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Article: Correlation between Helicobacter pylori infection, gastric inflammation and serum homocysteine concentration

TitleCorrelation between Helicobacter pylori infection, gastric inflammation and serum homocysteine concentration
Authors
Issue Date2001
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HEL
Citation
Helicobacter, 2001, v. 6 n. 2, p. 146-150 How to Cite?
AbstractBackground. Epidemiological studies have suggested a link between chronic Helicobacter pylori infection and ischemic heart disease but the underlying mechanism remains elusive. We hypothesized that H. pylori-associated chronic gastritis causes impairment of absorption of vitamin cofactors that are essential in the metabolism of homocysteine and results in hyperhomocysteinemia. Materials and Methods. Forty-nine dyspeptic patients were studied. H. pylori infection was defined by rapid urease test and histology. Fasting serum homocysteine level, which was measured by a validated commercial fluorescence polarization immunoassay, was correlated with H. pylori infection statuses and gastric histology. H. pylori-infected patients were followed up for 24 weeks post eradication for changes in serum homocysteine concentration. Results. Univariate analyses showed that serum homocysteine level correlated with increasing age (p < .001), male sex (p = .003) and smoking habit (p = .025). There was no significant difference in serum homocysteine levels between H. pylori infected and uninfected subjects (median 10.5 vs. 10.2 μmol/l). After successful eradication of the bacterium, there was no significant reduction in homocysteine level. Moreover, there was no correlation between homocysteine level and gastric histology including H. pylori density, activity and inflammation scores, presence of atrophy or intestinal metaplasia. Conclusions. The postulated link between H. pylori infection and ischemic heart disease, if it actually exists, is unlikely to be mediated through hyperhomocysteinemia.
Persistent Identifierhttp://hdl.handle.net/10722/162485
ISSN
2015 Impact Factor: 3.92
2015 SCImago Journal Rankings: 1.131
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorMa, PKen_US
dc.contributor.authorChoi, PCLen_US
dc.contributor.authorChing, JYLen_US
dc.contributor.authorNg, ACWen_US
dc.contributor.authorPoon, Pen_US
dc.contributor.authorWoo, KSen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:20:26Z-
dc.date.available2012-09-05T05:20:26Z-
dc.date.issued2001en_US
dc.identifier.citationHelicobacter, 2001, v. 6 n. 2, p. 146-150en_US
dc.identifier.issn1083-4389en_US
dc.identifier.urihttp://hdl.handle.net/10722/162485-
dc.description.abstractBackground. Epidemiological studies have suggested a link between chronic Helicobacter pylori infection and ischemic heart disease but the underlying mechanism remains elusive. We hypothesized that H. pylori-associated chronic gastritis causes impairment of absorption of vitamin cofactors that are essential in the metabolism of homocysteine and results in hyperhomocysteinemia. Materials and Methods. Forty-nine dyspeptic patients were studied. H. pylori infection was defined by rapid urease test and histology. Fasting serum homocysteine level, which was measured by a validated commercial fluorescence polarization immunoassay, was correlated with H. pylori infection statuses and gastric histology. H. pylori-infected patients were followed up for 24 weeks post eradication for changes in serum homocysteine concentration. Results. Univariate analyses showed that serum homocysteine level correlated with increasing age (p < .001), male sex (p = .003) and smoking habit (p = .025). There was no significant difference in serum homocysteine levels between H. pylori infected and uninfected subjects (median 10.5 vs. 10.2 μmol/l). After successful eradication of the bacterium, there was no significant reduction in homocysteine level. Moreover, there was no correlation between homocysteine level and gastric histology including H. pylori density, activity and inflammation scores, presence of atrophy or intestinal metaplasia. Conclusions. The postulated link between H. pylori infection and ischemic heart disease, if it actually exists, is unlikely to be mediated through hyperhomocysteinemia.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HELen_US
dc.relation.ispartofHelicobacteren_US
dc.subject.meshAdulten_US
dc.subject.meshAge Factorsen_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshAlcohol Drinkingen_US
dc.subject.meshFemaleen_US
dc.subject.meshGastritis - Blooden_US
dc.subject.meshHelicobacter Infections - Blooden_US
dc.subject.meshHelicobacter Pylorien_US
dc.subject.meshHomocysteine - Blooden_US
dc.subject.meshHumansen_US
dc.subject.meshHyperhomocysteinemia - Complicationsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMyocardial Ischemia - Etiologyen_US
dc.subject.meshSex Factorsen_US
dc.subject.meshSmokingen_US
dc.titleCorrelation between Helicobacter pylori infection, gastric inflammation and serum homocysteine concentrationen_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.1523-5378.2001.00021.xen_US
dc.identifier.pmid11422470-
dc.identifier.scopuseid_2-s2.0-0034956805en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034956805&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume6en_US
dc.identifier.issue2en_US
dc.identifier.spage146en_US
dc.identifier.epage150en_US
dc.identifier.isiWOS:000169428900010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridMa, PK=18836911500en_US
dc.identifier.scopusauthoridChoi, PCL=7102909169en_US
dc.identifier.scopusauthoridChing, JYL=7005086238en_US
dc.identifier.scopusauthoridNg, ACW=8060744200en_US
dc.identifier.scopusauthoridPoon, P=9336837000en_US
dc.identifier.scopusauthoridWoo, KS=7202574149en_US
dc.identifier.scopusauthoridSung, JJY=36847007300en_US

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