Helicobacter pylori infection and coagulation in healthy people

Introduction

Helicobacter pylori infection has recently been associated with an increased risk of developing ischaemic heart disease.1 2 It has been suggested that chronic gastritis related to H pylori infection may increase, through inflammatory mediators, the concentration of certain coagulation factors such as fibrinogen,3 which are predictors of ischaemic heart disease.4 We investigated the potential association between H pylori infection and abnormalities of plasma coagulation in healthy people, with particular emphasis on the possibility of H pylori inducing a tendency towards coagulation, thereby influencing the risk of ischaemic heart disease.

Subjects, methods, and results

Initially, 368 consecutive asymptomatic blood donors (unpaid volunteers) were recruited for this study. Exclusion criteria were age >51 years, any chronic drug treatment, recent intake of drugs interfering with blood coagulation, use of oral contraceptives, previous treatment for H pylori infection, pregnancy or breast feeding, and previous diagnosis of ischaemic heart disease, peptic ulcer, or any systemic chronic illness. Dietary habits, alcohol and cigarette consumption, and socioeconomic status were determined. A total of 300 subjects (229 men) aged 20-51 (mean 34.7) years fulfilled the inclusion criteria and were enrolled into the study. A resting venous blood sample was taken in all subjects and was analysed for concentrations of total cholesterol, C reactive protein, plasma fibrinogen, factor VII C, and haemoglobin; erythrocyte sedimentation rate; prothrombin time; partial thromboplastin time; and platelet and leucocyte count. Prothrombin cleavage fragment (factors I and II), an index of prothrombin activation,5 was also assayed. IgG antibodies specific to H pylori were determined by using a commercial ELISA kit (Helori test, Eurospital, Trieste, Italy); a cut off value of 19% was used, based on previous analysis of 200 patients (sensitivity compared with histology, 92%; specificity, 94%). Student's t test and the χ² test were used to compare characteristics of subjects and values of haemostatic factors in subjects with and without H pylori infection; multiple regression was used to assess the effects of covariates.

The overall prevalence of H pylori infection was 53% (158/300). Table 1) shows that subjects positive for H pylori were significantly older than those negative for H pylori. The groups did not differ significantly in other characteristics or in values for plasma fibrinogen, cholesterol, leucocyte and platelet count, erythrocyte sedimentation rate, prothrombin time, partial thromboplastin time, and C reactive protein. However, concentrations of factor VII C and prothrombin cleavage fragment were significantly higher in positive than in negative subjects, though the association disappeared after adjustment by multiple logistic regression for age, sex, and social class.

Comment

As plasma fibrinogen and total leucocyte count, which are well known risk factors for ischaemic heart disease,4 are increased in patients infected with H pylori,3 the increased risk of ischaemic heart disease in people positive for H pylori may be mediated through raised plasma fibrinogen concentrations. However, a large cross sectional population survey failed to find a significant association between H pylori and fibrinogen.2 These studies may be biased because they included patients with ischaemic heart disease, a condition which could be associated with increased concentrations of coagulation factors irrespective of patients' H pylori status. Comparing the concentrations of circulating coagulation factors in healthy people with and without H pylori infection, we found that H pylori infection is not associated with increased circulating concentrations of fibrinogen, factor VII:C, or prothrombin cleavage fragment, or with other haemostatic factors, which does not support the possibility of this infection inducing a tendency towards a procoagulant state. Thus it seems unlikely that H pylori infection predisposes the development of ischaemic heart disease through effects on the coagulation system.