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 esophagus was found in seven members of a single family. Two of these patients also had adenocarcinoma of the gastroesophageal junction. Among family members who did not have Barrett epithelium, one had esophageal ulcerations with dysplasia in squamous epithelium and another had an esophageal stricture. The pattern of involvement suggests autosomal dominant inheritance of Barrett esophagus and/or gastroesophageal reflux disease in this family, with a strong predisposition for adenocarcinoma of the esophagus.
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PMID:Familial Barrett esophagus and adenocarcinoma of the gastroesophageal junction. 834 64

Barrett's esophagus (i.e. columnar epithelial metaplasia in the distal esophagus) is an acquired condition that in most patients results from chronic gastroesophageal reflux. It is a disorder of the white male in the Western world with a prevalence of about 1/400 population. Due to the decreased sensitivity of the columnar epithelium to symptoms, Barrett's esophagus remains undiagnosed in the majority of patients. Gastroesophageal reflux disease in patients with Barrett's esophagus has a more severe character and is more frequently associated with complications as compared with reflux patients without columnar mucosa. This appears to be due to a combination of a mechanically defective lower esophageal sphincter, inefficient esophageal clearance function, and gastric acid hypersecretion. Excessive reflux of alkaline duodenal contents may be responsible for the development of complications (i.e., stricture, ulcer, and dysplasia). Therapy of benign Barrett's esophagus is directed towards treatment of the underlying reflux disease. Barrett's esophagus is associated with a 30- to 125-fold increased risk for adenocarcinoma of the esophagus. The reasons for the dramatic rise in the incidence of esophageal adenocarcinoma, which occurred during the past years, are unknown. High grade dysplasia in a patient with columnar mucosa is an ominous sign for malignant degeneration. Whether an esophagectomy should be performed in patients with high grade dysplasia remains controversial. Complete resection of the tumor and its lymphatic drainage is the procedure of choice in all patients with a resectable carcinoma who are fit for surgery. In patients with tumors located in the distal esophagus, this can be achieved by a transhiatal en-bloc esophagectomy and proximal gastrectomy. Early adenocarcinoma can be cured by this approach. The value of multimodality therapy in patients with advanced tumors needs to be shown in randomized prospective trials.
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PMID:Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management. 835 51

Barrett's esophagus, a premalignant condition associated with chronic gastroesophageal reflux, carries an approximate 40-fold increase in the incidence of adenocarcinoma. Between 1975 and 1994, 113 patients with Barrett's esophagus underwent antireflux procedures at the Mayo Clinic. The antireflux procedure was performed more than 3 months after the diagnosis of Barrett's disease in 39 patients (34.5%) and during the initial preoperative evaluation in 74 (65.5%). Uncut Collis-Nissen fundoplication was performed in 69 patients (61.1%), Nissen fundoplication was performed in 16 (14.2%), cut Collis-Nissen fundoplication was performed in 12 (10.6%), Belsey repair was performed in nine (8.0%), Collis-Belsey repair was performed in six (5.3%), and Nissen fundoplication with an anterior gastropexy was performed in one (0.9%). There was one operative death (0.9% mortality). Morbidity occurred in 41 patients (36.3%), including cardiac arrhythmia in eight (7.0%), pneumonia in six (5.3%), empyema in five (4.4%), hemorrhage in four (3.6%), myocardial infarction in two (1.8%), and wound dehiscence, wound infection, perforated duodenal ulcer, and postoperative leak in one each (0.9%). Median follow-up for the 112 survivors of operation was 6.5 years (range 4 months to 18.2 years). Excellent or good alleviation of symptoms was obtained in 92 patients (82.2%). Ninety-nine patients (88.4%) are currently alive and 13 (11.6%) have died. Three patients (2.7%) subsequently had adenocarcinoma of the esophagus after the antireflux procedure at 13, 25, and 39 months; two of these died of cancer. The incidence of esophageal carcinoma in this select group of patients was one in 273.8 patient-years of follow-up. We conclude that although antireflux procedures in patients with Barrett's esophagus result in long-term control of reflux symptoms, the possibility of esophageal cancer still exists. Endoscopic surveillance should therefore be recommended.
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PMID:Barretts's esophagus: does an antireflux procedure reduce the need for endoscopic surveillance? 864 13

Esophageal adenocarcinoma arises from Barrett's esophagus, which is induced by gastro-esophageal reflux. This refluxate often contains duodenal contents, whose backflow triggers gastric carcinoma, suggesting the hypothesis that refluxed duodenal contents cause esophageal carcinoma. This study examines the role of duodenal and gastric reflux in the absence of exogenous carcinogens in esophageal carcinogenesis. Wistar male rats, 120 in all, each weighing approximately 250 g, were used. Three experimental procedures were performed to produce gastro-duodeno-esophageal reflux, duodeno-esophageal reflux and gastro-esophageal reflux, for comparison with 2 control procedures, Roux-en-Y reconstruction and a sham operation. The animals were fed a standard diet and were examined 50 weeks after surgery. While no carcinoma was found among the 16 gastro-esophageal-reflux, 11 Roux-en-Y and 12 sham-operation animals, 10 of the 12 animals with gastro-duodeno-esophageal reflux (83%) and 10 of the 13 with duodeno-esophageal reflux (77%) developed esophageal carcinoma. The difference between groups was significant (p < 0.001). Two animals with gastro-duodeno-esophageal reflux had esophageal double and triple carcinomas respectively. Of the 23 carcinomas, 16 were adenocarcinoma, 4 adenosquamous carcinoma, and 3 squamous-cell carcinoma. Adenocarcinoma developed from the columnar-lined epithelium near the esophago-jejunostoma, while adenosquamous and squamous-cell carcinoma arose from the squamous esophagitis. These observations demonstrate that refluxed duodenal contents per so are responsible for esophageal carcinogenesis.
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PMID:Reflux of duodenal or gastro-duodenal contents induces esophageal carcinoma in rats. 876 May 98

Barrett's esophagus is a premalignant metaplastic change in the lining of the distal esophagus. It represents a peculiar form of healing which occurs in response to chronic gastroesophageal reflux disease. The condition should be considered in all patients undergoing endoscopy for symptoms of reflux disease and is confirmed when any biopsy shows the presence of specialized intestinal metaplasia irrespective of the macroscopic appearance of the distal esophagus. Endoscopic surveillance with multiple biopsy sampling of the esophageal mucosa is indicated for all medically fit patients with Barrett's esophagus. The diagnosis of dysplastic change within this abnormal mucosa requires histological examination of the biopsies by 2 independent but experienced pathologists. Identification of high-grade dysplasia heralds the development of invasive cancer and offers the physician an opportunity to intervene. Despite extensive endoscopic sampling of the esophageal mucosa the differentiation between high-grade dysplasia and invasive adenocarcinoma is unreliable. Esophagectomy remains the treatment of choice for patients with high-grade dysplasia since adenocarcinoma of the esophagus carries such a poor prognosis.
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PMID:Dysplasia in Barrett's esophagus: diagnosis, surveillance and treatment. 884 77

This article summarizes the pathophysiology of gastroesophageal reflux disease (GERD) and the wide spectrum in disease and symptom severity as they influence the selection of cost-effective treatment strategies. The vast majority of patients with GERD have mild symptoms, no gross endoscopic evidence of esophagitis, and little risk of developing complications. More than 85% of patients with GERD symptoms have uncomplicated disease. Diffuse ulcerations or complications (grade III or IV esophagitis) occur in only 3.5% of patients < 65 years of age. However, some patients with GERD can develop severe complications, including esophageal obstruction, significant blood loss, and, in rare circumstances, perforation. Furthermore, adenocarcinoma of the esophagus, which is increasing in incidence faster than any other cancer, is caused by GERD. Although severe ulcerations are uncommon in young patients, they occur in 20-30% of patients over age 65. Patients with ulcerative esophagitis are not only more prone to develop complications, they are also more resistant to treatment. Cost-effective medical management of GERD must take into account the wide spectrum of symptom and disease severity. Therapy consists of both nonpharmacologic treatment and the appropriate use of medications from several classes of drugs, either alone or in combination. Traditionally, prokinetic agents or histamine receptor antagonists have been used as primary therapy; proton-pump inhibitors are reserved for more resistant cases. The rationale for this and for alternative approaches is discussed.
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PMID:Influence of pathophysiology, severity, and cost on the medical management of gastroesophageal reflux disease. 893 25

The incidence of esophageal adenocarcinoma and adenocarcinoma of the gastric cardia has increased so substantially in the last two decades that adenocarcinoma now accounts for approximately one half of esophageal malignancies seen in the United States and Europe. The reasons for this histological change may be related to a parallel increase in the incidence of gastroesophageal reflux disease in the Western world and the subsequent development of Barrett's metaplasia. Controversies surrounding carcinoma of the esophagus that are currently the focus of study are the relationship of Barrett's esophagus to the development of adenocarcinoma; whether adenocarcinoma of the esophagus and cardia is the same disease; the correct way to stage the disease; the treatment of disease confined to the mucosa; the extent of surgical resection to cure disease beyond the mucosa; the role of adjuvant chemotherapy in the treatment of the disease; and the methods of palliating patients with incurable disease.
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PMID:Esophageal carcinoma: current controversies. 922 8

Barrett's esophagus is found in about 1% of the older population and in 3% to 5% of persons with gastroesophageal reflux. It is acquired more commonly by men and the prevalence increases with age. Most cases in the population remain undiagnosed. The incidence of adenocarcinoma of the esophagus and esophagogastric junction is increasing, both being related to Barrett's esophagus. Small areas of intestinal metaplasia are common but of uncertain significance.
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PMID:Epidemiology of columnar-lined esophagus and adenocarcinoma. 930 99

Columnar-lined esophagus or Barrett's esophagus is closely associated with gastroesophageal reflux disease. Animal and human studies have shown not only acid but duodenogastroesophageal reflux acting in synergy with acid causes the most esophageal injury. Patients with Barrett's esophagus manifest typical and atypical symptoms of reflux. Ten percent to 25%, however, have clinically silent reflux. Early diagnosis is essential for this disease as it is a risk factor for the development of adenocarcinoma of the esophagus.
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PMID:Gastroesophageal reflux disease in patients with columnar-lined esophagus. 930 4

Barrett's esophagus is an acquired condition with columnar metaplasia of the distal esophagus. Gastroesophageal reflux is the main pathophysiological factor, although genetic predisposition may play a role. The significance of Barrett's esophagus is that it is the only recognized risk factor for adenocarcinoma of the esophagus, which is one of the most rapidly rising types of cancer in North America. Cancer develops in Barrett's esophagus through a series of steps including mucosal dysplasia. High grade dysplasia is clearly a premalignant lesion and has been the focus of endoscopic surveillance strategies. Because dysplasia and adenocarcinoma develop predominantly in patients with specialized intestinal columnar epithelium, they make up the group that would be considered for surveillance programs. Endoscopic surveillance for dysplasia is only indicated for patients in whom esophagectomy would be considered if high grade dysplasia or carcinoma was found, at least until other endoscopic ablative techniques are proven to be beneficial. It has been recommended that endoscopy be performed every other year and be increased to yearly if low grade dysplasia is found. High grade dysplasia should be confirmed by another expert pathologist, and the patient should then be considered for esophagectomy. Flow cytometry and genetic markers may improve the ability to select patients for surveillance programs in the near future.
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PMID:Pathophysiology and investigation of Barrett's esophagus. 934 77


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