. RESULTS: Helicobacter pylori was found on the biopsy specimens of the gastric antrum in 14.0% (32/229) of the patients with benign disease. It was not related to the features of gastroesophageal reflux disease, including abnormal esophageal acid exposure, erosive esophagitis, or Barrett esophagus. The presence of inflamed cardiac mucosa at the GEJ or carditis was inversely related to H. pylori infection and strongly associated with increased esophageal acid exposure. There was no association between the presence of intestinal metaplasia and H. pylori infection. Helicobacter pylori was found in 22 (19.3%) of the 114 patients with esophageal adenocarcinoma, which was not different from the prevalence of H. pylori in patients with benign disease. CONCLUSION: Helicobacter pylori plays no role in the pathogenesis of gastroesophageal reflux disease or its complications.

Adolescent↗
PubMed1999

The pattern of esophageal acid exposure in gastroesophageal reflux disease influences the severity of the disease.

HYPOTHESIS: There is an independent association between the different patterns of esophageal acid exposure in gastroesophageal reflux disease and the severity of the disease. DESIGN: Case-comparison study. SETTING: Department of surgery at a university hospital. PATIENTS: A group of 401 patients with increased esophageal acid exposure divided into 4 groups according to the pattern of reflux: postprandial (n = 41), upright (n = 74), supine (n = 129), and bipositional (n = 157). MAIN OUTCOME MEASURES: The prevalence of mucosal injury and the status of the lower esophageal sphincter and esophageal motility were assessed in each group. RESULTS: The likelihood of having indicators of the severity of gastroesophageal reflux disease increases progressively from postprandial to upright, supine, and bipositional reflux. CONCLUSIONS: The pattern of esophageal acid exposure in gastroesophageal reflux disease is an objective predictor of the severity of disease and could be used for therapeutic decisions.

Case-Control Studies↗
PubMed1999

Endoscopic grading of the gastroesophageal valve in patients with symptoms of gastroesophageal reflux disease (GERD).

BACKGROUND: It has been suggested that endoscopic grading of the gastroesophageal flap valve is a good predictor of the reflux status. METHODS: To test this hypothesis, 268 symptomatic patients underwent endoscopic grading of the gastroesophageal valve using Hill's classification, with grades I through IV. Esophageal acid exposure, lower esophageal sphincter characteristics, and the degree of esophageal mucosal injury were compared among the groups. RESULTS: The prevalence of a mechanically defective sphincter, abnormal esophageal acid exposure, erosive esophagitis, and Barrett's esophagus increased with increasing alteration of the gastroesophageal valve. The presence of a grade IV valve indicated increased esophageal acid exposure in 75% of patients. As a predictor, this is similar to lower esophageal sphincter pressure but not as good as the presence of esophageal mucosal injury. CONCLUSIONS: Endoscopic grading of the gastroesophageal valve provides useful information about the reflux status but is less useful as an indicator of gastroesophageal reflux disease (GERD) than the presence of esophageal mucosal injury.

Adolescent↗