The gastric cardia in gastro-oesophageal disease

El‐Zimaity, Hala; Verghese, Vino J; Ramchatesingh, Jacqueline; Graham, David Y.

doi:10.1136/jcp.53.8.619

Cited by 29 publications

(22 citation statements)

References 40 publications

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“…20 Because the exposure of the gastric cardia to acid must be a frequent, perhaps normal phenomenon, 21 which is increased in reflux disease, we wanted to examine whether GORD would induce foveolar hyperplasia at the cardiac mucosa. We found no significant association between gastric cardiac foveolar hyperplasia and endoscopy positive GORD, a result which agrees with that reported by El-Zimaity et al 18 However, endoscopy positive GORD comprises less than half of all GORD cases and a closer study of the associations of cardiac foveolar hyperplasia with non-erosive GORD determined by 24 hour pH monitoring is needed. Our results may also be biased as a result of the exclusion of most of the original study population from our analysis.…”

Section: Discussionsupporting

confidence: 91%

“…In their study, H pylori positive patients were included, which certainly affected their results. 18 An even higher prevalence of 77% of foveolar hyperplasia (H pylori positive cases included) has also been reported. 19 In our study, foveolar hyperplasia was examined by five pathologists and this may have resulted in variations in the scoring of hyperplasia and may have reduced the reproducibility of the results.…”

Section: Discussionmentioning

confidence: 96%

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Foveolar hyperplasia at the gastric cardia: prevalence and associations

Voutilainen¹,

Juhola²,

Färkkilä³

et al. 2002

Journal of Clinical Pathology

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Aims: In the gastric antrum and body, foveolar hyperplasia is a feature of reactive gastritis resulting from-for example, duodenogastric bile reflux and the use of non-steroidal anti-inflammatory drugs (NSAIDs). The aim of this study was to examine the occurrence and clinical relevance of gastric cardiac foveolar hyperplasia. Methods: The study population was drawn from a consecutive series of 1698 patients sent for upper gastrointestinal endoscopy. Only cases without chronic gastritis or Barrett's oesophagus were included. The final study population consisted of 307 patients. Results: Foveolar hyperplasia was seen in the gastric cardiac mucosa in 31 (10%) patients with histologically normal stomach mucosa, but none had endoscopically noticeable hyperplastic polyps. Compared with patients without gastric cardiac hyperplasia, those with hyperplasia more often had chronic inflammation and complete intestinal metaplasia in the junctional biopsies (48% v 77% and 9% v 26%, respectively). Logistic regression analysis revealed that chronic cardiac inflammation (odds ratio (OR), 3.2; 95% confidence interval (CI), 1.3 to 7.8) and intestinal metaplasia of the complete type (OR, 2.8; 95% CI, 1.1 to 7.1) were independent risk factors for cardiac foveolar hyperplasia. In univariate analysis, endoscopic erosive oesophagitis (endoscopy positive gastro-oesophageal reflux disease) and the use of NSAIDs were not related to the presence of foveolar hyperplasia. Conclusions: Foveolar hyperplasia in the gastric cardiac mucosa occurs in patients with histologically normal non-gastritic stomachs and may develop as a consequence of chronic inflammation limited to the gastro-oesophageal junction ("junctitis"). It is not associated directly with endoscopy positive gastro-oesophageal reflux disease or the use of NSAIDs.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 96%

Foveolar hyperplasia at the gastric cardia: prevalence and associations

Voutilainen¹,

Juhola²,

Färkkilä³

et al. 2002

Journal of Clinical Pathology

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“…In these areas, pancreatic (acinar) metaplasia is frequently found and is associated with chronic gastritis. 4,5 Histologically, this type of metaplasia is characterized by acinus-like nests of epithelial cells producing pancreatic enzymes such as amylase, lipase and trypsinogen. 4 Furthermore, the so-called hyperplastic endocrine nodules can be regularly found in severe atrophic corpus gastritis.…”

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confidence: 99%

Gastric PDX-1 expression in pancreatic metaplasia and endocrine cell hyperplasia in atrophic corpus gastritis

et al. 2003

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The homeodomain transcription factor PDX-1 plays a key role in endocrine and exocrine differentiation processes of the pancreas. PDX-1 is also essential for differentiation of endocrine cells in the gastric antrum. The role of PDX-1 in the pathogenesis of endocrine cell hyperplasia and pancreatic metaplasia in corpus and fundus gastritis has not been evaluated. By immunohistochemistry and double-immunofluorescence, we investigated the expression of PDX-1 in 10 tissue specimens with normal human gastric mucosa, nonatrophic and atrophic gastritis and in pancreatic metaplasia, respectively. In normal corpus mucosa and in nonatrophic corpus gastritis, PDX-1 was mainly absent. In pancreatic metaplasia, PDX-1 was found in metaplastic cells and in adjacent gastric glands. In contrast to normal gastric corpus mucosa, PDX-1 could be strongly detected in the cytoplasm of the parietal cells surrounding metaplastic areas. Furthermore, PDX-1 expression was found in hyperplastic endocrine cells and in the surrounding gastric glands in chronic atrophic gastritis. Hyperplastic endocrine cells coexpressed the b-subunit of the gastric H,K-ATPase. We conclude that PDX-1 represents a candidate switch factor for glandular exocrine and endocrine transdifferentiation in chronic gastritis and that an impaired parietal cell differentiation might play a key role in disturbed gastric morphogenic processes. Keywords: PDX-1; gastritis; gastric atrophy; pancreatic metaplasia; endocrine cell hyperplasia In recent years, several factors have been characterized that play a key role in pancreatic organogenesis. 1 The homeobox transcription factor PDX-1 (pancreatic duodenal homeobox-1) also termed IPF-1 could be regarded as master switch for glandular exocrine and endocrine differentiation in the pancreas. Mutations within the PDX-1 gene are associated with type II diabetes mellitus or even with pancreatic agenesis. 2 In the stomach, PDX-1 has been shown to be essential for the differentiation of endocrine cells in the antropyloric region of mice and targeted deletion of PDX-1 leads to severely impaired development of gastrin cells in the antrum. 3 However, no study concerning the potential role of PDX-1 in glandular differentiation processes of the oxyntic mucosa in the corpus and fundus region has been undertaken. In these areas, pancreatic (acinar) metaplasia is frequently found and is associated with chronic gastritis. 4,5 Histologically, this type of metaplasia is characterized by acinus-like nests of epithelial cells producing pancreatic enzymes such as amylase, lipase and trypsinogen. 4 Furthermore, the so-called hyperplastic endocrine nodules can be regularly found in severe atrophic corpus gastritis. These nodules represent precursor lesions for neuroendocrine tumors within the gastric mucosa. 6 The molecular pathogenesis of both, pancreatic metaplasia and endocrine cell hyperplasia, is only poorly understood. To investigate the potential role of PDX-1 in these pathological conditions within the glandular compartment of the gastric mucos...

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“…Some authors reported the presence and/or extent of CM to correlate with GERD [3,4,30] The correlation between GERD and the extent of CM was also found in children [31]. However, other authors [6,8] reported a negative correlation of CM in biopsies from the EGJ with GERD symptoms, but a positive correlation with H. pylori infection. Their conclusion was that CM is metaplastic and expands distally in the cardia as a consequence of chronic gastritis.…”

Section: Anatomical Issuesmentioning

confidence: 83%

“…We have recently reviewed the literature on the prevalence of intestinal at the EGJ [Malfertheiner P: Gut 2004;in press]. Chronic inflammation of the cardia mucosa and intestinal metaplasia at an endoscopically normal EGJ were more often reported in association with H. pylori infection [6,7,9,33,35,39,[53][54][55] than with GERD. However, likewise powerful studies verified a stronger association of such histological features with GERD [7,11,50,55,56].…”

Section: Carditis and Intestinal Metaplasiamentioning

confidence: 99%

Carditis at the Interface between GERD and <i>Helicobacter pylori</i> Infection

Peitz

Malfertheiner²

2004

Dig Dis

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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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The gastric cardia in gastro-oesophageal disease

Cited by 29 publications

References 40 publications

Foveolar hyperplasia at the gastric cardia: prevalence and associations

Foveolar hyperplasia at the gastric cardia: prevalence and associations

Gastric PDX-1 expression in pancreatic metaplasia and endocrine cell hyperplasia in atrophic corpus gastritis

Carditis at the Interface between GERD and <i>Helicobacter pylori</i> Infection

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