Helicobacter pylori seropositivity and atherosclerosis risk factors

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dc.contributor.authorKöksal, A.
dc.contributor.authorEkmekci, Y.
dc.contributor.authorKaradeniz, Y.
dc.contributor.authorKöklü, S.
dc.contributor.authorApan, T.
dc.contributor.authorYilmaz, M.
dc.contributor.authorYildiz, A.
dc.date.accessioned2020-06-25T17:40:13Z
dc.date.available2020-06-25T17:40:13Z
dc.date.issued2004
dc.departmentKırıkkale Üniversitesi
dc.description.abstractCertain viral and bacterial infections may contribute to the initiation and progression of atherosclerosis. The aim of this study is to determine whether Helicobacter pylori ( HP) seropositivity contributes to conventional atherosclerosis risk factors in the development of an early sign of atherosclerosis: intima-media thickness (IMT) of the carotid artery. Eighty-four patients who had at least two conventional atherosclerosis risk factors and a control group of 50 patients having no risk factors for atherosclerosis were enrolled in the study. None of the patients had ever received HP eradication treatment. HP IgG antibodies were determined by enzyme-linked immunosorbent assay. Carotid artery IMT was measured 1 cm before the carotid bifurcation. Seventy-five percent of the study group was HP seropositive. HP seropositive ( n = 64) and seronegative ( n = 21) groups were identical in terms of sex distribution, smoking pattern, mean age, hemoglobin, leukocyte, platelet, C-reactive protein, erythrocyte sedimentation rate, glucose, cholesterol, triglyceride, low-density lipoprotein, high-density lipoprotein, systolic blood pressure and diastolic blood pressure levels. There was no significant difference between the mean carotid IMT of HP seropositive (0.8 +/- 0.3 mm) and negative ( 0.8 +/- 8 0.3 mm) patients in the study group. Similar to the study group, there was no statistically significant difference between mean carotid IMT of HP seropositive (0.56 +/- 0.19 mm) and negative patients (0.67 +/- 0.13 mm) in the control group ( p = 0.2). Future studies concerning virulent strains are needed to determine the probable role of HP in atherosclerosis. Copyright (C) 2004 S. Karger AG, Basel.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.1159/000083603
dc.identifier.endpage389en_US
dc.identifier.issn0257-2753
dc.identifier.issue4en_US
dc.identifier.pmid15812164
dc.identifier.scopus2-s2.0-21844464915
dc.identifier.scopusqualityQ2
dc.identifier.startpage386en_US
dc.identifier.urihttps://doi.org/10.1159/000083603
dc.identifier.urihttps://hdl.handle.net/20.500.12587/3346
dc.identifier.volume22en_US
dc.identifier.wosWOS:000228072200015
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherKargeren_US
dc.relation.ispartofDigestive Diseases
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectatherosclerosisen_US
dc.subjectHelicobacter pylorien_US
dc.subjectinfectionsen_US
dc.subjectcarotid arteryen_US
dc.subjectintima-media thicknessen_US
dc.titleHelicobacter pylori seropositivity and atherosclerosis risk factorsen_US
dc.typeArticle

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