Intestinal metaplasia at the gastro-oesophageal junction:<i>Helicobacter pylori</i> gastritis or gastro-oesophageal reflux disease?

Hackelsberger, Andreas; Günther, Thomas; Schultze, Viola; Manes, G.; Domínguez–Muñoz, J. Enrique; Roessner, Albert; Malfertheiner, Peter

doi:10.1136/gut.43.1.17

Cited by 145 publications

(80 citation statements)

References 29 publications

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“…Second, more than 95% of patients who had intestinal metaplasia in the present study had intestinal metaplasia originating in the gastric cardia, most of whom had a normalappearing Z line. This contrasts to endoscopy studies, in which the majority of intestinal metaplasia (approximately two thirds in most studies) occurs in short segments of esophageal columnarappearing mucosa identified at endoscopy (5,7,8,11,12). If the stomach, therefore, is the source of intestinal metaplasia in an asymptomatic general patient population, as the present study suggests, then a low rate of adenocarcinoma relative to a high frequency of intestinal metaplasia at the esophagogastric junction is not surprising, given the reduced likelihood of gastric intestinal metaplasia to progress to dysplasia or carcinoma (4 -12).…”

Section: Discussionmentioning

confidence: 82%

The Location and Frequency of Intestinal Metaplasia at the Esophagogastric Junction in 223 Consecutive Autopsies: Implications for Patient Treatment and Preventive Strategies in Barrett's Esophagus

et al. 2000

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The frequency of intestinal metaplasia at the esophagogastric junction is as high as 36% in endoscopy studies; the majority of cases (approximately 67%) occur in short segments of esophageal columnar mucosa. The validity of these studies has been questioned, however, because of heterogenous underlying diseases prompting endoscopy. To determine the frequency and origin of intestinal metaplasia at the esophagogastric junction, we histologically evaluated the entire esophagogastric junction for the presence of intestinal metaplasia using Alcian blue/periodic acid-Schiff mucin stains in 223 consecutive autopsies. Precise localization of the Z line in relation to the esophagogastric junction and tongues of esophageal columnar-appearing mucosa were noted in each case. Mean patient age was 47 years; 69% of patients were male, and 63% were white. Twenty five of 223 cases (11%) had intestinal metaplasia at the esophagogastric junction. Only 2 of 25 cases (8%) had intestinal metaplasia in the esophagus; the remaining 23 cases (92%) had intestinal metaplasia in the gastric cardia. Male gender, advanced age, white ethnic origin, and short tongues of esophageal columnar mucosa were not associated with gastric cardia intestinal metaplasia. An association of distal gastric intestinal metaplasia (P < .01) and chronic gastritis (P < .01) with gastric cardia intestinal metaplasia suggests a role for Helicobacter pylori infection in this process. The frequency of intestinal metaplasia at the esophagogastric junction in an unselected autopsy population is low (11%) even after exhaustive histologic evaluation using Alcian blue mucin stains. Furthermore, intestinal metaplasia is confined to the gastric cardia in more than 90% of cases with no association to male gender, white ethnic origin, advanced age, or the presence of short segments of esophageal columnar-appearing mucosa at endoscopy. These results demonstrate that caution is warranted when applying the findings of endoscopy studies to the development of preventive and screening strategies aimed at identifying Barrett's esophagus in an asymptomatic general population.

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Section: Discussionmentioning

confidence: 82%

The Location and Frequency of Intestinal Metaplasia at the Esophagogastric Junction in 223 Consecutive Autopsies: Implications for Patient Treatment and Preventive Strategies in Barrett's Esophagus

et al. 2000

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“…5 However, the pathogenesis of SIM, which is considered to be a precursor for EAC, still remains controversial. [6][7][8][9][10][11] It is a common assumption that an inverse statistically significant relationship of H. pylori infection with both BE and EAC, thus suggesting a protective role of the infection in these entities. 12,13 As for one of the possible mechanisms, a decrease in the acid production through H. pyloriinduced atrophic corpus gastritis, or through hyposecretion in the nonatrophic stomach may influence a reduced risk of these conditions.…”

mentioning

confidence: 99%

Effects of Helicobacter pylori infection on genetic instability, the aberrant CpG island methylation status and the cellular phenotype in Barrett's esophagus in a Japanese population

Moriichi

Watari

Das³

et al. 2008

Intl Journal of Cancer

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Genetic or epigenetic alterations in Barrett's esophagus (BE) with/without Helicobacter pylori (H. pylori) infection remain unclear. We examined the effects of H. pylori infection on genetic instability (GIN), the CpG island methylation status and a biomarker related to BE carcinogenesis. We analyzed 113 Japanese individuals with endoscopically suspected BE. The patients included, Group CLE (n 5 25): no specialized intestinal metaplasia (SIM) in a columnar lined epithelium (control); Group BE (n 5 88): all had SIM. Microsatellite instability and a loss of heterozygosity as GIN, the methylation status at hMLH1, E-cadherin, p16 and APC, and immunoreactivity using a monoclonal antibody (mAb) Das-1, which specifically reacts with BE, were evaluated. Nine additional patients with BE were prospectively followed up for 2 years after successful H. pylori eradication. The frequency of GIN, methylation at E-cadherin and APC, and mAb Das-1 reactivity in Group BE was significantly higher than that in Group CLE (p < 0.0001, p < 0.0001 and p < 0.005, and p < 0.0001, respectively). Furthermore, GIN, E-cadherin methylation and mAb Das-1 reactivity showed a significantly higher incidence in patients with H. pylori infection than in those without H. pylori infection (p < 0.01, p < 0.005, and p < 0.01, respectively). Interestingly, the patients from Group BE were observed to change to a stable state of molecular alterations in 60% for GIN, 42.9% for E-cadherin methylation and 55.6% for APC methylation, or a reduction of mAb Das-1 reactivity was noted in 25% following eradication. H. pylori infection may therefore affect these molecular alterations associated with the pathogenesis of BE, to some degree, in the Japanese population. '

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“…It has been shown in a number of studies from developed countries that IM is as common as 7-25% in a normal in appearance Z-line (IM-SCJ) in patients referred for upper GI endoscopy (6,(18)(19)(20)(21)(22). This wide range might be related with different patient selection criteria, staining techniques or the characteristics of study areas, such as low prevalence of HP, high income and obesity, etc.…”

Section: Discussionmentioning

confidence: 99%

“…Data on the roles of GERD and HP infection in the pathogenesis of IM at the GEJ are confusing and sometimes contradictory. Hackelsberger et al (22) suggested that the pathogenesis of IM at the SCJ is not uniform. They found that IM-SQJ is a sequela of HP gastritis, but endoscopic features BE are associated with GERD.…”

Section: Discussionmentioning

confidence: 99%

Is the prevalence of intestinal metaplasia at the squamocolumnar junction different in patients with progressive sytemic sclerosis?

Vardar¹,

Vardar²,

Bor³

2010

Turk J Gastroenterol

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Intestinal metaplasia at the gastro-oesophageal junction:Helicobacter pylori gastritis or gastro-oesophageal reflux disease?

Cited by 145 publications

References 29 publications

The Location and Frequency of Intestinal Metaplasia at the Esophagogastric Junction in 223 Consecutive Autopsies: Implications for Patient Treatment and Preventive Strategies in Barrett's Esophagus

The Location and Frequency of Intestinal Metaplasia at the Esophagogastric Junction in 223 Consecutive Autopsies: Implications for Patient Treatment and Preventive Strategies in Barrett's Esophagus

Effects of Helicobacter pylori infection on genetic instability, the aberrant CpG island methylation status and the cellular phenotype in Barrett's esophagus in a Japanese population

Is the prevalence of intestinal metaplasia at the squamocolumnar junction different in patients with progressive sytemic sclerosis?

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