Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Barrett's esophagus is an end-stage gastroesophageal reflux complication with a potential for malignant transformation. This condition probably is involved in esophageal cancer being perceived today as the most rapidly increasing cancer in Western countries. Numerous observations suggest that standard antireflux operations fail over time because of long-term inflammatory and fibrotic changes in the esophageal wall that cause shortening of the esophagus. The addition of esophageal elongation by gastroplasty provides a reliable repair by creation of a tension-free repair, whereas the durable antireflux effects are provided by the total fundoplication around the neoesophagus. The restored LES tone further helps control the mucosal damage and the chronic inflammatory changes. Complete regression of the abnormal mucosa still does not occur, and persistent irritation of that mucosa still entails the risk for progression toward dysplasia. The natural history of the columnar-lined mucosa in BE may be altered by medical or surgical intervention. It is too early to judge in which settings these interventions will be meaningful.
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PMID:Results of the Collis-Nissen gastroplasty to control reflux disease in patients who have Barrett's esophagus. 1190 25

The incidence rate of adenocarcinoma of the esophagogastric junction (AEG) is increasing in association with the epidemiologic rise in distal esophageal adenocarcinoma and gastric cardial (AEG type III) tumors. The overall survival rate is poor in most patients with AEG because lymph node or visceral metastases are frequently present at the time patients become symptomatic. A few patients are identified early in the disease because of screening for gastroesophageal reflux and Barrett's esophagus. Early stage AEG (T1N0 or T2NO, carcinoma in situ, or severe dysplasia ) can in many instances be cured with surgery alone. Ablative treatments for early stage AEG, including endoscopic fulguration by cautery and laser or photodynamic therapy, are investigational at this time. Locoregionally advanced AEG (T3, T4, N1, or M1a ) without distant systemic metastases (M1b) has a poor overall survival rate with surgery alone or definitive chemotherapy and radiation therapy without surgery. Analysis of the use of multimodality treatment strategies for locoregionally advanced AEG types I and II have demonstrated improved survival rates in two small phase III trials with preoperative concurrent chemoradiotherapy followed by surgical resection. In contrast, three small phase III trials with preoperative concurrent or sequential chemoradiotherapy in patients with predominantly squamous cell carcinoma did not demonstrate any clear survival advantage. Additionally, a randomized phase III study evaluating preoperative chemotherapy without radiation therapy in esophageal cancer (predominantly adenocarcinoma) has demonstrated no survival benefit. In light of these results, additional large randomized phase III studies are needed to confirm the potential benefit of preoperative concurrent chemoradiotherapy. At the present time, preoperative chemoradiotherapy remains investigational. For locoregionally advanced gastric adenocarcinoma, including AEG type III, postoperative concurrent 5-fluorouracil (5-FU)-based chemoradiotherapy is associated with improved survival as demonstrated in a recently completed random assignment trial (INT 0116). As a result, surgery with postoperative chemoradiotherapy has recently become the standard of care for patients with AJCC stage II and III gastric adenocarcinoma (including patients with AEG type III). Metastatic AEG (M1b) should be treated with palliative chemotherapy (in good performance patients) or supportive care (poor performance) in asymptomatic patients. Radiation therapy and endoscopic stent placement (expandable wire mesh) can be used to palliate dysphagia in patients with M1b disease. The development of expandable stents and improved radiotherapy has obviated surgical bypass to palliate patients with symptomatic, metastatic AEG.
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PMID:Gastroesophageal junction adenocarcinoma. 1205 46

Helicobacter pylori is uniquely adapted to colonize the human stomach. Infection leads to a range of subclinical and clinical outcomes that depend on properties of the infecting strain, the host, and the environment. Eradication therapy is indicated for infected persons who develop peptic ulcer disease or gastric lymphoma or who are beginning long-term treatment with nonsteroidal anti-inflammatory drugs. However, treatment may worsen gastroesophageal reflux disease and increase the risk of esophageal cancer. H. pylori infections can be diagnosed noninvasively and can be eradicated with approximately 85% success by a variety of multidrug, 7-14-day regimens. Unfortunately, antibiotic resistance is affecting treatment effectiveness in the United States and abroad. A more complete understanding of the variation in H. pylori pathogenesis should lead to clearer recommendations about treatment for infected persons who have neither peptic ulcer disease nor gastric lymphoma.
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PMID:Helicobacter pylori: consensus and controversy. 1211 96

In western industrialized countries, esophageal cancer is a rare entity. While smoking and alcohol are the major risk factors for squamous cell carcinoma, the most important etiological factor for adenocarcinoma is Barrett's esophagus caused by gastro-esophageal reflux. Over the past few decades there has been a dramatic increase in the incidence of adenocarcinoma. The prognosis for both types of esophageal cancer is poor, with a 5-year survival rate of < 10%. Only early stages have a good prognosis. While prevention of squamous cell carcinoma is limited to avoiding drinking and smoking, prevention of adenocarcinoma requires endoscopic surveillance of Barrett's esophagus and the treatment of any dysplasia arising in it.
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PMID:[Reflux, smoking, alcohol. Approach to prevention of esophageal carcinoma]. 1219 74

Adenocarcinoma of the esophagus and the gastroesophageal junction is the twentieth most common malignancy in the United States. In developed countries, the incidence of esophageal adenocarcinoma is increasing 5% to 10% per year. Despite the use of endoscopy for earlier detection, mortality from esophageal adenocarcinoma has not declined. Using an evidence-based approach, we review screening methods for esophageal adenocarcinoma, including the use of a symptom questionnaire, identification of patients with a family history of Barrett's esophagus, peroral or transnasal endoscopy, barium swallow, fecal occult blood testing, and brush and balloon cytology. Screening has not been shown to reduce rate of progression of Barrett's esophagus to esophageal cancer. Many treatment options for dysplastic Barrett's esophagus or early carcinoma appear effective, but long-term follow-up data are not available. There is currently insufficient evidence supporting population-based screening for Barrett's esophagus. Several risk factors, including severe reflux symptoms, male sex, and obesity, may identify patients with gastroesophageal reflux disease who are at the greatest risk of the development of cancer.
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PMID:Screening for esophageal adenocarcinoma: an evidence-based approach. 1242

Screening and surveillance for Barrett's esophagus have been proposed as strategies for preventing deaths from esophageal adenocarcinoma. A meaningful discussion on the cost efficacy of screening and surveillance for Barrett's esophagus requires a reasonable estimate of the risk of esophageal cancer in this condition. The primary goal of endoscopic screening for individuals with gastroesophageal reflux disease is to identify patients with Barrett's esophagus who will benefit from an intervention to prevent cancer. There is also indirect evidence to suggest that surveillance for Barrett's esophagus may be beneficial. However, there is much debate over the efficacy of these diagnostic procedures. In the absence of definitive data, investigators have used computer models to study the cost effectiveness of screening and surveillance for Barrett's esophagus. It is important for physicians to recognize that such models do not provide a single, definitive answer.
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PMID:Screening for Barrett's esophagus. 1247 41

Esophageal reflux of duodenal contents converts a rat nitrosamine esophageal cancer model from squamous cell carcinoma to adenocarcinoma. Further, there was a tendency for male rats to have a higher incidence of cancer than female rats. However, chemical castration with the gonadotropin-releasing hormone analog leuprolide did not protect male or female animals from developing cancer. We have identified an early (6-week) hyperproliferative epithelial cell reaction to duodenal reflux. We carried out experiments to assess the specificity of duodenal reflux in producing the hyperproliferative epithelial precursor lesion. Animals underwent specific surgical procedures to produce esophageal reflux of pure duodenal contents, mixed gastroduodenal, or bland intestinal contents. A hyperproliferative mucosal esophagitis developed in the group with duodenal reflux but not in the other groups. Mucosal thickness in the duodenal reflux group reached seven times that of normal mucosa at 6 weeks. These results suggest that esophageal reflux of duodenal contents plays an important role in the pathogenicity of proliferative esophagitis and the potential development of esophageal adenocarcinoma.
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PMID:Duodenal reflux produces hyperproliferative epithelial esophagitis--a possible precursor to esophageal adenocarcinoma in the rat. 1260 Apr 41

Most available information on the epidemiology of Barrettacute;s esophagus (BE) relates to patients with long segments (> 3 cm) of specialized intestinal metaplasia (SIM). Its prevalence is 3% in patients undergoing endoscopy for reflux symptoms and 1% in those undergoing endoscopy for any clinical indication. The latter prevalence is similar to the 1% found in autopsy series. A "silent majority" with BE remain unrecognized in the general population. BE is more common in men, and the prevalence rises with age. Recent endoscopic series document a rise in the diagnosis of endoscopically apparent short segments (< 3 cm) of BE (SSBE). The prevalence of SSBE in both unselected and reflux patients is 8% to 12%. Specialized intestinal metaplasia at the cardia, below a normal-appearing squamocolumnar junction, has been reported to vary from 6% to 25% in patients presenting for upper endoscopy. Unlike patients with long segment Barrett's esophagus (LSBE), the role of gastroesophageal reflux disease in the pathogenesis of SSBE and SIM of the cardia is controversial. Recent data suggest that the etiology of SIM of the cardia might be secondary to Helicobacter pylori infection, although the role of other environmental factors cannot be ruled out. The incidence of adenocarcinoma of the esophagus and esophagogastric juction (EGJ) has been increasing over the past 15 years in Western countries. Surgical series and population-based studies show that by 1994 adenocarcinomas of the esophagus accounted for half of all esophageal cancer among white men. LSBE and SSBE predispose to the development of adenocarcinoma of the esophagus and EGJ. The role of SIM of the cardia as a precursor lesion for EGJ adenocarcinoma is still unclear. The prevalences of dysplasia in LSBE and SSBE are around 6% and 8%, respectively. The incidence of adenocarcinoma in patients with LSBE is about 1 in 100 patient-years. Cancer risk for SSBE and SIM at the cardia is unknown. Smoking and obesity increase the risk for esophageal and EGJ adenocarcinomas.
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PMID:Trends in incidence and prevalence of specialized intestinal metaplasia, barrett's esophagus, and adenocarcinoma of the gastroesophageal junction. 1291 64

Barrett's esophagus is most often seen in white men with chronic heartburn who are generally older than 50 years of age. The prevalence of Barrett's esophagus is 10% to 15% in patients who are undergoing endosocopy for gastroesophageal reflux disease and 1% to 2% in asymptomatic American adults. Barrett's esophagus represents metaplastic columnar tissue with specialized intestinal metaplasia, and this condition carries an increased risk of esophageal adenocarcinoma. Patients with Barrett's esophagus have a risk of esophageal adenocarcinoma 30 to 60 times that of the general population with an incidence rate of over 100 times that of the general population. Esophageal adenocarcinoma has increased dramatically over the past few decades with specialized intestinal metaplasia being the most important risk factor for the development of dysplasia and cancer. Barrett's esophagus develops in the presence of persistent gastroesophageal reflux, which is an independent risk factor for adenocarcinoma. Other risk factors for adenocarcinoma in patients with Barrett's esophagus include length of Barrett's epithelium, low-grade dysplasia, and high-grade dysplasia. New data concerning the pathophysiology and biology of Barrett's epithelium may provide answers to prevent or treat esophageal cancer. This article briefly reviews Barrett's esophagus and focuses on the risk factors associated with its progression to adenocarcinoma.
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PMID:Barrett's esophagus and risk of esophageal adenocarcinoma. 1465 12

Complications of chronic gastroesophageal reflux disease (GERD) run the gamut from erosive esophagitis to esophageal cancer, but all are linked to repeated exposure of the esophagus to caustic gastric and duodenal acid. Progression from one complication to another is not clearly established across the GERD continuum, although there is a clear progression from the serious complication of Barrett's esophagus to esophageal adenocarcinoma. This review examines the range of complications that can arise from chronic GERD, underscoring the need to view heartburn as a symptom of a potentially serious condition.
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PMID:The continuum of GERD complications. 1470 80


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