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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 biopsy interpretation of GERD demonstration or exclusion of Barrett's esophagus and its complications (dysplasia and carcinoma) is the main task, especially in its differentiation to cardiac gastritis with intestinal metaplasia. Despite of all molecular-biological examinations till today no biomarker exists for the malignant potential of Barrett's esophagus, therefore regular surveillance is necessary. Differentiation of Barrett's esophagus from cardiac mucosa with intestinal metaplasia is not yet possible by using immunochemistry, also there is no marker for the differential diagnosis of low grade dysplasia versus reactive atypia and high grade dysplasia versus early cancer of mucosa type.
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PMID:[Biopsy differential diagnosis of gastroesophageal reflux (GERD)]. 1071 91

Adenocarcinomas of the cardia and distal esophagus have increased in incidence more rapidly than any other type of human cancer in recent years. Whereas the sequence of events leading to esophageal adenocarcinoma (esophagitis, Barrett's esophagus, dysplasia, and carcinoma) has been well described, that of cardiac adenocarcinoma has yet to be defined. We have examined 100 consecutive biopsies of the gastroesophageal (GE) junction in patients with symptoms of GERD, in order to answer the following questions: (1) What is the spectrum of cardiac pathology? (2) Can "carditis" due to GERD be histologically distinguished from carditis due to Helicobacter pylori (HP) infection? (3) Is intestinal metaplasia of the cardia more frequently related to GERD, or to HP infection? (4) What types of esophageal and gastric pathology coexist with carditis? Out of the 100 GE junction biopsies only 63 contained cardiac mucosa and all showed carditis. Carditis was related to HP in 8 cases. Distinguishing histologic features of non-HP carditis included the predominance of reactive epithelial changes over inflammatory changes, a villiform surface and a tendency of the inflammatory infiltrate to decrease with increasing distance from the squamo-columnar junction. Pancreatic metaplasia was seen in 9 cases (14%), none associated with HP. Intestinal metaplasia (IM) was seen in 15 cases (24%) and associated with HP in only 2. Non-HP carditis, with or without IM, was associated with normal or reactive esophageal squamous and distal gastric mucosa in the majority of cases. We conclude that, in our patient population, carditis and cardiac IM is primarily due to GERD and propose that the sequence of events leading to cardiac carcinoma is similar to that of esophageal adenocarcinoma.
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PMID:Pathology of the gastric cardia. 1071 92

The gastric cardia is a microscopic zone that is normally found in the most proximal portion of the stomach, although cardiac-type mucosa may arise in the distal esophagus as a metaplastic phenomenon secondary to gastroesophageal reflux disease (GERD). Inflammation of the native gastric cardia is strongly associated with Helicobacter pylori infection, although there may be a second form of 'carditis' in which metaplastic cardiac-type mucosa becomes inflamed secondary to GERD. Intestinal metaplasia of the cardia may be difficult to recognize because of the difficulty in accurately identifying the esophagogastric junction by endoscopy and the histologic similarities of intestinal metaplasia in the proximal stomach and distal esophagus. However, cytokeratin 7 and 20 immunoreactivity patterns appear to be useful in distinguishing between these forms of intestinal metaplasia. The preponderance of data suggests that intestinal metaplasia of the cardia is associated with H. pylori infection as opposed to GERD, and preliminary data suggest a lower risk of progression to dysplasia and adenocarcinoma when compared to intestinal metaplasia of the distal esophagus.
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PMID:Inflammation and intestinal metaplasia of the gastric cardia: Helicobacter pylori, gastroesophageal reflux disease, or both. 1072 33

Gastroesophageal reflux is a very common disorder. Typical symptoms are heartburn, regurgitation and chest pain. Recently, it has been demonstrated that gastroesophageal reflux may generate or worse extraesophageal symptoms such as asthma, chronic bronchitis, posterior laryngitis, and chronic cough. The diagnosis of gastroesophageal reflux is suggested by typical symptoms which improve under a therapy with proton pump inhibitors. pH-monitoring over 24 hours is able to establish directly the diagnosis by measuring acid reflux into the esophagus. Manometry detects the two most common causes of gastroesophageal reflux: insufficiency of the lower esophageal sphincter or esophageal motility abnormalities. Gastroesophageal reflux can lead to reflux esophagitis, which is diagnosed endoscopically. An endoscopy should routinely be performed in case of dysphagia, anemia, or loss of weight. A long-term sequela of gastroesophageal reflux is the development of Barrett's-esophagus, a condition which has to be verified by endoscopy and biopsy. This premalignant lesion is defined by a metaplastic change from the normal squamous mucosa to a specialized intestinal epithelium characterized by goblet cells. Because dysplasia in these metaplastic areas can lead to esophageal adenocarcinoma, regular endoscopic surveillance with biopsies is recommended. Gastroesophageal reflux can significantly impair the quality of life and can cause complications that include the neoplastic progression from Barrett's esophagus to carcinoma. Therefore, appropriate diagnostic procedures and adequate therapy are required. This article summarizes the diagnostic approach to patients with gastroesophageal reflux, reflux esophagitis and Barrett's-esophagus. The impact of endoscopy, pH-monitoring, esophageal manometry, radiology and scintigraphy are reviewed.
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PMID:[Diagnosis of gastroesophageal reflux and Barrett esophagus]. 1092 25

Adenocarcinoma of the esophagus and gastric cardia are the most rapidly increasing cancers in developed countries. Adenocarcinoma of the esophagus is associated with chronic gastroesophageal reflux, and Barrett's esophagus is a precursor. This disease most frequently affects middle-aged white men. Endoscopic surveillance should be performed on patients with Barrett's esophagus, and esophagectomy is often performed on persons with high-grade dysplasia. Ablation of Barrett's esophagus has been proposed to prevent cancer but the outcomes are unproven. Squamous carcinoma of the esophagus most often affects black men and is associated with alcohol and tobacco use. The diagnosis of esophageal cancer is made by endoscopy with biopsy. Optimal staging is with endoscopic ultrasonography for depth of invasion and regional nodes and CT scanning for distant metastases. Neoadjuvant chemotherapy and radiation therapy followed by surgery is widely practiced, but survival benefits remain to be proven. Palliation of dysphagia may be achieved with surgery, radiation therapy, or endoscopic means, with the latter having fewer complications.
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PMID:Esophageal cancer prevention, cure, and palliation. 1095 Apr 58

Barrett's esophagus is a premalignant lesion of the esophagus that arises as an abnormal tissue response to epithelial injury from gastroesophageal reflux. Barrett's esophagus has previously been considered an irreversible lesion that required life-long surveillance to prevent malignant transformation. Recently, combination therapy with pharmacologic or surgical control of acid reflux combined with endoscopic delivery of a mucosal injury appears to have the capability of reversing superficial Barrett's tissue, and perhaps deeper tissue as well. Whether Barrett's esophagus is cured and cancer/dysplasia prevented by these techniques will require long-term follow-up of these patients.
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PMID:Endoscopic ablation of Barrett's esophagus. 1098 Sep 51

The classic endoscopic diagnosis of a Barrett's esophagus (BE) is based on the finding of > or =3 cm, of distal esophagus covered by specialized columnar epithelium. However, currently, it is based on the finding of intestinal metaplasia (IM) at the squamous-columnar mucosal junction, independent of its extent. The aim of this study was to determine the prevalence of Barrett's esophagus by endoscopic and histological findings in control subjects and in patients with symptoms of gastroesophageal reflux (GER). Three hundred and six control subjects and 376 patients with symptoms of gastroesophageal reflux were included in this prospective study. Patients with Barrett's esophagus were classified in three groups as follows. 1. Intestinal metaplasia at the cardia. When endoscopy showed non-Barrett's esophagus, but histological intestinal metaplasia was found. 2. Short-segment Barrett's esophagus. When <3 cm, was covered with tongues or finger-like or creeping substitution of distal esophagus. 3. Long-segment Barrett's esophagus. When > 3 cm, of distal esophagus was covered by specialized columnar epithelium. Two biopsies at the antrum, four biopsies at the squamous-columnar junction and one or two at the distal esophagus were taken. In control subjects, 1.6% showed histological IM at the esophagogastric junction. In patients with GER without esophagitis or with erosive esophagitis, IM was found in 18% and 10.7% respectively. 'Short-segment' Barrett's esophagus was three times more frequent than 'long-segment' Barrett's esophagus. Patients with Barrett's esophagus were significantly older than the other groups. The presence of complications or erosions, peptic ulcer or stricture were significantly more frequent among patients with 'long-segment' Barrett's esophagus (p < 0.0001). The prevalence of dysplasia was similar in all groups of patients with Barrett's esophagus. Complications such as ulcers, stricture and dysplasia were exclusively seen among patients with BE, whereas non-Barrett's patients did not exhibit these complications. In control subjects, IM can be found in a low percentage of cases. Among patients with symptoms of GER, the classic endoscopic diagnosis of a Barrett's esophagus can underestimate this condition in 80% of the cases. Patients with intestinal metaplasia at the cardia already present 17% of the cases with low-grade dysplasia. In all patients with symptoms of GER, systematic biopsies at the squamous-columnar junction should be taken.
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PMID:Prevalence of Barrett's esophagus by endoscopy and histologic studies: a prospective evaluation of 306 control subjects and 376 patients with symptoms of gastroesophageal reflux. 1100 24

Many gastroenterologists are of the opinion that endoscopic diagnosis of gastro-oesophageal reflux disease (GORD) suffices and that additional biopsies are not necessary. The data obtained from 1068 consecutive patients with histologically confirmed Barrett's oesophagus were analysed retrospectively. In 37.9% of the patients, the histological diagnosis of Barrett's oesophagus was an incidental finding, whereas 32.7% of Barrett's carcinomas were diagnosed only at histology but not during endoscopy. Of the Patients with dysplasia, 92.4% were diagnosed only by the pathologist. Our analysis shows that an endoscopic diagnosis suspicious for Barrett's mucosa is made in 62.1% of the cases, carcinoma in 70%, and dysplasia in only 7.6% of the cases. Also, because neoplasia is detected for the most part at the invasive carcinoma state, but not in the dysplasia stage, the diagnosis of Barrett's oesophagus, with and without dysplasia, needs to be improved by additional biopsies for histopathological investigation.
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PMID:Barrett's mucosa, Barrett's dysplasia and Barrett's carcinoma: diagnostic endoscopy without biopsy-taking does not suffice. 1100 27

In recent years, the diagnosis of short segments of intestinal metaplasia lining the distal esophagus has increased. The aim of the present study was to determine the clinical, endoscopic, histologic and functional results in patients with intestinal metaplasia at the cardia (IMC), carditis and short-segment columnar epithelium (CE) lining the distal esophagus with and without intestinal metaplasia. Four groups were studied: 48 patients with carditis, 105 patients with IMC, 78 patients with short-segment CE (SSCE) without IM and 69 patients with short-segment CE with IM. All had clinical questionnaire, endoscopic and histological evaluation, manometric studies and measurements of acid and bilirubin exposition of the distal esophagus over 24 h. Patients without IM were found to be younger than those with IM. Erosive esophagitis was observed in similar proportions, but hiatal hernia was present in patients with SSCE with or without IM. Patients without IM had mainly cardial mucosa more than fundic mucosa. However, patients with IM had almost exclusively cardial mucosa. Low-grade dysplasia was observed only in patients with IM. Manometric evaluation demonstrated a structural defective lower esophageal sphincter in all groups. Acid and duodenal exposures of the distal esophagus over 24 h were significantly greater in patients with SSCE with IM. In the presence of pathologic gastroesophageal reflux (GER), there are several histological changes at the mucosa distal to the squamous columnar junction. The first metaplastic change is one from fundic to cardial mucosa and, when duodenal reflux occurs, a second metaplastic change to intestinal metaplasia from cardial mucosa occurs. Therefore, in all patients with symptoms of GER, biopsies specimens distal to the squamous columnar junction should be taken routinely.
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PMID:Comparison of clinical, endoscopic and functional findings in patients with intestinal metaplasia at the cardia, carditis and short-segment columnar epithelium of the distal esophagus with and without intestinal metaplasia. 1100 34

Barrett's esophagus occurs more frequently than previously anticipated. Detection of Barrett's esophagus is by endoscopic biopsy in which normal squamous epithelium of the esophagus is replaced by a specialized columnar epithelium of any length. Patients with more than five years of gastroesophageal reflux symptoms, particularly those 50 years of age or older, should have upper endoscopy to detect Barrett's esophagus. With recognition of Barrett's esophagus as a premalignant lesion, the crucial issue is surveillance for detection of dysplasia. Although the natural history of dysplasia is incompletely defined, it is clear that patients with dysplasia have a higher risk for adenocarcinoma than those without dysplasia. Dysplasia is not the ideal marker for selecting patients at high risk for adenocarcinoma, however; recent studies have shown that p53 protein accumulation appears to be earlier and more specific/sensitive marker of malignant potential in Barrett's esophagus. Management of Barrett's esophagus often involves a multidisciplinary evaluation and its current status is reviewed.
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PMID:Barrett's esophagus. 1100 23


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