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Cure of Helicobacter pylori infection in patients with reflux oesophagitis treated with long term omeprazole reverses gastritis without exacerbation of reflux disease: results of a randomised controlled trial

Identifieur interne : 001B45 ( Istex/Corpus ); précédent : 001B44; suivant : 001B46

Cure of Helicobacter pylori infection in patients with reflux oesophagitis treated with long term omeprazole reverses gastritis without exacerbation of reflux disease: results of a randomised controlled trial

Auteurs : E J Kuipers ; G F Nelis ; E C Klinkenberg-Knol ; P. Snel ; D. Goldfain ; J J Kolkman ; H P M. Festen ; J. Dent ; P. Zeitoun ; N. Havu ; M. Lamm ; A. Walan

Source :

RBID : ISTEX:90ECB6E19A2425EA04D2907BFE3DB28A49D281AE

English descriptors

Abstract

Background:Helicobacter pylori gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of H pylori gastritis. This prospective randomised study aimed to investigate whether H pylori eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD). Methods: A total of 231 H pylori positive GORD patients who had been treated for ⩾12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and H pylori density. Results: Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group, H pylori was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p<0.001, baseline v two years). Atrophic gastritis also improved in the corpus (p<0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p<0.01). H pylori eradication did not alter the dose of omeprazole required, or reflux symptoms. Conclusions: Most H pylori positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of H pylori eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H pylori eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of H pylori in GORD patients receiving long term acid suppression.

Url:
DOI: 10.1136/gut.53.1.12

Links to Exploration step

ISTEX:90ECB6E19A2425EA04D2907BFE3DB28A49D281AE

Le document en format XML

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<term>Aliment</term>
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<term>Antrum</term>
<term>Atrophic gastritis</term>
<term>Atrophy</term>
<term>Baseline</term>
<term>Biopsy</term>
<term>Centre</term>
<term>Corpus</term>
<term>Corpus gastritis activity</term>
<term>Endoscopy</term>
<term>Eradication</term>
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<term>Gastric atrophy</term>
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<term>Gastroenterology</term>
<term>Glandular</term>
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<term>Gord</term>
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<term>Helicobacter</term>
<term>Helicobacter pylori</term>
<term>Helicobacter pylori eradication</term>
<term>Helicobacter pylori gastritis</term>
<term>Helicobacter pylori infection</term>
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<term>Omeprazole dose</term>
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<term>Pylori infection</term>
<term>Pylori status</term>
<term>Pylorus</term>
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<term>Reflux</term>
<term>Reflux disease</term>
<term>Reflux oesophagitis</term>
<term>Reflux symptoms</term>
<term>Treatment group</term>
<term>Triple</term>
<term>Triple group</term>
<term>Triple groups</term>
<term>Value activity none</term>
<term>Variable score baseline</term>
<term>Visit baseline</term>
<term>atrophy</term>
<term>gastric cancer</term>
<term>gastritis</term>
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<term>Oesophagitis</term>
<term>Omeprazole</term>
<term>Omeprazole dose</term>
<term>Omeprazole maintenance therapy</term>
<term>Pharmacol</term>
<term>Present study</term>
<term>Pylori density</term>
<term>Pylori eradication</term>
<term>Pylori eradication therapy</term>
<term>Pylori infection</term>
<term>Pylori status</term>
<term>Pylorus</term>
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<term>Rectal ulcer</term>
<term>Reflux</term>
<term>Reflux disease</term>
<term>Reflux oesophagitis</term>
<term>Reflux symptoms</term>
<term>Treatment group</term>
<term>Triple</term>
<term>Triple group</term>
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<div type="abstract" xml:lang="en">Background:Helicobacter pylori gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of H pylori gastritis. This prospective randomised study aimed to investigate whether H pylori eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD). Methods: A total of 231 H pylori positive GORD patients who had been treated for ⩾12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and H pylori density. Results: Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group, H pylori was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p<0.001, baseline v two years). Atrophic gastritis also improved in the corpus (p<0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p<0.01). H pylori eradication did not alter the dose of omeprazole required, or reflux symptoms. Conclusions: Most H pylori positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of H pylori eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H pylori eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of H pylori in GORD patients receiving long term acid suppression.</div>
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<abstract>Background:Helicobacter pylori gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of H pylori gastritis. This prospective randomised study aimed to investigate whether H pylori eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD). Methods: A total of 231 H pylori positive GORD patients who had been treated for ⩾12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and H pylori density. Results: Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group, H pylori was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p>0.001, baseline v two years). Atrophic gastritis also improved in the corpus (p>0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p>0.01). H pylori eradication did not alter the dose of omeprazole required, or reflux symptoms. Conclusions: Most H pylori positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of H pylori eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H pylori eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of H pylori in GORD patients receiving long term acid suppression.</abstract>
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<note>Correspondence to:
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<p>Background:Helicobacter pylori gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of H pylori gastritis. This prospective randomised study aimed to investigate whether H pylori eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD). Methods: A total of 231 H pylori positive GORD patients who had been treated for ⩾12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and H pylori density. Results: Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group, H pylori was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p<0.001, baseline v two years). Atrophic gastritis also improved in the corpus (p<0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p<0.01). H pylori eradication did not alter the dose of omeprazole required, or reflux symptoms. Conclusions: Most H pylori positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of H pylori eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H pylori eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of H pylori in GORD patients receiving long term acid suppression.</p>
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<surname>Snel</surname>
<given-names>P</given-names>
</name>
<xref rid="AFF4">4</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Goldfain</surname>
<given-names>D</given-names>
</name>
<xref rid="AFF5">5</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Kolkman</surname>
<given-names>J J</given-names>
</name>
<xref rid="AFF6">6</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Festen</surname>
<given-names>H P M</given-names>
</name>
<xref rid="AFF7">7</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Dent</surname>
<given-names>J</given-names>
</name>
<xref rid="AFF8">8</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Zeitoun</surname>
<given-names>P</given-names>
</name>
<xref rid="AFF9">9</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Havu</surname>
<given-names>N</given-names>
</name>
<xref rid="AFF10">10</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Lamm</surname>
<given-names>M</given-names>
</name>
<xref rid="AFF11">11</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Walan</surname>
<given-names>A</given-names>
</name>
<xref rid="AFF11">11</xref>
</contrib>
<aff id="AFF1">
<label>1</label>
Department of Gastroenterology and Hepatology, Erasmus MC University Medical Centre, Rotterdam, the Netherlands</aff>
<aff id="AFF2">
<label>2</label>
Department of Gastroenterology, Sophia Hospital, Zwolle, the Netherlands</aff>
<aff id="AFF3">
<label>3</label>
Department of Gastroenterology, Free University Hospital, Amsterdam, the Netherlands</aff>
<aff id="AFF4">
<label>4</label>
Department of Gastroenterology, Slotervaart Hospital, Amsterdam, the Netherlands</aff>
<aff id="AFF5">
<label>5</label>
Department of Gastroenterology, Hopital Victor Jusselin, Dreux, France</aff>
<aff id="AFF6">
<label>6</label>
Department of Gastroenterology, Medical Spectrum Twente, Enschede, the Netherlands</aff>
<aff id="AFF7">
<label>7</label>
Department of Gastroenterology, Groot Ziekengasthuis, Den Bosch, the Netherlands</aff>
<aff id="AFF8">
<label>8</label>
Department of Gastroenterology, Royal Adelaide Hospital, Adelaide, Australia</aff>
<aff id="AFF9">
<label>9</label>
Department of Gastroenterology, Hopital Robert Derbre, Reims, France</aff>
<aff id="AFF10">
<label>10</label>
AstraZeneca R&D, Södertalje, Sweden</aff>
<aff id="AFF11">
<label>11</label>
AstraZeneca R&D, Mölndal, Sweden</aff>
</contrib-group>
<author-notes>
<corresp>Correspondence to:
 Professor E J Kuipers
 Department of Gastroenterology and Hepatology, Erasmus MC University Medical Centre, PO Box 2040, 3000 CA Rotterdam, the Netherlands;
<ext-link xlink:href="e.j.kuiperserasmusmc.nl" ext-link-type="email" xlink:type="simple">e.j.kuipers@erasmusmc.nl</ext-link>
</corresp>
</author-notes>
<pub-date pub-type="ppub">
<month>1</month>
<year>2004</year>
</pub-date>
<pub-date pub-type="epub">
<day>18</day>
<month>12</month>
<year>2003</year>
</pub-date>
<volume>53</volume>
<volume-id pub-id-type="other">53</volume-id>
<volume-id pub-id-type="other">53</volume-id>
<issue>1</issue>
<issue-id pub-id-type="other">gutjnl;53/1</issue-id>
<issue-id pub-id-type="other">1</issue-id>
<issue-id pub-id-type="other">53/1</issue-id>
<fpage>12</fpage>
<history>
<date date-type="accepted">
<day>27</day>
<month>05</month>
<year>2003</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright 2004 by Gut</copyright-statement>
<copyright-year>2004</copyright-year>
</permissions>
<self-uri content-type="pdf" xlink:role="full-text" xlink:href="gutjnl-53-12.pdf"></self-uri>
<abstract xml:lang="en">
<p>
<bold>Background:</bold>
<italic>Helicobacter pylori</italic>
gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of
<italic>H pylori</italic>
gastritis. This prospective randomised study aimed to investigate whether
<italic>H pylori</italic>
eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD).</p>
<p>
<bold>Methods:</bold>
A total of 231
<italic>H pylori</italic>
positive GORD patients who had been treated for ⩾12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and
<italic>H pylori</italic>
density.</p>
<p>
<bold>Results:</bold>
Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group,
<italic>H pylori</italic>
was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p<0.001, baseline
<italic>v</italic>
two years). Atrophic gastritis also improved in the corpus (p<0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p<0.01).
<italic>H pylori</italic>
eradication did not alter the dose of omeprazole required, or reflux symptoms.</p>
<p>
<bold>Conclusions:</bold>
Most
<italic>H pylori</italic>
positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of
<italic>H pylori</italic>
eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy.
<italic>H pylori</italic>
eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of
<italic>H pylori</italic>
in GORD patients receiving long term acid suppression.</p>
</abstract>
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<kwd>Helicobacter pylori</kwd>
<kwd>gastro-oesophageal reflux disease</kwd>
<kwd>gastritis</kwd>
<kwd>atrophy</kwd>
<kwd>gastric cancer</kwd>
<kwd>omeprazole</kwd>
<kwd>randomised controlled trial</kwd>
</kwd-group>
<kwd-group kwd-group-type="ABR" xml:lang="en">
<kwd>GORD, gastro-oesophageal reflux disease</kwd>
<kwd>PPI, proton pump inhibitor</kwd>
<kwd>OM, omeprazole</kwd>
<kwd>OAC, omeprazole, amoxycillin, clarithromycin</kwd>
<kwd>OMC, omeprazole, metronidazole, clarithromycin</kwd>
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</front>
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<abstract lang="en">Background:Helicobacter pylori gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of H pylori gastritis. This prospective randomised study aimed to investigate whether H pylori eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD). Methods: A total of 231 H pylori positive GORD patients who had been treated for ⩾12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and H pylori density. Results: Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group, H pylori was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p<0.001, baseline v two years). Atrophic gastritis also improved in the corpus (p<0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p<0.01). H pylori eradication did not alter the dose of omeprazole required, or reflux symptoms. Conclusions: Most H pylori positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of H pylori eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H pylori eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of H pylori in GORD patients receiving long term acid suppression.</abstract>
<note type="author-notes">Correspondence to:
 Professor E J Kuipers
 Department of Gastroenterology and Hepatology, Erasmus MC University Medical Centre, PO Box 2040, 3000 CA Rotterdam, the Netherlands; e.j.kuipers@erasmusmc.nl</note>
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<topic>omeprazole</topic>
<topic>randomised controlled trial</topic>
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<topic>GORD, gastro-oesophageal reflux disease</topic>
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