Effect of Helicobacter pylori infection on blood pressure: a community based cross sectional studyBMJ 2001; 323 doi: https://doi.org/10.1136/bmj.323.7307.264 (Published 04 August 2001) Cite this as: BMJ 2001;323:264
- Richard Harvey (), consultant gastroenterologistaa,
- Athene Lane, research associateb,
- Liam Murray, lecturer in public health medicineb,
- Ian Harvey, senior lecturer in health services researchb,
- Prakash Nair, special lecturer in medicinea,
- Jenny Donovan, reader in social medicineb
- a Frenchay Hospital, North Bristol NHS Trust, Bristol BS16 1LE
- b Department of Social Medicine, University of Bristol, Bristol BS8 2PR
- Correspondence to: R Harvey
- Accepted 23 March 2001
Many studies have reported an association between Helicobacter pylori infection and an increased risk of cardiovascular disease. The strength of the association has been hard to judge because of the varied methods of the studies and substantial heterogeneity of the findings. Mechanisms that may contribute to this association include abnormalities in the levels of certain blood proteins (for example fibrinogen or C reactive protein) secondary to the chronic infection 1 2 and raised blood pressure in people infected with H pylori.3–5
There are several methodological difficulties in carrying out studies to determine whether H pylori infection results in raised blood pressure. We have attempted to minimise such problems in a large prospective community based study of the association between H pylori infection and blood pressure.
Methods and results
The Bristol helicobacter project is a community based study centred on the northeastern suburbs of Bristol. The primary aims of the study are to assess the effects of H pylori infection (and its eradication, on a double blind basis) on digestive symptoms and their treatment and on various other aspects of health and quality of life. We have measured blood pressure prospectively in people who were recruited into this study and whose helicobacter status and other risk factors for raised blood pressure were known.
Of the 10 537 subjects enrolled in the project, 1634 (15.5%) were positive for H pylori infection on a 13C- urea breath test, using 100 mg 13C urea with a standard orange juice and citric acid test meal and a cut off of 3.5 δ 13C per ml. Blood pressure was measured with a random-zero sphygmomanometer (Hawksley, Lancing). Participants completed a questionnaire on demographic and lifestyle characteristics, and their height and weight were measured. Blood pressure in 1633 individuals with helicobacter infection was compared with twice that number (3267) of randomly selected non-infected subjects (total 4900). Multiple linear regression models (Stata version 6) were used, with systolic and diastolic blood pressure as the dependent variables, H pylori status as the predictor variable, and the potential confounders as covariables.
Systolic blood pressure was significantly higher in subjects with helicobacter infection before adjustment for age, sex, body mass index (weight (kg)/(height (m)2)), smoking, and high alcohol intake, but significantly lower after these adjustments (see table). No difference was found for diastolic blood pressure. Further analysis after the exclusion of 310 subjects who were taking treatment for previously known hypertension did not change these results significantly.
In multivariable analysis, older age (4.33 mm Hg/decade, 95% confidence interval 3.76 to 4.89), sex (4.1 mm Hg higher in men than in women; 3.20 to 4.94), increasing body mass index (0.74 mm Hg per unit, 0.65 to 0.84), and high alcohol intake, defined as >20 units per week for men and >13 units per week for women (2.64 mm Hg, 1.15 to 4.13), were all associated with a significantly increased systolic blood pressure. Conversely, current use of drugs for hypertension (−10.48 mm Hg, −12.31 to −8.65) was associated with a significant reduction in systolic blood pressure. Similar associations were found for diastolic blood pressure.
Our findings indicate that, contrary to some previous suggestions, the association that exists between cardiovascular disease and H pylori infection is not accounted for by any increase in blood pressure.
H pylori infection had little effect on blood pressure in the general population in the age groups studied when methods designed to minimise potential sampling biases and selection biases were used. Mean systolic blood pressure was higher in H pylori infected individuals than in those who were not infected and, although this is significant statistically, it is unlikely to be clinically important and may be explained by unknown residual confounding factors.
This research was presented at the American Gastroenterological Association meeting in May 2000 and subsequently published in abstract form (Gastroenterology 2000;118 (suppl 2):A723).
Contributors: RH initiated and helped to plan the project, and wrote the initial draft of the paper. AL ran the project from day to day, and helped with the analysis of the data and the final version of the paper. PN helped to set up the project and produce the final version of the paper. LM, IH, and JD helped to plan the project, analyse the results, and produce the final version of the paper. RH is the guarantor.
Funding This study was supported by the South and West Regional Research and Development Directorate and GlaxoSmithKline.
Competing interests RH and AL received financial support from GlaxoWellcome UK to attend the American Gastroenterological Association meeting in May 2000.