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

Inflammation of the gastric cardia, which is the most proximal portion of the stomach, in most instances is the result of either gastroesophageal reflux disease or H. pylori infection. Histologic distinction between these two entities is important because the treatment, natural history, and risk of malignancy are different. Moreover, multilayered epithelium, a possible precursor to Barrett's esophagus, has only recently been described in the gastric cardia, and its relationship to gastroesophageal reflux disease is unknown. The aim of this study was to compare the histologic features of the gastric cardia and the prevalence of multilayered epithelium in patients with reflux versus H. pylori-associated carditis. Routinely processed hematoxylin and eosin-stained mucosal biopsies of the gastric cardia from 30 patients with reflux-associated carditis, 25 with H. pylori-associated carditis, and 30 control patients (no reflux, no H. pylori) were evaluated for a wide variety of histologic features such as goblet cell metaplasia, presence of multilayered epithelium, type of glandular epithelium (mucous, oxyntic, mixed mucous/oxyntic), pancreatic metaplasia, overall degree of inflammation, and the quantity of individual types of inflammatory cells. The clinical and histologic features were compared between the two study groups and controls. Clinically, the reflux carditis group (male/female ratio: 21/9, mean age 56 years) had a significantly higher male/female ratio (p <0.01) and a slightly higher mean age in comparison with the H. pylori group (male/female ratio: 9/16, mean age 50 years). Histologically, the reflux group had significantly less overall inflammation (p <0.05), with fewer plasma cells (p <0.04) and neutrophils (p <0.006), but a higher prevalence of multilayered epithelium [9 of 30 (30%) vs 1 of 25 (4%) in the H. pylori group, p = 0.01]. In the reflux carditis group, multilayered epithelium was significantly associated with neutrophilic inflammation (p <0.05), but not any other features of chronic carditis or with any of the specific epithelial cell types. The control group showed less inflammatory activity in comparison with the H. pylori group and a lower prevalence of multilayered epithelium and eosinophilic inflammation in comparison with the reflux group. The clinical and pathologic features of reflux carditis are distinct from H. pylori carditis and are characterized by less overall inflammation and fewer neutrophils and plasma cells. Multilayered epithelium not uncommonly occurs in the cardia of patients with gastroesophageal reflux disease but without Barrett's esophagus, further supporting our hypothesis that multilayered epithelium may represent an early precursor in the development of columnar metaplasia in Barrett's esophagus.
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PMID:Pathologic features of reflux and Helicobacter pylori-associated carditis: a comparative study. 1282 88

Esophagus is often unregarded, being considered only a pathway for the food. As our knowledge has been rising, esophageal diseases become more frequently diagnosed. Gastroesophageal junction represents the region of contact between two different types of epithelium. Exact delimitation of the border is often very difficult. Also the region of cardia has not been yet precisely defined. The important component of the refluxate, which can impair the esophageal mucosa, is the duodenal content. One of the elemental causes of the reflux disease is probably transient relaxation of the lower esophageal sphincter, which is triggered by the central nervous system. When inflammatory changes are present in cardia, gastric carditis is diagnosed. Histological changes in cardia are related to the presence of Helicobacter pylori infection and also to the gastroesophageal reflux disease. If the aetiology of Helicobacter pylori infection cannot be proved, non-helicobacter solitary carditis is diagnosed. Barrett's esophagus represents an acquired serious impairment of the esophageal mucosa. Barrett's esophagus diagnose depends on the existence of histological changes in the biopsy samples form esophageal mucosa. The most effective treatment of the Barrett's esophagus is the early and long-lasting curing of the esophagus reflux disease. The conservative curing is based on the long-term suppression of gastric acid production by antisecretorics (most effective are inhibitors of proton pump). Functional gastric disorders represent an important group with the most recent international classification done in 1999 (Roma II).
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PMID:[The esophagus: organic and functional disorders--findings in literature in recent years]. 1507 66

Inflammation of the gastric cardia ('carditis') is a histological diagnosis. It seems reasonable to transfer histological criteria of the updated Sydney classification from the distal stomach to the cardia as long as a special classification of inflammation of the esophagogastric junction is lacking. The two best characterized causes of carditis are Helicobacter pylori infection and gastroesophageal reflux disease (GERD). However, the causal contribution and interference of these two factors are highly controversial, as is the clinical relevance of carditis in terms of eliciting symptoms or conferring an increased cancer risk. Variability of studies on carditis is based on conflicting concepts of the normal anatomy of the esophagogastric junction. Cardia-type mucosa (CM) apparently exists at birth as a tiny circular area, and extends to a larger area in adulthood. This implies that cardia-type mucosa is largely metaplastic. Metaplastic CM may evolve in the lower esophagus as a consequence of GERD. It is a general phenomenon that H. pylori-induced gastritis also involves the gastric cardia, irrespective whether the cardia is lined by fundus-type mucosa or CM. The contribution of GERD to inflammation of CM in H. pylori-negative individuals is, however, highly controversial. Prevalence of carditis in GERD patients fluctuates between 10 and 97%. Hence, because of its high frequency and low specificity, carditis can currently not be considered as a clinical entity. The role of carditis for the increasing incidence of cancer of the esophagogastric junction requires careful studies that include accurate description of the area with adequate biopsy protocols.
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PMID:Carditis at the interface between GERD and Helicobacter pylori infection. 1538 52

This study was conducted to assess the frequency of gastroesophageal reflux disease (GERD) and Barrett's esophagus among Sudanese patients with clinical symptoms of heartburn. One hundred and five patients were included in the study; forty seven patients had evidence of reflux oesophagitis, 61.7% of whom had grade B oesophagitis according to the modified Los Angeles classification and 10.6% had Barrett's oesophagus. 78.7% of the biopsies from the esophageal cardia revealed presenced of inflammation (Carditis). Dysplasia was documented in 21.3% of these biopsies. Helicobacter pylori was detected 59.6% of gastrooesophageal reflux disease patients and 56.8% of patients with carditis. However, 80% of patients with Barrett oesophagus were positive for Helicobacter pylori. It was concluded that gastro-oesophageal reflux disease affects all age groups with males being affected more than females and Helicobacter pylori infection did not play a major role in gastro-oesophageal reflux disease orits complications.
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PMID:Gastro-oesophageal reflux disease in Sudan: a clinical endoscopic and histopathological study. 1568 61

The gastroesophageal junction (GEJ), which is defined as the point where the distal esophagus joins the proximal stomach (cardia), is a short anatomic area that is commonly exposed to the injurious effects of GERD and/or Helicobacter pylori infection. These disorders often lead to inflammation and intestinal metaplasia (IM) of this anatomic region. The true gastric cardia is an extremely short segment (<0.4 mm) of mucosa that is typically composed of pure mucous glands, or mixed mucous/oxyntic glands that are histologically indistinguishable from metaplastic mucinous columnar epithelium of the distal esophagus. In patients with GERD, whether physiologic or pathologic, the length of cardia-type epithelium increases and extends proximally above the level of the anatomic GEJ into the distal esophagus. Columnar metaplasia of the distal esophagus represents a squamous to columnar metaplastic reaction that develops from an esophageal stem cell and may pass through an intermediate phase characterized by the presence of a type of epithelium that possesses a mixture of squamous and columnar features, termed multilayered epithelium. In contrast, IM of the gastric cardia represents a columnar to columnar cell metaplastic reaction that develops from a gastric stem cell located in the deep foveolar compartment of the gastric mucosa. Intestinal metaplasia, particularly the incomplete type, is widely believed to represent the precursor lesion upon which dysplasia and cancer arises. The frequency of IM is probably greater in metaplastic columnar epithelium in the esophagus secondary to GERD, than in cases of true gastric carditis secondary to H. pylori, and may be a reason why there is a higher risk of carcinoma in the former compared to the latter. A variety of clinical, endoscopic, histologic, and histochemical methods can be used to distinguish GERD-induced columnar metaplasia of the distal esophagus from H. pylori-induced inflammation of true gastric cardia, and these are outlined in this review, but further controlled studies are needed to critically evaluate these techniques. Further prospective trials are needed to adequately evaluate the different etiologic and pathogenetic mechanisms and, most importantly, the risk of malignancy in these two conditions.
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PMID:Unraveling the mystery of the gastroesophageal junction: a pathologist's perspective. 1645 56

The gastroesophageal junction (GEJ) is a poorly defined anatomic area that represents the junction etween the distal esophagus and the proximal stomach (cardia). The true anatomic GEJ corresponds to the most proximal aspect of the gastric folds, which represents an endoscopically apparent transition oint in most individuals. Many, if not most, adults, particularly those with either physiologic or logic GERD, have a proximally displaced Z-line indicating that the histologic squamocolumnar nction (SCJ) is located above the anatomic GEJ. The histologic characteristics of short segments of columnar mucosa located above the anatomic GEJ in these individuals are similar to the gastric cardia, ng composed of either pure mucous glands or mixed mucous glands/oxyntic glands. Although controversial, some authors believe that the cardia is normally composed, at birth, of surface mucinous columnar epithelium and underlying oxyntic glands identical to the gastric corpus, whereas others maintain that the true anatomic cardia is normally composed of mucinous columnar epithelium with underlying mucous glands or mixed mucous and oxyntic glands. However, the preponderance of evidence supports the latter theory and that the length of mucosa composed of either mucous, or mixed mucous glands/oxyntic glands, increases with age and is presumed to be related to ongoing GERD. Inflammation of the true gastric cardia (carditis), which is most often due to H. pylori infection, is difficult to distinguish from columnar metaplasia of the distal esophagus secondary to GERD. From a pathologist's perspective, the differential diagnosis of true gastric carditis from esophageal columnar metaplasia of the distal esophagus in GEJ biopsies is difficult, but a variety of clinical, pathologic, and immunohistochemical methods can be used to help separate these two disorders. Nearly one-third of patients who present for upper GI endoscopy without endoscopic evidence of BE reveal foci of intestinal metaplasia in the GEJ. There are some studies to suggest that the risk of dysplasia and cancer is different in patients with intestinal metaplasia in the cardia related to H. pylori infection versus those with metaplastic columnar epithelium in the distal esophagus related to GERD. Chronic inflammation is generally considered the predominant underlying stimulus for the development of columnar metaplasia in the GEJ, regardless of the etiology. Columnar metaplasia and intestinal metaplasia in the distal esophagus represents a squamous to columnar cell transition and there is some evidence that this occurs through an intermediate, or transitional, phase of intestinalization termed multilayered epithelium. In contrast, intestinal metaplasia that develops in the true gastric cardia secondary to H. pylori infection represents a columnar to columnar metaplastic reaction. This review will focus on the clinical, pathologic, and pathogenetic aspects of GERD and H. pylori-induced inflammation of the GEJ region.
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PMID:Pathology of the gastroesophageal junction. 1693 53

The etiology of inflammation of the gastric cardia (carditis) is controversial, and gastroesophageal reflux disease (GERD) and H. pylori infection have been proposed as etiological factors. This study aimed to investigate the effect of acid suppression on histological changes in the gastric cardia. Gastric cardia biopsies of reflux patients were evaluated at baseline and after proton pump inhibitor (PPI) therapy. The updated Sydney classification was used to score the biopsies, and carditis scores (pre- and post-PPI therapy) were compared. A total of 31 patients were included, of which 5 patients were excluded, as cardiac mucosa was not documented in either pre- or post-PPI biopsies. The mean duration of PPI therapy was 30 months (SE, 3.04 months). There was no significant change in carditis scores post-PPI therapy. The mean mononuclear and neutrophil scores were 1.23 and 0.35 pre-PPI therapy and 1.73 and 0.62 post-PPI therapy, respectively. No change in mean intestinal metaplasia and atrophy scores was identified. In conclusion, acid suppressive therapy with PPI did not lead to a significant reduction in carditis scores. These results suggest that GERD probably does not play a major role in the pathogenesis of inflammation in the gastric cardia.
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PMID:Effect of proton pump inhibitor therapy on inflammatory changes in the gastric cardia (carditis). 1823 53

"Carditis" (inflammation of the gastric cardiac mucosa) may be associated with gastroesophageal reflux disease (GERD), whereas other studies argue that Helicobacter pylori could play a significant role in the chronic cardiac damage. We examined prospectively histologic features of gastric cardia, esophagitis, and H. pylori status in 204 consecutive subjects with GERD symptoms (57.3% male, 42.7% female mean age 49.2 y) undergoing upper gastrointestinal endoscopy with multiple biopsies in the distal esophagus, cardiac region, and stomach. These were assessed for esophagitis landmarks [Ismail Beigi grading (g0-3)], gastritis, and H. pylori infection (Sydney classification). The average symptom duration was 10.8 months. Endoscopy showed no erosive disease in 54.5% patients, grade "A" esophagitis in 37.6%, "B" in 8%, and "C" in 1 case. Histologic examination disclosed g0 in 8.3% patients, g1 in 78.4%, g2 in 12.8%, and g3 in 1; analysis of the cardia showed oxyntic mucosa in 27.9% patients and chronic cardiac mucosa inflammation in 72.1%. Carditis was significantly related to macroscopic esophagitis (P=0.044) and heartburn score (P=0.001). H. pylori cardiac infection was present in 27.4% cases (73.2% associated with cardiac mucosa). Gastric H. pylori infection was demonstrated in 35% patients. H. pylori in the cardiac region was associated with gastric H. pylori infection (P=0.001) and with paucity of GERD symptoms (P=0.05). A good correlation between carditis and GERD, concerning symptoms and macroscopic esophagitis was found in this study. H. pylori-related carditis is likely to be differently compared with the GERD-related type.
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PMID:The pathology of gastric cardia: a prospective, endoscopic, and morphologic study. 1822 43

The primary cause of the gastroesophageal reflux disease is the impairment of motility and not that of acidic secretion. The reflux disease develops when the balance between aggressive and defensive factors becomes disequilibriated. Among the aggressive factors the gastro-oesophageal (duodeno-gastro-oesophageal) reflux is classified. In its pathogenesis, the major role has the concentration of the hydrochloric acid, presence of bile and of pancreatic enzymes. These factors may be potentiated by the hiatal hernia, gastric dysmotility, insufficient pyloric competency, and subsequent duodeno-gastric reflux. Key factor in the development of the gastroesophageal reflux disease is the length of esophageal exposition to the refluxed gastric content. The role of duodenal content is not yet clear. Mucosal impairment probably comes from the synergistic effects of hydrochloric acid and the bile. The antireflux barrier, luminal clearance, and the tissue resistance may serve as protective factors. The first line of defence is the antireflux barrier--the retrograde flow of the gastric content is blocked by the competence of the lower esophageal sphincter and by the contractile activity of the diaphragm. Transition of epithels in the region of gastro-oesophageal junction is not yet fully understood. When inflammatory and reactive changes are found in the cardiac mucosa, the case is classified as carditis. Three potential mechanisms of incompetence in the region of gastro-oesophageal junction been described: Transient relaxation of the lower oesophageal sphincter, hypotension of the lower oesophageal sphincter, anatomical disruption of the gastro-oesophageal junction, which is frequently connected with hiatal hernia. Majority of papers indicates that the essential causes of the gastroesophageal reflux disease are transient relaxations of the lower esophageal sphincter and diaphragm. In patients with massive reflux esophagitis, pressure of the lower esophageal sphincter is weak and amplitude of esophageal contractions is low. Gradient in the region of the lower esophageal sphincter is formed in the vicinity of the functioning valve, which is formed by musculo-mucosal fold located in transition of esophagus and stomach. In healthy persons, refluxed fluid is quickly removed from the esophagus, which is the second line of defence. Reduction of the frequency or the power of peristaltic contractions causes delayed esophageal clearance. Gravitation and neutralisation of acids by bicarbonates in saliva assist the clearance. Pathogenic processes can be augmented by the retardation of gastric emptying. Composition of the refluxed fluid reflects the seriousness of the disease. Two mechanisms of impaired esophageal emptying has been identified: Peristaltic dysfunction and "re-reflux" related to some hiatal hernias. The third line of defence is the less known and it is represented by "tissue resistance". The role of eicosanoids in the gastroesophageal reflux disease is not yet known because their levels do not correlate with the seriousness of the symptoms. Increased prevalence of the reflux disease during the last years is often correlated with decreased incidence of Helicobacter pylori infections. Ethiopathogenesis of the reflux disease is multifactorial and can include deficient antireflux mechanisms, frequency of reflux episodes, volume and effectiveness of the refluxed fluid, mucosal resistance, deficient esophageal clearance and emptying of the stomach. Among the serious factors may belong the frequency and magnitude of the gastro-oesophageal reflux, however, the key role probably plays the dysfunction of the lower esophageal sphincter.
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PMID:[Ethiopathogenesis of gastroesophageal reflux disease]. 2266 24

Esophageal adenocarcinoma has shown a significant increase in incidence in recent years. It is thought that the development of gastroesophageal reflux disease (GERD), followed by columnar-lined esophagus and the development of dysplasia, leads to invasive adenocarcinoma. The exact pathogenesis of this process, the diagnosis and differentiation of the metaplastic and dysplastic esophageal lesions have yet to be determined. The purpose of this immunohistochemical study was to investigate the expression of pro-tumorigenic enzyme platelet 12-lipoxygenase (p12LOX) using two new available antibodies in non-dysplastic and dysplastic Barrett's esophagus. The stem cell markers nestin, CD117 and CD44, were then evaluated. The comparative group included GERD carditis, gastric intestinal metaplasia and colorectal adenoma. The overexpression of p12LOX detected by two specific antibodies in the non-dysplastic and dysplastic Barrett's mucosa clearly demonstrated that this enzyme plays an important role in the development of esophageal adenocarcinoma.
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PMID:Platelet 12-lipoxygenase and stem cells in Barrett's esophagus. 2296 80


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