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)

Postnasal drip, asthma and gastroesophageal reflux disease are the underlying causes in almost 90% of cases with chronic cough. Causal treatment is successful in the majority of patients, although in the event of a long-standing cough, it might need to be continued over several weeks. Smoking complicates the identification of cough as a clinical early symptom of an underlying tumor. Cardiac causes are rare, and in most cases are due to the use of ACE-inhibitors. Cough may be triggered by a variety of causes and the therapeutic palette must include several spectra. Since the individual causes often cannot be unequivocally identified, it may be necessary to take a polypragmatic therapeutic approach targeting the three most common causes simultaneously for 7-10 days.
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PMID:[Differential diagnosis and treatment of chronic cough]. 1553 30

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

The definition of BE has evolved over time. BE is the key premalignant lesion for developing EAC. The epidemiology and pathophysiology of BE is outlined, and risk factors for BE and EAC are reviewed. GERD plays a crucial role in the pathophysiology and the clinical identification of BE. Endoscopy with biopsy is the best tool for diagnosing and surveying patients with BE. Detection of early neoplasia is the present approach to reduce EAC mortality. Novel technology should assist in the early detection of dysplasia to enable targeted therapy. Effective chemopreventive strategies may reduce the risk of progression to EAC.
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PMID:Epidemiology, pathophysiology, and treatment of Barrett's esophagus: reducing mortality from esophageal adenocarcinoma. 1565 28

Several articles have been published during the last year that may affect the management of patients with gastroesophageal reflux disease (GERD) and/or Barrett's esophagus in the near future. A new method of measuring esophageal pH has been introduced that does not require an indwelling transnasal catheter and may allow a more physiological assessment of esophageal acid exposure. Several articles discussed the use of endoscopic antireflux procedures, and a sham-controlled randomized study was published concerning the Stretta procedure. A long-term follow-up study and a decision analysis study have again fueled the debate concerning the relevance of surveillance of Barrett's patients, whereas other studies focused on techniques that may improve the detection of specialized intestinal metaplasia and dysplasia within the Barrett's segment. Finally, several studies have reported promising results with the endoscopic treatment of Barrett's metaplasia and early neoplasia using ablation techniques or endoscopic resection modalities. This review summarizes the most important articles in the field of GERD and Barrett's esophagus that have been published in peer-reviewed journals during the last year that are relevant to the practicing endoscopist.
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PMID:Gastroesophageal reflux disease and Barrett's esophagus. 1565 52

The cyclin-dependent kinase (cdk) inhibitor p27 preferentially inactivates cdk complexes required for progression through the G1/S transition. Loss of p27 is associated with aggressive behavior in a variety of tumors, including Barrett's associated adenocarcinoma (BAA). We have previously shown that gastroduodenal-esophageal reflux (GDER) together with N-methyl-N-benzylnitrosamine (MBN) induces Barrett's esophagus (BE) and malignant transformation of the esophageal mucosa in mice. This process is enhanced in a p27 null background. Here, we show that chronic flavopiridol administration sharply reduced the prevalence of BE in GDER/MBN-treated p27 knockout mice when compared to animals treated with diluent only (7 vs 26%, P=0.0079). Similarly, flavopiridol reduced the prevalence of BAA (11 vs 32%, P=0.0098) and overall cancer prevalence (15 vs 60%, P<0.0001). In addition, appropriate molecular targeting by flavopiridol in tumor cells was confirmed by downregulation of cyclin D1, a known target of this pan-cdk inhibitor. The results of this study represent the experimental basis for chemoprevention with cdk inhibitors in human BE and BAA.
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PMID:Flavopiridol reduces malignant transformation of the esophageal mucosa in p27 knockout mice. 1567 36

Helicobacter pylori infection and gastro-oesophageal reflux disease (GERD) account for most upper gastrointestinal pathologies with a wide spectrum of clinical manifestations. The interplay of both conditions is complex, in part intriguing, and has become a matter of debate because of conflicting results. The cardia is an area where both H pylori and abnormal GERD exert their damaging potential, inducing inflammation and its consequences, such as intestinal metaplasia. While the role of intestinal metaplasia within columnar lined epithelium (Barrett's oesophagus) in the context of GERD is well established as a risk for neoplasia development, the role of intestinal metaplasia at the cardia in the context of H pylori infection is unclear. A particular challenge is the distinction of intestinal metaplasia as a consequence of GERD or H pylori if both conditions are concomitant. Available data on this issue, including follow up of a small patient series, are presented, but more studies are required to shed light on this issue because they will help to identify those patients that need surveillance.
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PMID:The interplay between Helicobacter pylori, gastro-oesophageal reflux disease, and intestinal metaplasia. 1571 Oct 3

Despite advances in diagnosis and therapy, esophageal adenocarcinoma remains an aggressive and usually lethal tumor. This review focuses on the epidemiology of esophageal adenocarcinoma and its presumed precursor lesion, Barrett's esophagus; the pathogenesis of the cancer; advances in treatment of adenocarcinoma and Barrett's esophagus; and strategies for cancer prevention. Emphasis is placed on recent literature. Although the absolute number of cases of adenocarcinoma in the United States is still small, the incidence of this cancer has increased dramatically in the last 40 years, and adenocarcinoma is now the predominant form of esophageal cancer in this country. Recent evidence suggests that Barrett's esophagus is more prevalent in asymptomatic individuals than previously appreciated. The pathogenesis of Barrett's esophagus is poorly understood. Given that some subjects will have repeated bouts of severe erosive esophagitis and never develop Barrett's esophagus, host factors must play an important role. The utility of neoadjuvant radiation and chemotherapy in those with adenocarcinoma, although they are widely practiced, is not of clear benefit, and some authorities recommend against it. Ablative therapies, as well as endoscopic mucosal resection, hold promise for those with superficial cancer or high-grade dysplasia. Most series using these modalities feature relatively short follow-up, and longer-term data will be necessary to better describe the effects of these therapies. The value of chemoprevention in subjects with dysplastic Barrett's esophagus by use of cyclooxygenase 2 inhibitors, nonsteroidal anti-inflammatory drugs, or proton pump inhibitors is unknown. Similarly, although endoscopic screening is widely practiced, its value in patients with chronic gastroesophageal reflux disease symptoms is of unproven value, and recommending bodies are divided as to its practice.
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PMID:Advances in Barrett's esophagus and esophageal adenocarcinoma. 1588 51

Barrett's esophagus is a premalignant condition and remains the number one risk factor for developing adenocarcinoma. Gastro-esophageal reflux disease is a strong risk factor for both esophageal adenocarcinoma and the precancerous lesion Barrett's esophagus. Both of these conditions are related to the reflux of acid and bile into the esophagus. This results in inflammation and cell damage which initiates a sequence of events termed the metaplasia-dysplasia sequence in which the squamous epithelium is replaced by columnar epithelium exhibiting increasing degrees of dysplasia and overt malignancy. The underlying disease mechanisms remain unclear, but tumor suppression genes (p53, p16, APC) and, oncogenes (K-ras, cyclin D1, c-erb-2) seem to cause the malignant transformation of Barrett's esophagus, and the genetic or epigenetic alterations of these genes have been reported.
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PMID:[Carcinogenesis of Barrett's esophagus]. 1610 Dec 21

The development and progression of Barrett's epithelium are accompanied with the acquisition of many molecular changes of the oesophageal mucosa. Gastro-oesophageal reflux and inflammation cause the oxidative stress and free-radical generations, which result in the expression of oxidative-stress-related genes and the induction of DNA damage. The development of Barrett's epithelium follows a metaplasia-dysplasia-adenocarcinoma sequence, characterized by the accumulation of many genetic and epigenetic alterations, which are seen in carcinogenesis. Abnormalities in the expression of tumor suppressor genes, such as p53, p16, APC, and a number of molecules involved in cell proliferation, apoptosis or angiogenesis are observed. These genetic alterations affecting the cancer hallmarks provide a better understanding of the etiology and pathogenesis of the disease.
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PMID:[Molecular events associated with Barrett's oesophagus]. 1610 Dec 22

The causal relationship between GERD and esophageal adenocarcinoma, although unclear just a few decades ago, now is established fairly well. The physiologic changes and the biocellular alterations of the damaged esophageal mucosa are documented better. Despite this knowledge, the dramatic increase in the incidence of esophageal cancer cannot be explained. The absolute risk of esophageal adenocarcinoma arising from GERD is low, and, at present, does not justify population-screening programs. Still, with the notion that adenocarcinoma of the esophagus is an aggressive cancer once documented, important questions still are in need of answers for patients suffering from reflux symptoms. Patients who have reflux disease are not necessarily symptomatic. It remains unclear if patients experiencing reflux symptoms should undergo mandatory endoscopy with biopsies at the esophagogastric junction. Furthermore, metaplasia of the lower esophagus often is not readily recognizable at endoscopy, and only biopsies can document abnormal histology. A severe and prolonged history of reflux always should orient to the possibility of a reflux-related columnar-lined esophagus. Once documented, Barrett's esophagus needs to be seen as a premalignant condition not necessarily leading to adenocarcinoma formation; despite their increased risk of tumor formation, most patients who have Barrett's esophagus die of other causes. During regular endoscopic follow-up, multilevel circumferential biopsies should document the evolution of the histologic changes in the lower esophagus and at the gastroesophageal junction of these patients. It is the only method available to document the appearance of dysplasia. It still is unclear if medicine or surgery provides the best quality of life and the best protection against the development of dysplasia and the possible progression toward adenocarcinoma formation when intestinal metaplasia is present in the esophagus.
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PMID:Gastroesophageal reflux and cancer. 1610 25


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