The relation between Helicobacter pylori and atherosclerosis cannot be explained by a high homocysteine concentration

Background Recent studies have suggested that a chronic infection with Helicobacter pylori might be an independent risk factor for atherosclerosis. However, a direct role in atherogenesis is not plausible, since the bacterium has not been isolated from atherosclerotic lesions. An indirect mechanism...

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Veröffentlicht in:European journal of clinical investigation 2002-08, Vol.32 (8), p.549-555
Hauptverfasser: Bloemenkamp, D. G. M., Mali, W. P. Th. M., Tanis, B. C., Rosendaal, F. R., Van Den Bosch, M. A. A. J., Kemmeren, J. M., Algra, A., Visseren, F. L. J., Van Der Graaf, Y.
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container_end_page 555
container_issue 8
container_start_page 549
container_title European journal of clinical investigation
container_volume 32
creator Bloemenkamp, D. G. M.
Mali, W. P. Th. M.
Tanis, B. C.
Rosendaal, F. R.
Van Den Bosch, M. A. A. J.
Kemmeren, J. M.
Algra, A.
Visseren, F. L. J.
Van Der Graaf, Y.
description Background Recent studies have suggested that a chronic infection with Helicobacter pylori might be an independent risk factor for atherosclerosis. However, a direct role in atherogenesis is not plausible, since the bacterium has not been isolated from atherosclerotic lesions. An indirect mechanism that could link H. pylori with atherosclerosis might be through an increase in plasma homocysteine concentration caused by deficiencies of vitamin B12 and folate in plasma. Materials and methods  In 150 female patients with peripheral arterial disease (PAD) and in 412 healthy control women from a nation‐wide population‐based case–control study, blood samples were collected to determine the antibody titre against H. pylori and to measure plasma homocysteine, folate and vitamin B12 levels. First, the odds ratio for PAD in women with a positive antibody titre against H. pylori was calculated and adjusted for homocysteine level. Secondly, mean concentrations of vitamin B12, folate and homocysteine were compared in healthy controls with a positive or negative antibody titre against H. pylori. Thirdly, the relation between H. pylori and PAD in individuals with a normal or high homocysteine level was investigated. Results  A positive immunoglobulin G antibody titre against H. pylori was found in 42% of the PAD patients and in 27% of the controls. The age‐ and socio‐economic‐status (SES) adjusted odds ratio for PAD was 1·5 (95%CI; 1·0–2·2). Additional adjustment for homocysteine plasma concentration did not essentially change the odds ratio. Secondly, among the healthy controls, the homocysteine plasma concentration did not depend on the immunoglobulin G titre, neither did the folate plasma concentration. The concentration of vitamin B12 was slightly higher in women with a positive titre. Thirdly, H. pylori infection was a risk factor for PAD in subjects with a normal homocysteine concentration [OR 2·0 (95%CI 1·3–3·1)]. Conclusions  This study shows a relationship between a positive immunoglobulin G antibody titre against H. pylori and PAD in young women. Moreover, this study does not support the hypothesis that H. pylori infection is related to atherosclerosis via an increase in plasma homocysteine concentration.
doi_str_mv 10.1046/j.1365-2362.2002.01022.x
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G. M. ; Mali, W. P. Th. M. ; Tanis, B. C. ; Rosendaal, F. R. ; Van Den Bosch, M. A. A. J. ; Kemmeren, J. M. ; Algra, A. ; Visseren, F. L. J. ; Van Der Graaf, Y.</creator><creatorcontrib>Bloemenkamp, D. G. M. ; Mali, W. P. Th. M. ; Tanis, B. C. ; Rosendaal, F. R. ; Van Den Bosch, M. A. A. J. ; Kemmeren, J. M. ; Algra, A. ; Visseren, F. L. J. ; Van Der Graaf, Y.</creatorcontrib><description>Background Recent studies have suggested that a chronic infection with Helicobacter pylori might be an independent risk factor for atherosclerosis. However, a direct role in atherogenesis is not plausible, since the bacterium has not been isolated from atherosclerotic lesions. An indirect mechanism that could link H. pylori with atherosclerosis might be through an increase in plasma homocysteine concentration caused by deficiencies of vitamin B12 and folate in plasma. Materials and methods  In 150 female patients with peripheral arterial disease (PAD) and in 412 healthy control women from a nation‐wide population‐based case–control study, blood samples were collected to determine the antibody titre against H. pylori and to measure plasma homocysteine, folate and vitamin B12 levels. First, the odds ratio for PAD in women with a positive antibody titre against H. pylori was calculated and adjusted for homocysteine level. Secondly, mean concentrations of vitamin B12, folate and homocysteine were compared in healthy controls with a positive or negative antibody titre against H. pylori. Thirdly, the relation between H. pylori and PAD in individuals with a normal or high homocysteine level was investigated. Results  A positive immunoglobulin G antibody titre against H. pylori was found in 42% of the PAD patients and in 27% of the controls. The age‐ and socio‐economic‐status (SES) adjusted odds ratio for PAD was 1·5 (95%CI; 1·0–2·2). Additional adjustment for homocysteine plasma concentration did not essentially change the odds ratio. Secondly, among the healthy controls, the homocysteine plasma concentration did not depend on the immunoglobulin G titre, neither did the folate plasma concentration. The concentration of vitamin B12 was slightly higher in women with a positive titre. Thirdly, H. pylori infection was a risk factor for PAD in subjects with a normal homocysteine concentration [OR 2·0 (95%CI 1·3–3·1)]. Conclusions  This study shows a relationship between a positive immunoglobulin G antibody titre against H. pylori and PAD in young women. Moreover, this study does not support the hypothesis that H. pylori infection is related to atherosclerosis via an increase in plasma homocysteine concentration.</description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1046/j.1365-2362.2002.01022.x</identifier><identifier>PMID: 12190953</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adolescent ; Adult ; Age Factors ; Antigens, Bacterial - blood ; Arteriosclerosis - blood ; Arteriosclerosis - immunology ; Arteriosclerosis - microbiology ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Case-Control Studies ; Chronic Disease ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Female ; Folic Acid Deficiency - blood ; Helicobacter Infections - blood ; Helicobacter Infections - complications ; Helicobacter Infections - immunology ; Helicobacter pylori ; Helicobacter pylori - immunology ; homocysteine ; Homocysteine - blood ; Humans ; Immunoglobulin G - blood ; Medical sciences ; Middle Aged ; Odds Ratio ; peripheral arterial disease ; Peripheral Vascular Diseases - blood ; Peripheral Vascular Diseases - immunology ; Peripheral Vascular Diseases - microbiology ; Risk Factors ; Socioeconomic Factors ; Vitamin B 12 Deficiency - blood</subject><ispartof>European journal of clinical investigation, 2002-08, Vol.32 (8), p.549-555</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. 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G. M.</creatorcontrib><creatorcontrib>Mali, W. P. Th. M.</creatorcontrib><creatorcontrib>Tanis, B. C.</creatorcontrib><creatorcontrib>Rosendaal, F. R.</creatorcontrib><creatorcontrib>Van Den Bosch, M. A. A. J.</creatorcontrib><creatorcontrib>Kemmeren, J. M.</creatorcontrib><creatorcontrib>Algra, A.</creatorcontrib><creatorcontrib>Visseren, F. L. J.</creatorcontrib><creatorcontrib>Van Der Graaf, Y.</creatorcontrib><title>The relation between Helicobacter pylori and atherosclerosis cannot be explained by a high homocysteine concentration</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description>Background Recent studies have suggested that a chronic infection with Helicobacter pylori might be an independent risk factor for atherosclerosis. However, a direct role in atherogenesis is not plausible, since the bacterium has not been isolated from atherosclerotic lesions. An indirect mechanism that could link H. pylori with atherosclerosis might be through an increase in plasma homocysteine concentration caused by deficiencies of vitamin B12 and folate in plasma. Materials and methods  In 150 female patients with peripheral arterial disease (PAD) and in 412 healthy control women from a nation‐wide population‐based case–control study, blood samples were collected to determine the antibody titre against H. pylori and to measure plasma homocysteine, folate and vitamin B12 levels. First, the odds ratio for PAD in women with a positive antibody titre against H. pylori was calculated and adjusted for homocysteine level. Secondly, mean concentrations of vitamin B12, folate and homocysteine were compared in healthy controls with a positive or negative antibody titre against H. pylori. Thirdly, the relation between H. pylori and PAD in individuals with a normal or high homocysteine level was investigated. Results  A positive immunoglobulin G antibody titre against H. pylori was found in 42% of the PAD patients and in 27% of the controls. The age‐ and socio‐economic‐status (SES) adjusted odds ratio for PAD was 1·5 (95%CI; 1·0–2·2). Additional adjustment for homocysteine plasma concentration did not essentially change the odds ratio. Secondly, among the healthy controls, the homocysteine plasma concentration did not depend on the immunoglobulin G titre, neither did the folate plasma concentration. The concentration of vitamin B12 was slightly higher in women with a positive titre. Thirdly, H. pylori infection was a risk factor for PAD in subjects with a normal homocysteine concentration [OR 2·0 (95%CI 1·3–3·1)]. Conclusions  This study shows a relationship between a positive immunoglobulin G antibody titre against H. pylori and PAD in young women. Moreover, this study does not support the hypothesis that H. pylori infection is related to atherosclerosis via an increase in plasma homocysteine concentration.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Age Factors</subject><subject>Antigens, Bacterial - blood</subject><subject>Arteriosclerosis - blood</subject><subject>Arteriosclerosis - immunology</subject><subject>Arteriosclerosis - microbiology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Chronic Disease</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Female</subject><subject>Folic Acid Deficiency - blood</subject><subject>Helicobacter Infections - blood</subject><subject>Helicobacter Infections - complications</subject><subject>Helicobacter Infections - immunology</subject><subject>Helicobacter pylori</subject><subject>Helicobacter pylori - immunology</subject><subject>homocysteine</subject><subject>Homocysteine - blood</subject><subject>Humans</subject><subject>Immunoglobulin G - blood</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>peripheral arterial disease</subject><subject>Peripheral Vascular Diseases - blood</subject><subject>Peripheral Vascular Diseases - immunology</subject><subject>Peripheral Vascular Diseases - microbiology</subject><subject>Risk Factors</subject><subject>Socioeconomic Factors</subject><subject>Vitamin B 12 Deficiency - blood</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EotPCKyALie4S_BN7kgULNCptpQqKVNSl5Th3iAePPdiJOnl7nM6olbpiY1v2d47vvQchTElJSSU_b0rKpSgYl6xkhLCSUMJYuX-FFk8Pr9GCEFoVrFmyE3Sa0oYQUlPO3qITymhDGsEXaLzrAUdwerDB4xaGBwCPr8BZE1ptBoh4N7kQLda-w3roIYZk3LzahI32PgxZhmG_c9p66HA7YY17-7vHfdgGM6UB8j02wRvwQ3z86B16s9YuwfvjfoZ-fbu4W10VNz8ur1dfbwpTScIKEJ3hQmtatRLarquFMaJbSwAueO6BNbwmupGCVQCyzhJCuGkk1y3PdMXP0PnBdxfD3xHSoLY2GXBOewhjUktG2JKxOoMfX4CbMEafa1O0aSgVjM9u9QEyufsUYa120W51nBQlas5FbdQ8fjWPX825qMdc1D5LPxz9x3YL3bPwGEQGPh0BnYx266i9semZ43VNKiEz9-XAPVgH038XoC5W1_Mp64uD3uZc9k96Hf8oueRLoe6_X6qK1bf3q1uhfvJ_xG24tA</recordid><startdate>200208</startdate><enddate>200208</enddate><creator>Bloemenkamp, D. 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M. ; Tanis, B. C. ; Rosendaal, F. R. ; Van Den Bosch, M. A. A. J. ; Kemmeren, J. M. ; Algra, A. ; Visseren, F. L. J. ; Van Der Graaf, Y.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4602-e5dc35aa14b6ebdd85cc5df6ee35312129380a96524ee68602003c963ab3dd843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Age Factors</topic><topic>Antigens, Bacterial - blood</topic><topic>Arteriosclerosis - blood</topic><topic>Arteriosclerosis - immunology</topic><topic>Arteriosclerosis - microbiology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Chronic Disease</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Folic Acid Deficiency - blood</topic><topic>Helicobacter Infections - blood</topic><topic>Helicobacter Infections - complications</topic><topic>Helicobacter Infections - immunology</topic><topic>Helicobacter pylori</topic><topic>Helicobacter pylori - immunology</topic><topic>homocysteine</topic><topic>Homocysteine - blood</topic><topic>Humans</topic><topic>Immunoglobulin G - blood</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>peripheral arterial disease</topic><topic>Peripheral Vascular Diseases - blood</topic><topic>Peripheral Vascular Diseases - immunology</topic><topic>Peripheral Vascular Diseases - microbiology</topic><topic>Risk Factors</topic><topic>Socioeconomic Factors</topic><topic>Vitamin B 12 Deficiency - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bloemenkamp, D. G. M.</creatorcontrib><creatorcontrib>Mali, W. P. Th. 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J.</creatorcontrib><creatorcontrib>Van Der Graaf, Y.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bloemenkamp, D. G. M.</au><au>Mali, W. P. Th. M.</au><au>Tanis, B. C.</au><au>Rosendaal, F. R.</au><au>Van Den Bosch, M. A. A. J.</au><au>Kemmeren, J. M.</au><au>Algra, A.</au><au>Visseren, F. L. J.</au><au>Van Der Graaf, Y.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The relation between Helicobacter pylori and atherosclerosis cannot be explained by a high homocysteine concentration</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2002-08</date><risdate>2002</risdate><volume>32</volume><issue>8</issue><spage>549</spage><epage>555</epage><pages>549-555</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract>Background Recent studies have suggested that a chronic infection with Helicobacter pylori might be an independent risk factor for atherosclerosis. However, a direct role in atherogenesis is not plausible, since the bacterium has not been isolated from atherosclerotic lesions. An indirect mechanism that could link H. pylori with atherosclerosis might be through an increase in plasma homocysteine concentration caused by deficiencies of vitamin B12 and folate in plasma. Materials and methods  In 150 female patients with peripheral arterial disease (PAD) and in 412 healthy control women from a nation‐wide population‐based case–control study, blood samples were collected to determine the antibody titre against H. pylori and to measure plasma homocysteine, folate and vitamin B12 levels. First, the odds ratio for PAD in women with a positive antibody titre against H. pylori was calculated and adjusted for homocysteine level. Secondly, mean concentrations of vitamin B12, folate and homocysteine were compared in healthy controls with a positive or negative antibody titre against H. pylori. Thirdly, the relation between H. pylori and PAD in individuals with a normal or high homocysteine level was investigated. Results  A positive immunoglobulin G antibody titre against H. pylori was found in 42% of the PAD patients and in 27% of the controls. The age‐ and socio‐economic‐status (SES) adjusted odds ratio for PAD was 1·5 (95%CI; 1·0–2·2). Additional adjustment for homocysteine plasma concentration did not essentially change the odds ratio. Secondly, among the healthy controls, the homocysteine plasma concentration did not depend on the immunoglobulin G titre, neither did the folate plasma concentration. The concentration of vitamin B12 was slightly higher in women with a positive titre. Thirdly, H. pylori infection was a risk factor for PAD in subjects with a normal homocysteine concentration [OR 2·0 (95%CI 1·3–3·1)]. Conclusions  This study shows a relationship between a positive immunoglobulin G antibody titre against H. pylori and PAD in young women. Moreover, this study does not support the hypothesis that H. pylori infection is related to atherosclerosis via an increase in plasma homocysteine concentration.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12190953</pmid><doi>10.1046/j.1365-2362.2002.01022.x</doi><tpages>7</tpages></addata></record>
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subjects Adolescent
Adult
Age Factors
Antigens, Bacterial - blood
Arteriosclerosis - blood
Arteriosclerosis - immunology
Arteriosclerosis - microbiology
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Case-Control Studies
Chronic Disease
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Female
Folic Acid Deficiency - blood
Helicobacter Infections - blood
Helicobacter Infections - complications
Helicobacter Infections - immunology
Helicobacter pylori
Helicobacter pylori - immunology
homocysteine
Homocysteine - blood
Humans
Immunoglobulin G - blood
Medical sciences
Middle Aged
Odds Ratio
peripheral arterial disease
Peripheral Vascular Diseases - blood
Peripheral Vascular Diseases - immunology
Peripheral Vascular Diseases - microbiology
Risk Factors
Socioeconomic Factors
Vitamin B 12 Deficiency - blood
title The relation between Helicobacter pylori and atherosclerosis cannot be explained by a high homocysteine concentration
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