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Article: Dysfunction of oesophageal motility in Helicobacter pylori-infected patients with reflux oesophagitis

TitleDysfunction of oesophageal motility in Helicobacter pylori-infected patients with reflux oesophagitis
Authors
Issue Date2001
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APT
Citation
Alimentary Pharmacology And Therapeutics, 2001, v. 15 n. 12, p. 1913-1919 How to Cite?
AbstractBackground: Helicobacter pylori infection has been suggested to be protective against gastro-oesophageal reflux disease. However, a significant proportion of patients with gastro-oesophageal reflux disease are infected by H. pylori. Aim: To study oesophageal motor function in H. pylori-infected patients with reflux oesophagitis. Methods: Patients with erosive reflux oesophagitis were recruited prospectively for stationary oesophageal manometry and 24-h ambulatory oesophageal pH monitoring. H. pylori status was determined by biopsy urease test. Non-reflux volunteers were recruited as controls. Results: Seventy-four patients with erosive oesophagitis (34 H. pylori-positive, 40 H. pylori-negative) and 48 non-reflux patient controls (22 H. pylori-positive, 26 H. pylori-negative) were recruited. There was no difference in severity of oesophagitis (median grade, 1; P = 0.53) or oesophageal acid exposure (total percentage time oesophageal pH < 4, 7.6% vs. 6.8%; P = 0.57) between H. pylori-positive and H. pylori-negative groups. Compared to H. pylori-negative patients, H. pylori-positive patients had significantly lower basal lower oesophageal sphincter pressure (12.2 mmHg vs. 15.3 mmHg; P = 0.03) and amplitude of distal peristalsis (56.9 mmHg vs. 68.4 mmHg: P = 0.03). Ineffective oesophageal motility (14% vs. 7%; P = 0.02) and failed oesophageal peristalsis were also significantly more prevalent in H. pylori-positive patients. Conclusions: Among patients with a similar degree of reflux oesophagitis, H. pylori-infected patients have more severe oesophageal dysmotility and lower oesophageal sphincter dysfunction. Oesophageal motor dysfunction probably plays a dominant role in the development of gastro-oesophageal reflux disease in patients with H. pylori infection.
Persistent Identifierhttp://hdl.handle.net/10722/162543
ISSN
2015 Impact Factor: 6.32
2015 SCImago Journal Rankings: 2.833
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWu, JCYen_US
dc.contributor.authorLai, ACWen_US
dc.contributor.authorWong, SKHen_US
dc.contributor.authorChan, FKLen_US
dc.contributor.authorLeung, WKen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:20:55Z-
dc.date.available2012-09-05T05:20:55Z-
dc.date.issued2001en_US
dc.identifier.citationAlimentary Pharmacology And Therapeutics, 2001, v. 15 n. 12, p. 1913-1919en_US
dc.identifier.issn0269-2813en_US
dc.identifier.urihttp://hdl.handle.net/10722/162543-
dc.description.abstractBackground: Helicobacter pylori infection has been suggested to be protective against gastro-oesophageal reflux disease. However, a significant proportion of patients with gastro-oesophageal reflux disease are infected by H. pylori. Aim: To study oesophageal motor function in H. pylori-infected patients with reflux oesophagitis. Methods: Patients with erosive reflux oesophagitis were recruited prospectively for stationary oesophageal manometry and 24-h ambulatory oesophageal pH monitoring. H. pylori status was determined by biopsy urease test. Non-reflux volunteers were recruited as controls. Results: Seventy-four patients with erosive oesophagitis (34 H. pylori-positive, 40 H. pylori-negative) and 48 non-reflux patient controls (22 H. pylori-positive, 26 H. pylori-negative) were recruited. There was no difference in severity of oesophagitis (median grade, 1; P = 0.53) or oesophageal acid exposure (total percentage time oesophageal pH < 4, 7.6% vs. 6.8%; P = 0.57) between H. pylori-positive and H. pylori-negative groups. Compared to H. pylori-negative patients, H. pylori-positive patients had significantly lower basal lower oesophageal sphincter pressure (12.2 mmHg vs. 15.3 mmHg; P = 0.03) and amplitude of distal peristalsis (56.9 mmHg vs. 68.4 mmHg: P = 0.03). Ineffective oesophageal motility (14% vs. 7%; P = 0.02) and failed oesophageal peristalsis were also significantly more prevalent in H. pylori-positive patients. Conclusions: Among patients with a similar degree of reflux oesophagitis, H. pylori-infected patients have more severe oesophageal dysmotility and lower oesophageal sphincter dysfunction. Oesophageal motor dysfunction probably plays a dominant role in the development of gastro-oesophageal reflux disease in patients with H. pylori infection.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APTen_US
dc.relation.ispartofAlimentary Pharmacology and Therapeuticsen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshEsophagitis, Peptic - Microbiology - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGastritis - Microbiology - Physiopathologyen_US
dc.subject.meshGastroesophageal Reflux - Microbiology - Physiopathologyen_US
dc.subject.meshHelicobacter Infections - Microbiology - Physiopathologyen_US
dc.subject.meshHelicobacter Pylorien_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.titleDysfunction of oesophageal motility in Helicobacter pylori-infected patients with reflux oesophagitisen_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2036.2001.01132.xen_US
dc.identifier.pmid11736722-
dc.identifier.scopuseid_2-s2.0-0035659488en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035659488&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume15en_US
dc.identifier.issue12en_US
dc.identifier.spage1913en_US
dc.identifier.epage1919en_US
dc.identifier.isiWOS:000172788300010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridWu, JCY=7409253910en_US
dc.identifier.scopusauthoridLai, ACW=7102226209en_US
dc.identifier.scopusauthoridWong, SKH=24345849900en_US
dc.identifier.scopusauthoridChan, FKL=7202586434en_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US

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