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

Patients with severe GERD resistant to medical therapy are benefited greatly by laparoscopic fundoplication provided that there is careful preoperative patient selection and evaluation. Preoperative evaluation should include contrast esophagography, EGD with biopsies, stationary manometry, and 24-hour pH analysis. Significant esophageal shortening or severe dysplasia are contraindications to laparoscopic fundoplication. A short, loose Nissen fundoplication should be performed in patients with adequate esophageal body function, whereas patients with esophageal dysmotility should be offered a partial fundoplication such as the Toupet procedure. If these guidelines are followed, long-term good results can be expected, with minimal complications, and all of the advantages of the minimally invasive approach.
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PMID:The technique of laparoscopic Nissen fundoplication. 758 30

A new stimulus for research into the etiology and pathogenesis of Barrett's columnar-lined lower esophagus has been provided by the discovery that Barrett's esophagus has a very high prevalence in the general population and that adenocarcinoma of the esophagus and cardia is the fastest-growing cancer in the United States. Gastroesophageal reflux disease is the single most important factor in the pathogenesis of Barrett's esophagus, and duodenal juices may play a key role in the development of complications of stricture, ulceration, and possibly even malignant degeneration. Treatment is, therefore, aimed at abolishing all forms of reflux. Acid suppression, if used, needs to be given in massive doses to be effective in gastric hypersecretion and has no effect on other constituents of the refluxed material. Antireflux surgery has been shown to be superior to all forms of medical treatment. Regression is rare after any therapy, but continued surveillance is essential, with increased vigilance in patients with dysplasia or DNA abnormalities on flow cytometry. The role of cigarettes and alcohol in malignant degeneration is refuted.
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PMID:Barrett's esophagus. 758 62

Barrett's esophagus is a complication of gastroesophageal reflux disease that is diagnosed with increasing frequency in connection with the increased utilization of upper endoscopy. It remains unclear why some patients with gastroesophageal reflux disease develop Barrett's esophagus while others do not. The association of Barrett's esophagus and adenocarcinoma is well established; if not for this fact, Barrett's esophagus would be of little clinical importance. Endoscopic surveillance with a rigorous biopsy protocol for the detection of dysplasia or early adenocarcinoma is indicated in any patient with Barrett's esophagus who is a candidate for surgery. New therapeutic strategies, including profound acid suppression with proton pump inhibitors, laser ablation of Barrett's epithelium, and photodynamic therapy, are currently under evaluation for the treatment of Barrett's esophagus.
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PMID:Barrett's esophagus. 781 46

Phonomicrosurgical treatment of premalignant vocal fold epithelium and microinvasive cancer combines principles of surgical oncology with advanced laryngoscopic microsurgical-techniques. This treatment is guided by mucosal-wave theory of voice production and strives not only to cure the disease but also to achieve optimal vocal function. Surgical techniques developed during the past two centuries have improved methods for vocal fold visualization, tissue retrieval, and tissue evaluation. Examination of the evolution of these surgical techniques reveals the incomplete convergence of laryngoscopic surgical theory with both the concept of premalignancy and the anatomical-physiological principles of voice production. This historical review, which helps to explain the lack of consensus about current treatment options, led to a series of four investigations. They were conducted with the aim of developing a laryngoscopic (phonomicrosurgical) management approach for improving the treatment of premalignant and microinvasive vocal fold epithelium. In the first of four investigations, 42 patients (each of whom had a significant smoking history) underwent microlaryngoscopic biopsy of 52 vocal fold lesions. These lesions, which were suspicious for atypia or malignancy and were confined to the musculomembranous vocal fold, were mapped according to surface involvement and depth of penetration. Review of the maps revealed that 27 of the 52 lesions involved only the superior/ventricular surface. For these patients, the entire layered vocal fold structure could potentially be preserved on the medial/vocalizing surface. Twenty-five of the 52 lesions involved both the superior/ventricular surface and the medial/vocalizing surface. No lesion involved only the medial surface. These data suggest that (in smokers) geographic localization of keratotic and erythroplastic lesions on the superior/ventricular surface of the musculomembranous vocal fold are likely to contain atypia. This characteristic facilitates the appropriate selection of patients for biopsy and may spare individuals, who have lesions resulting from hyperfunctional dysphonia and/or gastroesophageal reflux, from unnecessary biopsy. These two disorders typically result in pathology on the medial and/or posterior glottal surfaces. In order to determine whether a directed biopsy or an excisional biopsy approach is preferable for obtaining an accurate diagnosis, all specimens underwent whole-mount sectioning for three-dimensional histopathological analysis. Keratosis was noted: without atypia in 14; with atypia in 27; and with carcinoma in 11. The severity of the atypia usually varied throughout each specimen. The surface appearance of the lesion was not a reliable prognosticator of the severity of dysplasia either between patients or in different areas of the same lesion; therefore, excisional biopsy and whole-mount, multiple-section histopathological analysis were necessary for obtaining an accurate diagnosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Premalignant epithelium and microinvasive cancer of the vocal fold: the evolution of phonomicrosurgical management. 788 66

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.
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PMID:[Barrett esophagus. Current situation of the risk and surveillance policy]. 789 14

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.
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PMID:Barrett's esophagus, dysplasia, and adenocarcinoma. 792 21

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.
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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.
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PMID:Barrett's oesophagus and carcinoma. Recent insights into its development and possible prevention. 801 73

Hiatus hernia with reflux can be asymptomatic or can lead to severe, complicated esophagitis or even to metaplasia, dysplasia and carcinoma. Ideally all refluxing patients with esophagitis who are not easily and completely controlled with medical therapy should undergo anti-reflux surgery before complications such as ulcers, stricture or columnar metaplasia (Barrett's esophagus) occur. When esophagitis is long-lasting or severe, shortening of the esophagus is common. In such cases the esophagus must be "lengthened" before an anti-reflux procedure can be performed safely. This is the Collis gastroplasty. We have performed 17 Collis-Nissen procedures over 5 years for complicated gastroesophageal reflux disease (GERD). Results were good to excellent in 8 cases, satisfactory in 6 and poor in 3. We conclude that a complete preoperative workup with esophagoscopy (and biopsies), 24-hour pH monitoring and esophageal manometry must be performed in all patients with complicated GERD to allow the best operative procedure to be chosen (gastroplasty-fundoplication, resection or total duodenal diversion). The role of alkaline reflux is also discussed.
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PMID:[Treatment of irreducible hiatal hernia with reflux esophagitis by Collis-Niessen gastroplasty-fundoplication. Indications, technique, results of a series of 17 cases]. 803 23

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.
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PMID:Barrett's oesophagus. 804 32


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