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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We systematically reviewed the literature on gastroesophageal reflux disease (GERD) related to Helicobacter pylori therapy, and classified the GERD according to various aspects. Preexisting GERD is active GERD before H. pylori therapy, and a substantial proportion of the GERD patients improve after successful H. pylori therapy. If the GERD does not persist or recur after cessation of acid-suppressive therapy combined with H. pylori therapy, it may have been cured (cured GERD). If it recurs, it may have been masked by acid-suppressive therapy and unmasked with cessation of the therapy (pharmacologically masked and unmasked GERD). Newly developed GERD after successful H. pylori therapy is a kind of unmasked GERD arising after cure of infection (de novo unmasked GERD). The possible mechanism of the improvement of cured GERD is normalized hyperacidity associated with an improved cytokine-somatostatin-gastrin system followed by normalized G-cell activity and parietal cell mass. Preexisting GERD is not a reason to avoid eradication therapy. De novo unmasked GERD develops in a substantial proportion of patients with cured infection. The possible mechanism is increased acid exposure in the esophagus due to gastric acid increase, which is caused by a loss of neutralizing effect by ammonia, normalized cytokine-acid suppression and improvement of corpus atrophy. De novo unmasked GERD is important because GERD is recurrent and may induce adenocarcinoma of the esophagus. However, it is expected that cure of infection lowers gastric cancer incidence. Eradication therapy is recommended irrespective of the possibility that de novo unmasked GERD may have a slight increase of the risk of esophageal adenocarcinoma.
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PMID:Active and inactive gastroesophageal reflux diseases related to Helicobacter pylori therapy. 1295 Jun

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

Duodenogastric reflux is the retrograde flow of duodenal contents into the stomach that then mix with acid and pepsin. These agents can reflux into the esophagus (ie, duodenogastroesophageal reflux ) and cause gastroesophageal reflux disease (GERD) and its complications, including stricture, Barrett's esophagus, and adenocarcinoma of the esophagus. Medical and surgical treatments of DGER can be difficult. Best medical treatment is proton-pump inhibitors, which decrease DGER by inhibiting both gastric acidity and volume, making less gastric contents available to reflux into the esophagus. The addition of the gamma-aminobutyric (GABA(B)) receptor agonist baclofen may further reduce DGER in patients not responding to proton-pump inhibitors. Bile acid-binding agents (aluminum-containing antacids, cholestyramine, sucralfate, urosodeoxycholic acid) have physiologic rationale, but their efficacy is unproven. Prokinetic agents can reduce DGER and its upper gastrointestinal symptoms by promoting increased gastric emptying. In patients with medically refractory symptoms, a Roux-en-Y diversion or duodenal switch operation may be helpful.
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PMID:Duodenogastric Reflux-induced (Alkaline) Esophagitis. 1472 38

Gastroesophageal reflux disease (GERD) is a chronic condition that affects a large proportion of the adult population. Persistent untreated GERD can lead to esophageal strictures, premalignant Barrett's esophagus, and an increased risk of adenocarcinoma of the esophagus. Currently, the most effective medical treatment targets gastric acid suppression, allowing healing of erosive/peptic lesions and controlling symptoms. Most patients take over-the-counter medication or are successfully treated by their primary care physician. Gastroenterologists and gastrointestinal surgeons see patients with complications, refractory symptoms despite acid-suppressive therapy, or atypical symptoms. For the medical management of GERD, proton pump inhibitors are potent acid suppressants with favorable side-effect profiles and long-term efficacy and safety. Medical therapy can heal 80% to 100% of patients with erosive esophagitis with 30% to 60% of patients reporting sustained resolution of heartburn. Surgery may be offered to patients with GERD as an alternative to long-term antireflux medication. Careful selection of appropriate surgical candidates is important, and the risk of developing new or recurrent symptoms requiring medication should be disclosed to patients contemplating the surgical alternative.
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PMID:Gastroesophageal reflux disease: natural history and long-term medical and surgical outcomes. 1510 95

The demographics of esophageal and gastric cancer have been changing dramatically in the United States over the past several decades. While incidence rates for esophageal squamous cell carcinoma and distal gastric carcinoma have been declining, the trends for adenocarcinoma of the esophagus and proximal stomach have been rising rapidly, particularly among white males. The incidence of these upper gastrointestinal (GI) malignancies varies widely based on geographic location, race, and socioeconomic status. The primary causes of squamous cell carcinoma of the esophagus are tobacco use and alcohol consumption, whereas the main risk factors for adenocarcinoma of the esophagus are gastroesophageal reflux disease and obesity. Dietary factors and Helicobacter pylori infection play an important role in the development of gastric cancer. Understanding the epidemiology and etiologies of esophageal and gastric carcinomas will lead to the development of interventions for screening and prevention in high-risk populations.
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PMID:Epidemiology of upper gastrointestinal malignancies. 1529 38

This review summarizes key results of epidemiologic studies published in peer-reviewed journals between April 2003 and March 2004. The prevalence of H. pylori infection continues to vary strongly between developing countries and developed countries, and according to ethnicity, place of birth and socioeconomic factors among people living in the same country. Intrafamilial spread appears to play a central role in transmission of the infection in both developing and developed countries. The role of H. pylori infection in development of noncardia gastric cancer appears to be even much stronger than previously assumed, whereas the lack of an association with cardia cancer and an inverse association with adenocarcinoma of the esophagus could be confirmed. Suggestions for an inverse association of the infection with atopic diseases have recently received further support, whereas evidence concerning the role of the infection (or its eradication) in GERD and a large variety of other extragastric diseases, including cardiovascular disease, remains inconclusive.
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PMID:Epidemiology of Helicobacter pylori infection. 1534 99

Limited available data specifically addressing nocturnal gastroesophageal reflux indicate its association with more severe injuries such as esophagitis and stricture, adenocarcinoma of the esophagus, respiratory and ENT disorders as well as sleep disturbances, diminished quality of life and undesired changes in activities of daily living. In a recent survey, altogether 79% of respondents reported experiencing heartburn at night. Among those, 75% reported that symptoms affected their sleep, 63% believed that heartburn negatively affected their ability to sleep well, and 40% believed that nocturnal heartburn impaired their ability to function the following day. Of the 791 respondents with nighttime heartburn, 71% reported taking over-the-counter medicine for it, only 29% of these rated this approach extremely effective. Forty-one percent reported trying prescription medicines and 49% of these rated this approach extremely satisfactory. This recent understanding of the prevalence and impact of nighttime heartburn is an indicator of nocturnal acid reflux events and suggests that nighttime heartburn occurs in a large majority of adults with gastroesophageal reflux disease. The fact that expected result from implemented therapy for heartburn is not achieved by a sizable percentage of patients can have significant management implications.
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PMID:Nighttime GERD: clinical implications and therapeutic challenges. 1558 93

The diagnosis of Barrett's esophagus is rendered based on proof of intestinal metaplasia in the tubular portion of the esophagus. Barrett's develops in a percentage of patients with gastroesophageal reflux disease; risk factors include a long history of the disease, age over 40 years and Caucasian skin. Specifics about a genetic predisposition have not become known to date. Each year, around one out of every 200 patients with Barrett's epithelium develop adenocarcinoma of the esophagus, the incidence of which has risen dramatically over the past two decades. Apart from the early stages, the prognosis for this type of Barrett's carcinoma is extremely unfavorable, even after esophagectomy. It therefore appears sensible to examine patients with a long history of reflux and/or frequently recurrent reflux symptoms and to develop screening strategies for timely detection of persons with Barrett's esophagus along with subsequent monitoring. This would involve regular endoscopic studies accompanied by biopsies aimed at excluding or demonstrating the intraepithelial neoplasms that count as direct precursors to cancer. Treatment of nonneoplastic Barrett's esophagus can be symptomatic. Although theoretically logical, the benefits of normalizing esophageal acid exposure have not been proven. When high-grade intraepithelial neoplasms or mucosal carcinomas have been confirmed, local endoscopical resection and/or ablation appear sufficient, since the risk of lymph node metastasis is extremely low. Previous studies on this subject have been very promising, but should be continued and/or verified. Definitive therapy of more advanced tumor stages is currently given according to multimodal concepts established in an interdisciplinary manner.
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PMID:[Barrett's esophagus]. 1565 5

Oesophageal adenocarcinoma has a low incidence and still remains an uncommon cancer; however, it has been on the rise over the past 20 years. Barrett's oesophagus, a complication of gastro-oesophageal reflux disease, is the only known precursor of this adenocarcinoma. It can often be asymptomatic and probably goes undiagnosed in the majority of the population. There are no direct data supporting the practice of screening for Barrett's oesophagus and oesophageal adenocarcinoma among the general population or even in patients with chronic reflux symptoms. However, many argue that the detection of neoplasms at a curable state in a high risk population can perhaps justify screening endoscopy. No prospective, controlled trials have been conducted to support the effectiveness of surveillance, but some indirect evidence does exist. The cost effectiveness of surveillance programmes needs to be further assessed in prospective studies. Ultimately, the use of better tools to diagnose Barrett's oesophagus and dysplasia and the identification of high risk groups for progression to oesophageal adenocarcinoma could potentially make screening and surveillance a cost effective practice.
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PMID:Are screening and surveillance for Barrett's oesophagus really worthwhile? 1571 Oct 5


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