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The relation between Helicobacter pylori and atherosclerosis cannot be explained by a high homocysteine concentration
Author(s) -
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.
Publication year - 2002
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2002.01022.x
Subject(s) - homocysteine , helicobacter pylori , vitamin b12 , odds ratio , titer , medicine , hyperhomocysteinemia , antibody , risk factor , immunology , population , antibody titer , gastroenterology , endocrinology , environmental health
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 B 12 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 B 12 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 B 12 , 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 B 12 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.