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Query: UMLS:C0017168 (gastroesophageal reflux disease)
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Histologic changes indicative of gastroesophageal reflux disease (GERD) are found on both sides of the squamocolumnar junction (Z-line). In the gastric cardia, inflammation is found as part of GERD in the absence of Helicobacter pylori or other causes of gastritis (carditis). The squamous mucosa is the location most likely to show inflammatory changes, such as neutrophils or eosinophils, close to the Z-line, whereas traditional reactive changes in the squamous mucosa are found only in biopsies taken at least 3 cm above the Z-line. Endoscopic criteria for GERD have a morphologic counterpart in capillary congestion and hemorrhage into the papillae, which have largely been ignored by pathologists as secondary to biopsy trauma. A biopsy protocol that maximizes the chances of detecting changes of GERD is suggested. The traditional definition of Barrett's esophagus as requiring 3 cm of glandular mucosa extending into the esophagus is no longer tenable. However, even the concept of short-segment Barrett's esophagus, in which less than 3 cm of intestinalized mucosa is present, often as tongues, is being challenged because random biopsies immediately distal to the Z-line may also show intestinal metaplasia when Barrett's esophagus is unsuspected endoscopically. Moreover, it is difficult or impossible to determine whether these changes indicate the earliest lesion of Barrett's esophagus or intestinal metaplasia in native cardiac mucosa. It is suggested that Barrett's esophagus be redefined as intestinal metaplasia in the lower esophagus. It is presently unclear whether patients with such minimal Barrett's epithelium are at increased risk for adenocarcinoma or require surveillance. Successful therapy for GERD results in healing of disease in squamous mucosa and may result in regression of Barrett's epithelium. In the stomach it may be associated with temporary regression of H. pylori and associated inflammation, migration of H. pylori into the oxyntic mucosa, hypertrophy and hyperplasia of parietal cells, and a variant of fundic gland polyps. Some patients may be at risk for accelerated atrophic gastritis if inflammation is present before therapy.
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PMID:The biopsy diagnosis of gastroesophageal reflux disease, "carditis," and Barrett's esophagus, and sequelae of therapy. 869 47

A novel pathophysiology of Barrett's esophagus and a new method of assessing biopsy specimens in patients with gastroesophageal reflux disease (GERD) are presented. This is based on the observation in autopsy studies of patients without GERD that the squamous epithelium of the esophagus transitions directly to fundic mucosa in many people and that the cardiac mucosa is of very short length in others. Available evidence suggests that what is termed gastric cardiac mucosa is in reality an abnormal mucosa resulting from metaplasia of the squamous epithelium of the esophagus as a result of GERD. The severity of GERD correlates with the length of metaplastic cardiac mucosa and further changes occurring in it, permitting development of a system that provides good correlation between biopsy histology and severity of GERD. Intestinal metaplasia ("Barrett's esophagus") always occurs in this metaplastic cardiac mucosa. The recognition of this new pathophysiology of Barrett's esophagus permits identification of the entire sequence whereby GERD leads to adenocarcinoma: GERD-->cardiac metaplasia of squamous epithelium-->reflux carditis-->intestinal metaplasia-->dysplasia-->adenocarcinoma. This article also attempts to develop a terminology that avoids use of the confusing term "Barrett's esophagus," which should be discarded.
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PMID:Pathophysiology of Barrett's esophagus. 926 45

In a prospective endoscopic and bioptic study, 141 control subjects and 359 patients with symptoms of gastroesophageal reflux (GER) were included to determine the prevalence of cardial epithelium inflammation or 'carditis' and to determine the prevalence of Helicobacter pylori in this area. Two biopsies at the antrum, four distal to the squamous-columnar junction and two proximal in the esophageal mucosa, were taken. Patients with gastroesophageal reflux were divided into four groups, according to the severity of endoscopic findings: patients without esophagitis, patients with erosive esophagitis, patients with short-segment and long-segment Barrett's esophagus (BE). Control subjects had normal histological findings at the cardia in 90% of cases, fundic mucosa being present twice as cardial epithelium. Carditis was present in 8% of cases and intestinal metaplasia (IM) in 2%. On the contrary, patients with GER had carditis in nearly 50% of cases. Intestinal metaplasia was present in 12% of cases with GER without esophagitis or erosive esophagitis, in 35% of cases with short-segment BE and in 65% of the cases with long-segment BE. IM at the antrum was present in only 5% of cases. Helicobacter pylori at the squamous-columnar junction was present in 13% of control subjects and in 30% of the patients with GER. It is concluded that carditis is an easy and objective marker for the presence of chronic gastroesophageal reflux and the presence of Helicobacter pylori at this region must be carefully evaluated in order to determine some pathogenic role for the development of Barrett's esophagus.
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PMID:'Carditis': an objective histological marker for pathologic gastroesophageal reflux disease. 977 65

To explore the potential contributions of gastroesophageal reflux disease, as opposed to Helicobacter pylori infection, to the development of gastric carditis, we evaluated gastric carditis (using the criteria of the updated Sydney system for the classification of gastritis), clinical and morphologic features of esophagitis, and H. pylori infection (evaluation of Steiner stains) in biopsy specimens from the gastroesophageal squamocolumnar junction. We correlated clinical, endoscopic, and histologic features in an unselected group of 116 patients. Some degree of carditis was found in 107 (92%) of the patients. The mean age of the patients increased with increasing severity of carditis (P < .05). The various groups of patients with different degrees of carditis did not differ significantly in sex ratio, ethnic background, presence of obesity, percentage having symptoms of gastroesophageal reflux disease (such as heartburn, regurgitation, dysphagia, or odynophagia), endoscopic evidence of esophagitis and columnar epithelium in the distal esophagus, or histologic evidence of active esophagitis. The presence, however, of active gastritis and H. pylori infection in the distal stomach and/or in the cardia was significantly associated with carditis. In patients without carditis, H. pylori was not detected in any cardiac or distal gastric biopsy specimen. In contrast, H. pylori was demonstrated in gastric tissue samples (either from the cardia or distally) of patients with carditis, with the prevalence rate increasing with greater degrees of cardiac inflammation. The H. pylori prevalence rate was 12% in the group with mild carditis, 40% in those with moderate carditis, and 57% in patients with marked carditis (P = .0001). In summary, carditis is commonly found in patients with symptoms related to upper gastrointestinal diseases. From analysis of our study cohort, we concluded that carditis was significantly associated with H. pylori infection and active gastritis but not with symptoms or signs of gastroesophageal reflux disease. These findings suggest that carditis with histologic features similar to those of gastritis in the distal stomach was a sequel of H. pylori infection and represented a part of an H. pylori--associated gastric inflammation.
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PMID:Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis. 979 21

Intestinalized epithelium in traditional long-segment Barrett's esophagus (BE) shows increased proliferative activity, which is postulated to be an early step in the metaplasia-dysplasia-carcinoma sequence. The aim of this study was to evaluate the proliferative activity of intestinalized epithelium of the distal esophagus and gastroesophageal junction (IMEGEJ). Tissue sections from 78 consecutive patients (20 with IMEGEJ, 58 without IMEGEJ) who had elective upper gastrointestinal endoscopy over a 6-month period were immunohistochemically stained with MIB-1, the Ki-67 proliferation-antigen-associated marker, for evaluation of the crypt MIB-1 proliferation index (PI), size of the proliferative zone (PZ), and the presence of surface epithelial staining. Data from the IMEGEJ and non-IMEGEJ groups, and from 15 age-matched patients with traditional long-segment BE (>3.0 cm), were compared statistically. IMEGEJ patients showed a statistically significant increase in the mean crypt PI compared with non-IMEGEJ controls (21.9+/-19.5 v 14.3+/-9.3; P=.01). In addition, IMEGEJ cases showed an increase in the mean crypt PZ (52.3+/-16.4 v 45.2+/-17.2; P=.05), and a trend toward an increase in the percentage of cases with MIB-1-positive surface epithelial cells (50% v 33%, P=.18). Patients with IMEGEJ did not differ from patients without IMEGEJ with respect to any other clinical or histological feature, including signs or symptoms of gastroesophageal reflux disease and presence or absence of esophagitis or carditis. The MIB-1 results of the patients with long-segment BE (MIB-1 PI = 22.6+/-20.5, MIB-1 PZ = 51.8+/-19.6, proportion of cases with MIB-1-positive surface cells = 66%) were similar to those with IMEGEJ. Intestinalized epithelium in the distal esophagus or gastroesophageal junction shows increased proliferative activity in comparison with patients without intestinalized epithelium. This finding supports an increased risk of carcinogenesis in patients with IMEGEJ.
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PMID:Proliferative characteristics of intestinalized mucosa in the distal esophagus and gastroesophageal junction (short-segment Barrett's esophagus): a case control study. 1020 62

Adenocarcinomas at the gastroesophageal junction appear to arise from foci of intestinal metaplasia that develop either in the distal esophagus or the proximal stomach (the gastric cardia). Metaplasia is usually a consequence of chronic inflammation, and it is logical to assume that intestinal metaplasia at the gastroesophageal junction develops as a result of chronic inflammation in the epithelia that normally line the junction region. Intestinal metaplasia in the esophagus is known to be a sequela of chronic inflammation in squamous epithelium caused by gastroesophageal reflux disease, whereas intestinal metaplasia in the distal stomach is often a consequence of chronic gastritis caused by Helicobacter pylori infection. For the gastric cardia, the contributions of gastroesophageal reflux disease, H. pylori infection, and other factors to inflammation, metaplasia, and neoplasia are not clear. If physicians are to develop meaningful preventive strategies and specific therapies for tumors of the proximal stomach, a clear understanding of pathogenesis is important. Recent studies on pathogenetic factors for inflammation in cardiac epithelium (gastric carditis) have yielded contradictory results, perhaps because of fundamental differences in the techniques used by different investigators for identifying and sampling the gastric cardia. This report explores the roots of the controversy regarding the role of gastric carditis in the development of metaplasia and neoplasia at the gastroesophageal junction and suggests practical guidelines for biopsy protocols to be used in future studies that will be necessary to resolve these disputes.
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PMID:The role of gastric carditis in metaplasia and neoplasia at the gastroesophageal junction. 1038 31

Heartburn is a common symptom affecting 21-44% of the adult population on a monthly basis. Oesophagitis is less common, affecting 2% of individuals. Epidemiological studies have shown that patients with gastro-oesophageal reflux disease (GORD) have similar incidence rates of Helicobacter pylori infection as do controls. Some groups have reported that there is a lower incidence, deducing that infection does not cause, and in some way confers protection against GORD. Additional supportive evidence is available from reports of GORD development following successful H pylori eradication. The mechanisms involved are complicated. Individuals with H pylori induced pangastritis and subsequent hypochlorhydria may be protected whereas those with an antral predominant gastritis, as in duodenal ulcer disease, with an increased acid output may be prone to development of GORD. Recent evidence has linked H pylori infection with the development of inflammation of the gastric cardia---carditis. Reports are available which show that carditis is a frequent finding in patients with GORD. The incidence of both cardia and oesophageal carcinoma is increasing. The relation between GORD, carditis, intestinal metaplasia, and cardia carcinoma is unclear. Intestinal metaplasia may result from multifocal atrophic gastritis, linked to H pylori infection or from GORD and the development of Barrett's oesophagus. Long term follow up studies will be required to assess the malignant potential of these histological entities and whether or not H pylori infection has an aetiological role.
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PMID:Gastro-oesophageal reflux disease and Helicobacter pylori: an intricate relation. 1045 30

Laparoscopic Nissen fundoplication has been applied with increasing frequency in the treatment of gastroesophageal reflux disease. The aim of this study was to determine the variables that predict outcome of laparoscopic Nissen fundoplication. A multivariate analysis was performed on data from 199 consecutive patients undergoing laparoscopic Nissen fundoplication. Variables included age, sex, body mass index, primary symptoms, clinical response to acid suppression therapy, erosive esophagitis, 24-hour esophageal pH score, and the percentage of time the esophageal pH was less than 4 on 24-hour pH monitoring, lower esophageal sphincter competence, status of the esophageal body motility, hiatal hernia, carditis, intestinal metaplasia of cardiac epithelium limited to the gastroesophageal junction, and Barrett's esophagus of any length. Clinical outcome was obtained from all patients at a median follow-up of 15 months (range 6 to 74 months) after surgery. One hundred seventy-three patients had an excellent or good outcome (87%) and 26 had a fair or poor outcome. Three factors were significantly predictive of a successful outcome: an abnormal 24-hour pH score (odds ratio = 5.4; 95% confidence interval [CI] = 1. 9-15.3), a typical primary symptom (odds ratio = 5.1; 95% CI = 1. 9-13.6), and a clinical response to acid suppression therapy (odds ratio = 3.3; 95% CI = 1.3-8.7). We conclude that 24-hour pH monitoring provides the strongest outcome predictor of laparoscopic Nissen fundoplication and that outcome is based more on the correct identification of the disease than on its severity.
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PMID:Multivariate analysis of factors predicting outcome after laparoscopic Nissen fundoplication. 1048 Nov 22

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

AIMS: There is an increasing awareness that short (less than 3 cm) segments of Barrett's epithelium and macroscopically normal cardia epithelium may harbour specialized intestinal metaplasia (SIM), a premalignant phenotype. This was a prospective study of both the prevalence of SIM in an unselected population of patients attending for endoscopy, and the association of SIM with symptoms, lifestyle, medication, endoscopic oesophagitis and carditis. METHODS: Two hundred consecutive patients underwent endoscopy. Biopsies taken from just below the squamocolumnar junction were stained for SIM, and were analysed for carditis and Helicobacter pylori infection. A detailed questionnaire of symptoms, tobacco consumption and the use of proton pump inhibitors was completed. RESULTS: Forty-two patients (21 per cent) had SIM, 19 of 126 (15 per cent) in an endoscopically normal oesophagus, 15 of 63 (24 per cent) in a short segment of Barrett's epithelium and eight of 11 in classical Barrett's oesophagus. Comparative analysis between the SIM positive and negative groups with respect to potential risk factors is outlined below. Table 1. CONCLUSION: SIM is prevalent in patients undergoing endoscopy, does not correlate with symptoms or with H. pylori infection, but is significantly associated with endoscopic and pathological markers of gastro-oesophageal reflux.
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PMID:Specialized intestinal metaplasia: analysis of prevalence, risk factors and association with gastro-oesophageal reflux disease 1071 66

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