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)

Esophageal carcinoma is a highly lethal disease with increasing prevalence and an equally dramatic epidemiologic shift. Its causal association with gastroesophageal reflux disease and adenocarcinoma of the esophagus is well established, 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 have significant limitations. The extent of surgical resection for esophageal carcinoma remains controversial. Disease confined to the mucosa and submucosa is more common, and endoscopic ablative techniques have been proposed. However, preoperative evaluation of tumor depth and regional nodal metastases remains inadequate in these very early lesions and urges caution before adoption of therapies that may compromise cure. Patients with disease confined to the mucosa or submucosa should undergo resectional therapy aimed at removing the entire esophageal wall, including the periesophageal and perihiatal lymph nodes. For disease penetrating the submucosa, the extent of surgical therapy must be tailored to the objectives of treatment (cure vs palliation) and preoperative stage. Although data from seven prospective, randomized trials are encouraging, no clear survival benefit has been documented for neoadjuvant combined-modality therapy. Surgical resection remains the standard of care and best chance for cure in the treatment of esophageal malignancy, with combined-modality therapy reserved for prohibitive surgery candidates.
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PMID:Surgical management of esophageal malignancy. 1273 40

Barrett's esophagus (BE), a premalignant lesion to esophageal adenocarcinoma is associated with long-standing, gastroesophageal reflux disease (GERD). BE is a multi-phase process: during the initiation phase, genetically predisposed individuals (mostly white men) suffering from clinical or occult reflux damage their distal esophagus and form a new cell phenotype (incomplete intestinal metaplasia). During the formation phase, this phenotype occupies an area of variable surface (short or long-segment BE). During the progression phase, the metaplastic epithelium either remains dormant or progresses to dysplasia and adenocarcinoma. We review the recent clinical and basic research literature that explores the interaction of the refluxate (acid, bile, etc.) with BE. Acid and bile reflux variably affect BE and may cause dysplasia or adenocarcinoma. Regardless of the underlying biology, a patient with BE may suffer from GERD symptoms or may remain asymptomatic. Acid may be synergistic to bile or it could be antagonistic and protective. Acid suppressive therapy, if profound and continuous enough to abolish symptoms and esophageal acid exposure, may decrease proliferation, increase differentiation and reduce BE surface. Overexpression of cyclooxygenase-2 (COX-2), not entirely independent of acid/bile reflux, may increase proliferation and increase the invasiveness and metastatic potential of Barrett's metaplasia and neoplasia. Clinically, both acid and bile reflux need to be inhibited, either with potent acid-suppressing drugs or anti-reflux surgery. Cyclooxygenase inhibition using aspirin, NSAIDs or the safer COX-2 inhibitors added to these anti-reflux therapies may enhance the therapeutic benefit. Many questions remain unanswered. We still do not know why only a fraction of patients with GERD develop BE, what factors of the refluxate (acid, bile, etc.) initiate metaplasia and/or promote carcinogenesis, which patients are at risk for malignancy, and what is the best chemopreventive strategy. Ablation therapies and endoscopic mucosal resection are still under study.
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PMID:Management of Barrett's esophagus with and without dysplasia. 1279 81

Because of effective surveillance programs in patients with known Barrett's esophagus, adenocarcinoma of the distal esophagus is increasingly diagnosed at early stages. With the introduction of limited surgical and endoscopic treatment modalities, the need for radical esophagectomy and extensive lymphadenectomy in such patients has been questioned. When selecting the approach to early Barrett's cancer, the precancerous nature of the underlying Barrett's esophagus, the frequent multicentricity of neoplastic alterations within the Barrett mucosa, the inaccuracy of current staging modalities, and the presence of lymph node metastases should be taken into account. Invasiveness and morbidity of the procedures, as well as quality of life aspects, should also be considered. From an oncologic point of view the minimum extent of a resection for early Barrett's cancer should include a full-thickness removal of the entire segment of the distal esophagus covered by intestinal metaplasia together with a regional lymphadenectomy. In appropriately selected patients this can be achieved by a limited surgical procedure involving transhiatal resection of the distal esophagus, but not by endoscopic mucosal ablation or endoscopic mucosa resection. Our experience with 49 limited surgical resections with regional lymphadenectomy indicates that this procedure is oncologically adequate and safe. Reconstruction with an interposed jejunal loop prevents postoperative gastroesophageal reflux and is associated with good quality of life. In contrast, endoscopic interventions are plagued by a high tumor recurrence rate, probably from persistence of Barrett's mucosa and gastroesophageal reflux.
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PMID:Approach to early Barrett's cancer. 1291 59

From a clinical and biological point of view, the term "adenocarcinoma of the esophagogastric junction" (AEG) encompasses several distinct tumor entities. The topographic anatomic classification into adenocarcinoma of the distal esophagus (AEG I), true carcinoma of the cardia (AEG II), and subcardiac gastric cancer (AEG III) also reflects differences regarding the pathogenesis of these tumors and is increasingly accepted worldwide. Associated Barrett's esophagus, which usually develops as a consequence of chronic gastroesophageal reflux, can be documented in practically all patients with AEG I tumors and constitutes the most important precancerous lesion. A metaplasia-dysplasia-carcinoma sequence has been confirmed for these tumors. Barrett's esophagus is thus considered a model for studies on carcinogenesis and the prevention of esophageal adenocarcinoma. Its pathogenetic role in AEG II and III tumors must, however, be discussed differently. Our own experience shows that pathogenetic mechanisms similar to those in AEG I tumors may be present in up to 30% of tumors classified as AEG II. The majority of AEG II tumors, however, show morphologic, biologic and pathogenetic similarities with AEG III tumors and proximal gastric cancer.
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PMID:[Carcinoma of the oesophagogastric junction and Barrett's esophagus: an almost clear oncologic model?]. 1292 90

The relation between Helicobacter pylori and gastroesophageal reflux disease is unclear. Recent reports have suggested a possible protective role for H. pylori, particularly in preventing the complications of gastroesophageal reflux disease (GERD). The purpose of this article is to present a brief overview of the recent literature regarding the role of H. pylori in the genesis of the complications of GERD, focusing on Barrett's esophagus and esophageal adenocarcinoma. The prevalence of H. pylori infection in the population of the West is around 40% and is not different in cohorts of patients with GERD. When the infection induces pangastritis or corpus-predominant gastritis, there may be concomitant reduced gastric acid secretion. Eradication of the bacteria in this subgroup of patients may enhance gastric acid secretion and provoke reflux symptoms. H. pylori organisms do not colonize the specialized intestinal metaplasia characteristic of Barrett's esophagus. H. pylori infection rates in gastric mucosa of patients with Barrett's esophagus occur at a similar or slightly lower frequency than is found in controls. Gastric infection with cagA-positive strains of H. pylori appears to be uncommon in patients with Barrett's esophagus. Furthermore, epidemiologic studies indicate that cagA-positive strains are protective against esophageal adenocarcinoma. Several investigators have proposed that the decreasing prevalence of H. pylori infection might be an important factor in the rising incidence of this tumor.
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PMID:Effect of Helicobacter pylori infection in Barrett's esophagus and the genesis of esophageal adenocarcinoma. 1456 Mar 64

The patient was a 22-year-old woman who had presented in early childhood with gastroesophageal reflux and who subsequently underwent surgery. It was commented upon by the surgeons at that time that the esophagus was abnormally thickened. The patient subsequently presented during her first pregnancy with a vulval tumor, which proved histologically to be a leiomyoma. She was also found to have a grossly dilated esophagus and was thought to have achalasia. However, endoscopic ultrasound imaging showed gross hypertrophy of the mid- and distal esophageal wall, with only mild symptoms of dysphagia, which had been long-standing. The appearance of the esophagus was consistent with diffuse esophageal leiomyomatosis. In view of the associated vulval leiomyoma, the patient demonstrated esophagovulvar syndrome.
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PMID:Diffuse esophageal leiomyomatosis: another cause of pseudoachalasia. 1460 10

Zenker's diverticulum is the single most common diverticular event arising in the esophagus. Its physiopathology is universally recognized. Lack of coordination between the propulsive pharyngeal contractions and the release of the upper esophageal sphincter creates abnormally high pressure in the pharyngeal chamber, resulting in the collapse of the posterior wall of the hypopharynx, i.e., the Laimer-Killian triangle (or Killian's dehiscence). The mucosal hernia that develops constitutes the diverticulum, which grows in volume and above all in length and is compressed between two rigid structures, namely, the spine posteriorly and the trachea anteriorly. Swallowing progressively fills the diverticulum, which in turn leads to compression of the esophagus and hence to the characteristic symptom of "delayed dysphagia" or "dysphagia of the 3rd bite". These physiopathological considerations underpin the rationale for surgical treatment, namely upper esophageal sphincter myotomy and diverticulectomy, which is the standard approach used in the 44 cases presented here. A diverticulopexy was performed only once due to the patient's advanced age. Myotomy alone was performed in only one case, given the small size of the diverticulum. In two patients the standard procedure was carried out following emergency therapy for iatrogenic perforation of the diverticulum. The patient with cancer underwent chemo-radiotherapy after futile surgical attempts. Complications included transitory salivary leakage (1 case), and a transitory laryngeal nerve deficit (1 case). Gastroesophageal reflux disease was present in two-thirds of the patients. A Nissen-Rossetti fundoplication was performed one year after treatment of the diverticulum in 5 patients. The following important aspects emerged: i) the incidence of neoplasia on the diverticulum; ii) the association and possible pathogenetic relationship with gastro-esophageal reflux disease iii) the validity of myotomy plus diverticulectomy as a treatment option in view of the negligible complications and the absence of relapse and/or persistence of dysphagia.
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PMID:[Our experience with pharyngo-esophageal Zenker's diverticulum]. 1472 16

Gastroesophageal reflux disease (GERD) is a common GI disorder, particularly frequent in the primary care setting, with a high direct and indirect economic burden on society. Despite the high prevalence and costs of the disease, the epidemiology and natural history of GERD have not been fully elucidated. It has recently been suggested to abandon the current model of GERD as a "spectrum" disease and to adopt a new conceptual framework, e.g., categorizing GERD into three unique groups of patients: nonerosive reflux disease, erosive esophagitis, and Barrett's esophagus. In the present review we present arguments against this proposal, and argue that the concept of a single disease, potentially progressing from mild nonerosive forms toward metaplasia and neoplasia (adenocarcinoma), still holds true and may in fact help us in planning the diagnostic and therapeutic approach as well as in allocating financial resources much better than the proposed model of a "tripartited" disease. Independently from the conceptual model adopted, however, more data on the natural history of patients with GERD are eagerly needed.
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PMID:Gastroesophageal reflux disease: a typical spectrum disease (a new conceptual framework is not needed). 1512 65

We performed laparoscopic intragastric surgery (LIGS) for gastric stromal tumors located at the esophago-cardiac junction (ECJ) in 7 patients. The tumors measured 27 to 75 mm in diameters. Histologically, there were 4 cases of gastrointestinal stromal tumors, 2 leiomyomas, and 1 schwannoma. LIGS was performed with 1 camera port (10 mm) inserted by the open method and two 5-mm working ports inserted by puncturing the stomach. Tumors were enucleated or resected with appropriate margins confirming the muscle layer of the stomach wall and retrieved orally by gastrofiberscope. The mean surgical duration was 141.4 minutes. Recent patients took their first meal on day 3 postoperatively and were discharged within a week. There were no complications including stenosis or gastroesophageal reflux in any patient to date. LIGS is a feasible surgical option for gastric stromal tumors located at ECJ.
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PMID:Laparoscopic intragastric resection of gastric stromal tumor located at the esophago-cardiac junction. 1525 76

Premalignant esophagogastric (EG) lesions develop against a background of chronic inflammation, called a premalignant condition. For esophageal squamous cell cancer, causal factors include alcohol, tobacco, hot beverages, oral consumption of opioids, and probably infectious agents. For adenocarcinoma in the Barrett's esophagus (BE), gastroesophageal reflux disease (GERD) is the principal causal factor. At the EG junction, adenocarcinoma arises either from the esophagus or from the proximal stomach (cardia). In the distal stomach, chronic gastritis with atrophy is the premalignant condition related to Helicobacter pylori infection. A high intake of salt and low intake of antioxidants also play a role. The histopathology of EG premalignant lesions is now included in the groups low-grade and high-grade intraepithelial neoplasia (IEN) of the revised Vienna classification. Endoscopy is the gold standard for detection of the lesions at the preclinical stage and their appearance is described in subtypes of the type 0 of the Japanese classification, with a distinction between protruding and nonprotruding lesions. There is a priority for primary prevention of causal factors rather than for mass screening, which is justified only in Japan for the prevention of stomach cancer. The trend to early detection of premalignant lesions justifies the development of mini-invasive endoscopic procedures of treatment.
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PMID:Premalignant lesions of the esophagogastric mucosa. 1529 42


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