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

In Barrett's esophagus, the squamous lining of the lower esophagus is replaced by columnar epithelium. Barrett's esophagus is associated with gastroesophageal reflux and an increased risk of the development of esophageal cancer. Endoscopy shows red columnar epithelium in the lower esophagus. Biopsy is needed to confirm intestinal metaplasia. Some cases progress from dysplasia to invasive adenocarcinoma. Medical or surgical antireflux treatment controls symptoms and esophagitis, but Barrett's esophagus remains. Patients are usually followed up by endoscopy for detection of dysplasia or early cancer. For patients with low-grade dysplasia, follow-up is adequate; however, for those with high-grade dysplasia, esophagectomy or experimental endoscopic mucosal ablation is advised.
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PMID:Management of Barrett's esophagus. 958 88

In Barrett's esophagus, stratified squamous mucosa of the lower third of the esophagus is replaced by columnar mucosa, as a complication of chronic gastroesophageal reflux. The presence of Barrett's esophagus appears to be a major factor in the progression to adenocarcinoma of the lower third of the esophagus. Therefore it is crucial to identify the subset of patients at risk for the development of adenocarcinoma. Dysplasia is an important histologic feature to evaluate because it identifies those patients who require follow-up. The diagnosis of biopsies with lesser degrees of abnormalities, however, makes microscopic evaluation less helpful in identifying patients who need more frequent endoscopic biopsy surveillance. DNA ploidy and the use of monoclonal antibodies, such as suppressor gene product p53, oncogene cerbB-2, and Ki-67, have added dramatically to our understanding of the biology of Barrett's metaplasia and have given us objective indicators to predict the presence of an increased risk of developing cancer.
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PMID:The histopathology and biologic prognostic factors of Barrett's esophagus: a review. 964 22

Barrett's esophagus (BE) is a premalignant condition, due to chronic gastroesophageal reflux. Effective antireflux therapy may diminish cancer risk. To evaluate this option an intermediate marker is needed. We developed a methodology for measurement of epithelial cell proliferative activity of Barrett's mucosa as an intermediate marker and correlated the activity with traditional cancer risk markers and other parameters. Fifty-six patients (21-74 years of age) with Barrett's esophagus and established acid gastroesophageal reflux were included. Biopsies were taken from Barrett's mucosa at 3-cm intervals. Reflux was measured by 24-hr pH-metry. Proliferative activity was determined using in vitro labeling with 5-bromodeoxyuridine and immunohistochemistry and was expressed as labeling index (LI). The length of BE correlated with erect acid reflux (P=0.002). LI in specialized columnar metaplasia was higher than in gastric metaplasia, especially in crypt epithelium (P < 0.05). Multiple regression analysis revealed independent positive correlations for surface LI with dysplasia (P=0.011), distance from the incisors (P=0.041), and crypt LI (P=0.000). Crypt LI showed an independent positive correlation with the length of BE (P=0.033) and type of metaplasia (P=0.007). In conclusion, epithelial cell proliferative activity of BE correlates with several known risk factors for cancer. Proliferative activity is an attractive intermediate marker to evaluate the effects of interventional measures to decrease cancer risk in Barrett's esophagus.
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PMID:Epithelial cell proliferative activity of Barrett's esophagus: methodology and correlation with traditional cancer risk markers. 969 Mar 86

Since 1992 there have been reports of proton pump inhibitors being associated with fundic gland-type gastric polyps. Endoscopic and histologic characteristics and natural history of these polyps have not been clearly defined. We performed a retrospective study of patients on long-term treatment with proton pump inhibitors who developed gastric polyps. Gastric polyps developed in 17 (10 males and 7 females, 7.3%) of the 231 patients who underwent 2 or more upper endoscopies for complicated gastroesophageal reflux disease and who were receiving long-term treatment with proton pump inhibitors. The mean interval of proton pump inhibitor use after which an endoscopy revealed gastric polyps was 32.5 months. In 1 patient, discontinuation of treatment resulted in disappearance of the polyps within 3 months. The polyps recurred 4 months after the treatment was restarted. Endoscopy established that typical polyps were generally small (<1 cm), sessile, multiple, and whitish pink with a mottled partially translucent surface. The polyps were most often present in the proximal/midgastric body. Of the 15 polyps removed endoscopically, 9 were of the fundic gland type, 4 were of the hyperplastic type, and 2 were of the inflammatory type. Eight of 9 polyps with typical endoscopic appearance were of the fundic gland type. None of the polyps contained dysplasia or carcinoma. Long-term use of proton pump inhibitors may be associated with the presence of small gastric fundic gland polyps and hyperplastic polyps. A prospective study is required to establish their incidence, natural history, and clinical significance.
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PMID:Proton pump inhibitor-associated gastric polyps: a retrospective analysis of their frequency, and endoscopic, histologic, and ultrastructural characteristics. 1051 Jun 76

Experimental studies have shown that the severity of esophageal mucosal injury in gastroesophageal reflux disease is related to the reflux of both gastric and duodenal juice. The purpose of this study was to determine whether duodenal juice potentiates esophageal injury in patients with reflux disease or, in fact, causes no harm allowing acid and pepsin to do the damage. A total of 148 consecutive patients who had no previous gastric or esophageal surgery underwent endoscopy and biopsy, manometry, and 24-hour esophageal pH and bilirubin monitoring. Esophageal injury was defined by the presence of erosive esophagitis, stricture, or biopsy-proved Barrett's esophagus. Exposure to duodenal juice, identified by the absorbance of bilirubin, was defined as an exposure time exceeding the ninety-fifth percentile measured in 35 volunteers. To separate the effects of gastric and duodenal juice, patients were stratified according to their acid exposure time. One hundred patients had documented acid reflux on pH monitoring, and in 63 of them it was combined with reflux of duodenal juice. Patients with combined reflux (50 of 63) were more likely to have injury than patients without combined reflux (22 of 37; P < 0.05). When the acid exposure time was greater than 10%, patients with injury (n = 40) had a greater exposure to duodenal juice (median exposure time 17.2% vs. 1.1%, P = 0.006) than patients without injury (n = 5), but there was no difference in their acid exposure (16.9% vs. 13.4%). Patients with dysplasia of Barrett's epithelium (n = 9) had a greater exposure to duodenal juice (median exposure time 30.2% vs. 7.2%, P = 0.04) compared to patients without complications (n = 25), whereas acid exposure was the same (16.4% vs. 15%). Duodenal juice adds a noxious component to the refluxed gastric juice and potentiates the injurious effects of gastric juice on the esophageal mucosa.
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PMID:Duodenogastric reflux potentiates the injurious effects of gastroesophageal reflux. 983 27

The significance of finding specialized intestinal epithelium localized to the region of the gastroesophageal junction is unclear. We tested the hypothesis that short segments of specialized intestinal epithelium are a consequence of gastroesophageal reflux disease and are premalignant. Two hundred forty-one patients with reflux symptoms underwent gastroscopy with rigorous biopsy. Barrett's esophagus was diagnosed when specialized intestinal epithelium was present on biopsy. Patients with Barrett's esophagus were subdivided according to the length of Barrett's mucosa: short-segment Barrett's (<3 cm) and extended Barrett's (> or =3 cm). Esophageal function was evaluated by manometry and 24-hour pH monitoring. In another 16 patients with small noncircumferential adenocarcinomas, the endoscopic length of Barrett's mucosa was recorded. Thirty-three patients (14%) had short-segment Barrett's and 37 (15%) had extended Barrett's esophagus. Patients with short-segment Barrett's esophagus had significantly more acid exposure than patients without specialized intestinal epithelium. Eighty-one percent of patients with short-segment Barrett's esophagus had increased esophageal acid exposure as did 100% of those with extended Barrett's esophagus. All lengths of Barrett's mucosa were associated with poor esophageal sphincter function and reduced contraction amplitudes in the distal esophagus. Twelve percent of patients with short-segment Barrett's esophagus had dysplasia. The length of Barrett's mucosa was > or =3 cm in 25% (4 of 16) of patients with early Barrett's adenocarcinoma. Short-segment Barrett's esophagus is commonly associated with gastroesophageal reflux disease. Further, short segments of specialized intestinal epithelium are premalignant in nature.
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PMID:Short-segment Barrett's esophagus: A prevalent complication of gastroesophageal reflux disease with malignant potential. 983 37

Barrett's esophagus is a premalignant metaplastic change in the lining of the distal esophagus. It represents a peculiar form of healing which occurs in response to chronic gastroesophageal reflux. The etiology of this condition is unknown but clinical and experimental data points to esophageal exposure to duodenal juice as the key factor in its development. Barrett's esophagus should be considered in all patients undergoing endoscopy for symptoms of reflux disease. It is confirmed by the presence of intestinal metaplasia in an area of columnar mucosa, regardless of the macroscopic appearances of the distal esophagus. Endoscopic surveillance with multiple biopsy of the columnar mucosa is indicated for all medically fit patients with Barrett's esophagus. Identification of intestinal metaplasia with high-grade dysplasia heralds the development of invasive cancer and offers the physician an opportunity to intervene. Esophagectomy is the treatment of choice for patients with high-grade dysplasia, since occult early adenocarcinoma is identified in up to 50 percent of the esophageal specimens.
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PMID:Barrett's esophagus. Update of pathophysiology and management. 984 64

The development of columnar lined epithelium with intestinal metaplasia in the distal esophagus is a possible, but not a necessary, end stage of advanced gastroesophageal reflux disease. Currently, research is focused on the carcinogenesis of Barrett's carcinoma and the metaplasia-dysplasia carcinoma sequence, since it is a malignoma with the highest increasing incidence in Western industrial countries. Possible causes of the above-mentioned sequence are excessive acid, duodenogastric reflux, and genetic factors. A curative surgical approach is the radical R-0 resection. Some centers prefer the transmediastinal esophagectomy. Others prefer the transthoracic en bloc esophagectomy. Reconstruction can be done with the stomach and the colon. Patients with advanced disease probably benefit best from multimodal therapy with neoadjuvant radiochemotherapy.
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PMID:[Barrett carcinoma as a tumor entity with special therapy consequences]. 993 28

Gastroesophageal reflux disease (GERD) is a common clinical problem. New information suggests that infection with Helicobacter pylori may protect patients from developing GERD and its complications. Endoscopy may be used by clinicians to tailor GERD therapy, but an empirical trial of a proton-pump inhibitor may be an alternative diagnostic approach. Studies continue to show that laparoscopic antireflux surgery is a cost-effective treatment option for patients requiring maintenance therapy with proton-pump inhibitors. However, the minimally invasive nature of the operation should not alter the indications for antireflux surgery, especially for patients with atypical symptoms. It remains unclear why some patients with GERD develop Barrett's esophagus, whereas others do not. Recent guidelines suggest that patients with long-standing GERD symptoms, especially white men over 50 years of age, should undergo endoscopy at least once to screen for Barrett's esophagus. Debate concerning short-segment Barrett's esophagus continues. Intestinal metaplasia at a normal-appearing gastroesophageal junction may be associated with intestinal metaplasia of the stomach and infection with H. pylori, whereas short tongues of intestinal metaplasia in the esophagus are associated with GERD. Cancer surveillance is indicated in short-segment Barrett's esophagus, as dysplasia may develop in these patients. Barrett's esophagus is the only known risk factor for the development of esophageal adenocarcinoma, but the incidence of adenocarcinoma may be lower than previously reported. New clinical guidelines for endoscopic surveillance suggest that the surveillance interval should be lengthened to every two years in patients without dysplasia. Newer treatment options, such as thermal ablation and photodynamic therapy, continue to show promise, but are not yet ready for routine clinical use.
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PMID:Reflux disease and Barrett's esophagus. 1008 5

Barrett's oesophagus represents the replacement of stratified squamous epithelium by metaplastic columnar epithelium for 3 cm of the distal oesophagus. Gastro-oesophageal reflux, which affects 40% of the adult population, is the principal aetiological factor. This results in predominantly acid but also bile reflux (due to duodenogastrooesophageal reflux) through the lower oesophageal sphincter, transient relaxation of which accounts for the main mechanism of reflux. Conventional Barrett's oesophagus is reported in 11-13% of patients with symptomatic reflux and short segment Barrett's oesophagus (< 3.0 cm) in 18%. Approximately 50% of these patients have recognised complications on presentation, eg, carcinoma (15%). The disparity between clinical symptoms and endoscopic severity is due to reduced oesophageal mucosal sensitivity as a consequence of prolonged mucosal acid exposure. These rather alarming figures combined with the knowledge that Barrett's oesophagus is a pre-malignant condition (the diagnosis is associated with a 25-130-fold increase of malignancy) may account for the substantial increase in junctional gastrooesophageal malignancies. Symptomatic Barrett's oesophagus should be managed with full-dose proton pump inhibitors, eg, lansoprazole. Anti-reflux surgery should be reserved for the medically fit patient with recurrent symptomatic relapse in the histological absence of premalignant change. There is no evidence suggesting that surgery can be used as a prophylactic measure against malignancy. Encouraging short-term results have been obtained with photodynamic therapy in the management of high-grade dysplasia. However, columnar epithelium has been found underlying the regenerated squamous epithelium, suggesting that life-long surveillance is warranted.
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PMID:Barrett's oesophagus. 1019 95


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