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Hyperhomocysteinaemia, Helicobacter pylori, and coronary heart disease
  1. P H WHINCUP
  1. Department of Primary Care and Population Sciences,
  2. Royal Free Hospital School of Medicine,
  3. London NW3 2PF, UK
  4. Department of Medicine,
  5. St George’s Hospital Medical School,
  6. London SW17 0RE, UK
  7. Department of Epidemiology and Public Health,
  8. University College, Cork, Republic of Ireland
  9. Department of Public Health Sciences,
  10. St George’s Hospital Medical School,
  11. London SW17 0RE, UK
    1. M A MENDALL
    1. Department of Primary Care and Population Sciences,
    2. Royal Free Hospital School of Medicine,
    3. London NW3 2PF, UK
    4. Department of Medicine,
    5. St George’s Hospital Medical School,
    6. London SW17 0RE, UK
    7. Department of Epidemiology and Public Health,
    8. University College, Cork, Republic of Ireland
    9. Department of Public Health Sciences,
    10. St George’s Hospital Medical School,
    11. London SW17 0RE, UK
      1. I J PERRY
      1. Department of Primary Care and Population Sciences,
      2. Royal Free Hospital School of Medicine,
      3. London NW3 2PF, UK
      4. Department of Medicine,
      5. St George’s Hospital Medical School,
      6. London SW17 0RE, UK
      7. Department of Epidemiology and Public Health,
      8. University College, Cork, Republic of Ireland
      9. Department of Public Health Sciences,
      10. St George’s Hospital Medical School,
      11. London SW17 0RE, UK
        1. D P STRACHAN
        1. Department of Primary Care and Population Sciences,
        2. Royal Free Hospital School of Medicine,
        3. London NW3 2PF, UK
        4. Department of Medicine,
        5. St George’s Hospital Medical School,
        6. London SW17 0RE, UK
        7. Department of Epidemiology and Public Health,
        8. University College, Cork, Republic of Ireland
        9. Department of Public Health Sciences,
        10. St George’s Hospital Medical School,
        11. London SW17 0RE, UK

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          Sung and Sanderson1 have suggested that the development of hyperhomocysteinaemia in subjects with Helicobacter pyloriinfection (due to malabsorption and consequent B vitamin deficiency2 ) might provide a link between these two possible causes of coronary heart disease.

          Sir,—Sung and Sanderson1have suggested that the development of hyperhomocysteinaemia in subjects with Helicobacter pylori infection (due to malabsorption and consequent B vitamin deficiency2) might provide a link between these two possible causes of coronary heart disease.

          We have examined this issue within the framework of our earlier prospective case control study of H pylori infection, based on a comparison of incident cases of myocardial infarction (fatal and non-fatal) and controls within the British regional heart study.3 Residual serum samples were available for 110 of 135 cases of myocardial infarction and 118 of 136 controls for measurement of total homocysteine by reverse phase high performance liquid chromatography with fluorescence detection.4 Within the control group, geometric mean total homocysteine concentrations were very similar in subjects seropositive (n = 63) or seronegative (n = 55) for H pylori (11.9 v11.9 μmol/l; p = 0.98).

          In an analysis adjusted for age and town, total homocysteine was positively related to risk of myocardial infarction. For each 5 μmol/l increase in total homocysteine, the odds ratio (OR) increased by 1.38 (95% confidence interval (CI) 1.02 to 1.86; p = 0.03). H pylori seropositivity was positively but non-significantly related to risk of myocardial infarction (OR = 1.56; 95% CI 0.86 to 2.82; p = 0.14). However, mutual adjustment had little effect on the respective odds ratios: for total homocysteine, adjusted OR = 1.35; 95% CI 1.00 to 1.83; p = 0.04; for H pylori, adjusted OR = 1.47; 95% CI 0.81 to 2.68; p = 0.20.

          The findings of this study, while consistent with earlier reports of an association between homocysteine and coronary risk,5do not provide strong support for the hypothesis that hyperhomocysteinaemia and H pylori infection have interrelated effects on coronary risk.

          Acknowledgments

          Analyses of total homocysteine were carried out in the department of pharmacology, University of Bergen, Norway (Professors H Refsum and P M Ueland).

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