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

Primary adenocarcinoma of the esophagus, previously considered a rare neoplasm, has shown a dramatic increase in its incidence rate among White men in the United States since 1970. The reason for this increase is unknown. Since the presence of Barrett's esophagus is essential for the development of most esophageal adenocarcinomas, the increasing incidence of esophageal adenocarcinoma may be related to an increasing prevalence of Barrett's esophagus, and its precursor, gastroesophageal reflux. An association between this increasing incidence and an increasing use of pharmaceutical agents that relax the lower esophageal sphincter is proposed. The data on the dollar amount and approximate quantity in milligrams purchased per capita through retail pharmacies and hospitals in the United States from 1957 to 1986 are presented for four categories of such agents. An upward trend is observed for all four categories.
 ...
PMID:Rising incidence rate of esophageal adenocarcinoma and use of pharmaceutical agents that relax the lower esophageal sphincter (United States). 782 45

Barrett's esophagus is the condition wherein columnar epithelium replaces squamous epithelium in the esophagus. The condition is named for the late Mr Normal Barrett, an English surgeon whose most renowned publication, ironically, is a treatise contending that the esophagus cannot be lined by columnar epithelium. The eponym is used commonly despite Mr Barrett's mistaken contention, although some European authors still prefer to call the condition "endobrachyesophagus." Barrett's esophagus appears to be a sequela of gastroesophageal reflux disease (GERD), and it is the major known risk factor for esophageal adenocarcinoma. Barrett's esophagus is usually discovered during endoscopic evaluation of patients who have symptoms caused by GERD or esophageal cancer. Consequently, data on the clinical features of Barrett's esophagus are derived primarily from studies on symptomatic patients in whom the condition was recognized endoscopically. Recent investigations suggest that more than 90% of cases of Barrett's esophagus in the general population are not recognized by physicians, and many of these unrecognized patients have few or no symptoms of GERD. It is important to appreciate, therefore, that conclusions drawn from studies on patients with clinically apparent disease are not necessarily applicable to the "silent majority" of individuals with Barrett's esophagus.
 ...
PMID:Barrett's esophagus. 786 34

Barrett's oesophagus is a condition in which a metaplastic columnar mucosa replaces the normal squamous epithelium of the lower oesophagus. Barrett's oesophagus develops as a complication of gastro-oesophageal reflux and predisposes to the development of oesophageal adenocarcinoma. Most adenocarcinomas arising in Barrett's mucosa are far advanced at the time of diagnosis, and prognosis is consequently poor. Regular endoscopic surveillance of patients with Barrett's oesophagus is recommended to detect the oesophageal malignancy in an early presymptomatic stage. The concept of screening is based on the notion that regular surveillance can reduce the mortality, but there is yet little evidence that this is the case in Barrett's oesophagus. Screening is generally carried out by regular endoscopy with multiple biopsies in an attempt to detect dysplasia. Unfortunately, dysplasia is not an ideal biomarker of malignant potential in Barrett's oesophagus. There is an interest in research into more sensitive and effective predictors of heightened risk for development of malignancy. DNA content flow cytometry and p53 protein expression might be useful in managing the cancer risk in Barrett's patients. However these new techniques need further evaluation before they can be applied to routine clinical investigation.
 ...
PMID:[Barrett esophagus. Current situation of the risk and surveillance policy]. 789 14

The natural history of gastroesophageal reflux disease is usually that of a chronic disorder. Spontaneous remission is rare, and cure even more so, especially in more severe cases. Treatment of esophagitis has been eased in most cases with current drugs, but recurrence is almost the rule after discontinuation of therapy. Therefore, long-term treatment is required in many patients. The drugs of preference for long-term treatment are acid inhibitors given at the lowest dose that suppresses symptoms. Surgical treatment should be reserved for the rare patient who cannot be managed satisfactorily with conservative treatment. Because of the high risk of adenocarcinoma in Barret's esophagus, endoscopic surveillance of all patients with acceptable surgical risk is recommended.
 ...
PMID:[Therapy of gastroesophageal reflux disease]. 790 54

In Barrett's esophagus the normal stratified squamous epithelium lining the esophagus becomes replaced by metaplastic columnar epithelium containing goblet cells; it develops as a complication of chronic gastroesophageal reflux disease and predisposes the patient to adenocarcinoma. The frequency with which it leads to adenocarcinoma is not established with certainty, but the reported prevalence averages approximately 10% when the diagnosis of Barrett's esophagus is first made. The estimated incidence of adenocarcinoma varies from one in 152 to one in 441 cases per patient year, or a 30- to 125-fold excess risk. Esophageal adenocarcinoma arises only in patients with metaplastic columnar epithelium. Dysplasia precedes adenocarcinoma in Barrett's esophagus and arises from the metaplastic epithelium; it has been proposed as a marker for detecting patients at high risk for developing carcinoma. Problems with the use of dysplasia as a marker for cancer risk include difficulty in differentiating it from reactive change, variability in diagnosis and grading between observers and when the same observer interprets the sections on different occasions, and lack of understanding of its natural history. Methods other than dysplasia for detecting patients at highest risk for developing carcinoma have been sought, but flow cytometric analysis of DNA content is the only one proven to be valuable to date. Flow cytometric abnormalities correlate well with histological progression in Barrett's esophagus. The prevalence of elevated S phase and G2/tetraploid fractions and of aneuploid cell populations increases with histological progression from metaplasia to indefinite/low grade dysplasia to high grade dysplasia and cancer. Flow cytometric abnormalities in endoscopic biopsy specimens identify those patients with a higher risk of progression to high grade dysplasia or adenocarcinoma.
 ...
PMID:Barrett's esophagus, dysplasia, and adenocarcinoma. 792 21

After the skin, the gastrointestinal tract is the second most common target of systemic sclerosis. The major clinical manifestations include gastroesophageal reflux, small bowel bacterial overgrowth, malnutrition, and intestinal pseudoobstruction. Treatment is symptomatic and supportive. Gastroesophageal reflux can usually be adequately managed with prokinetic drugs, omeprazole, and judicious use of antireflux surgery. If Barrett's esophagus is present, periodic endoscopic monitoring for development of dysplastic changes or adenocarcinoma is indicated. Bacterial overgrowth usually responds to rotating antibiotics and prokinetic drugs. Malnutrition and intestinal pseudoobstruction remain the major problems and often home total parenteral nutrition is required. Intestinal pseudoobstruction occurs in two phases: an early, neuropathic phase may respond to prokinetic drugs (metoclopramide, cisapride, octreotide, and erythromycin) and dietary modification (low-residue diets, vitamin supplementation). In the late myopathic phase, therapy is usually ineffective. Treatment consists of nutritional support. Careful manometric and radiographic localization of affected segments of stomach and small and large intestines may allow judicious surgical resection or venting procedures to reduce symptoms in this unfortunate group of patients.
 ...
PMID:Gastrointestinal motility disorders in scleroderma. 870 62

Barrett esophagus has become a common lesion in the esophagus; it is presumably caused by reflux esophagitis. Double-contrast barium esophagraphy improves radiographic evaluation of Barrett esophagus. The presence of midesophageal stricture, mucosal reticular pattern, and deep esophageal ulceration suggests the presence of Barrett esophagus. Other findings, such as hiatal hernia, thickened mucosal folds, and gastroesophageal reflux, are also frequently seen in Barrett esophagus but are not specific. Adenocarcinoma may complicate Barrett mucosa, usually with severe dysplasia. Adenocarcinoma has morphologic forms similar to squamous cell carcinoma in the esophagus. Barium esophagram, CT scans, and endoscopic sonography are used to evaluate and stage adenocarcinoma in the esophagus.
 ...
PMID:Barrett esophagus and adenocarcinoma. 797 6

Barrett's oesophagus or columnar epithelium-lined oesophagus is a condition due to chronic gastro-oesophageal reflux. In addition to acid-peptic reflux, reflux of duodenal contents may have a role in its aetiology. The clinical importance of Barrett's oesophagus is the increased risk for development of oesophageal adenocarcinoma. Measures to prevent cancer development have so far been limited to regular screening and early oesophagectomy in the case of severe dysplasia or early cancer. Other modes of intervention, directed toward prevention of dysplasia and possibly regression of Barrett's epithelium, should be sought. Early markers of development toward dysplasia and cancer are necessary if we are to be able to evaluate such measures. Determination of epithelial cell proliferative activity has the potential to be such a marker. A study is now being performed to evaluate the effect of elimination of acid reflux on proliferative activity of Barrett's epithelium in conjunction with the effects of inflammation and development of dysplasia.
 ...
PMID:Barrett's oesophagus and carcinoma. Recent insights into its development and possible prevention. 801 73

Barrett's oesophagus is defined as the occurrence of columnar epithelium extending for more than 3 cm up into the tubular part of the oesophagus. The average age at the time of diagnosis is 55 years. The condition is most often seen in men and is rare among negroid populations. The condition is caused by a combination of pronounced gastro-oesophageal reflux, hypersecretion of acid by the stomach, motoric and sensory dysfunction in the oesophagus, as well as increased aggressiveness of the refluxed material. The diagnosis is made by endoscopy, taking biopsies. Three types of histological epithelium occur: specialized columnar epithelium, junctional-type epithelium and gastric fundus-type epithelium. Barrett's oesophagus is a premalignant condition. Severe dysplasia is correlated with the development of oesophageal adenocarcinoma. The incidence of the latter varies between 1:441 and 1:52 per patient-year. The treatment of Barrett's oesophagus is either medical treatment or surgery. The medical treatment includes H2 receptor antagonists or omeprazole. Antireflux surgery is indicated in cases resistant to medical treatment. Resection is the only possible curative treatment when severe dysplasia or adenocarcinoma is present. Recommendations are made, based on the available literature, as to the treatment and follow-up of patients with Barrett's oesophagus.
 ...
PMID:Barrett's oesophagus. 804 32

Upper thoracic esophageal tumors adjacent to the trachea often require a preliminary thoracotomy to accomplish resection. Between January 1985 and July 1992, 49 consecutive patients (38 men and 11 women) underwent extended esophagectomy for esophageal cancer where the neoplasm was mobilized through an initial right thoracotomy and then resected and reconstructed through an abdomino-cervical approach. Ages ranged from 40 to 80 years (median 63.4 years). The tumor was located in the upper third of the thoracic esophagus in 44 patients and in the middle third in five. Thirty-three patients had squamous cell carcinoma, 14 had adenocarcinoma, and two had adenosquamous cell carcinoma. Complications occurred in 35 patients (71.4%) and included anastomotic leak in 15, vocal cord paralysis in 11, atrial arrhythmia in nine, pneumonia in six, wound infection in five, and postoperative bleeding in one. Three patients required tracheostomy. There was one postoperative death (2.0%). Median survival was 0.9 years (range 1 month to 5.1 years). Thirty-one patients were alive at the time this article was written, 28 without evidence of cancer. Cause of death was recurrent disease in 13 patients, unrelated to cancer in three, and unknown in one. Overall actuarial 3- and 5-year survivals were 48.6% and 18.2%, respectively. Four-year survival for stage II disease was 44.6% as compared to 24.9% for stage III (p < 0.02). The presence of lymph node metastases significantly affected survival. Three-year survival for patients with N0 disease was 77.9% compared with 20.9% for patients with N1 disease (p < 0.01). Age, sex, and cell type had no effect on survival. Ten patients had late dysphagia, four had gastroesophageal reflux, and one had dumping symptoms. Although associated with significant morbidity, we conclude that extended esophagectomy is an acceptable method of management for tumors of the upper thoracic esophagus. Mortality is low, and long-term results are reasonable.
 ...
PMID:Extended esophagectomy in the management of carcinoma of the upper thoracic esophagus. 812 21


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>