Helicobacter pylori seropositivity is associated with enhanced platelet activation in patients with intermittent claudication.
OBJECTIVE
Patients with intermittent claudication have a significantly increased risk of mortality from cardiovascular and cerebrovascular causes. Helicobacter pylori infection and abnormal platelet function have been shown to be associated with atherosclerosis as well as with acute ischemic events. The aim of this study was to assess for the first time the relation between H pylori serology status, platelet activation, and endothelial injury in patients with intermittent claudication. Design of study : A prospective observational study of 125 patients with intermittent claudication suitable for angioplasty was conducted at the Vascular Unit of the Aberdeen Royal Infirmary. Main outcome measures Main outcome measures were (1) H pylori serology using ELISA kit for immunoglobulin G antibody to H pylori and (2) whole blood flow cytometric analysis of resting platelet P-selectin expression and fibrinogen binding as measures of platelet activation. Results are presented as platelet percentage. von Wildebrand factor levels were measured using ELISA as a marker of endothelial injury. Carstair deprivation scores were calculated for all patients.


RESULTS
H pylori serology was positive in 62 patients (49.6%), negative in 56 (44.8%) and equivocal in 7 (5.6%). Median P-selectin expression was significantly increased in H pylori-positive patients compared with seronegative patients (0.815 vs 0.65; P =.039). Median platelet fibrinogen binding was higher in seropositive patients, but this failed to reach statistical significance (2.135 vs 1.85%; P =.11). There was no difference in von Wildebrand factor levels between the two groups (P =.51). There was no difference in socioeconomic status between the two groups.


CONCLUSIONS
Patients with intermittent claudication who are H pylori positive show enhanced platelet activation that does not appear to be mediated by means of endothelial cell injury.
Cassar
Kevin
K
Department of Vascular Surgery, the health Services Research Unit, University of Aberdeen, Aberdeen, Scotland, UK. k.cassar@abdn.ac.uk
Bachoo
Paul
P
Ford
Isobel
I
McGee
Magnus
M
Greaves
Mike
M
Brittenden
Julie
J
D000368:Aged; D015415:Biomarkers / Q000097:blood; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology*; D005260:Female; D005340:Fibrinogen / Q000032:analysis / Q000096:biosynthesis / Q000378:metabolism; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori; D006801:Humans; D007383:Intermittent Claudication / Q000097:blood / Q000276:immunology* / Q000382:microbiology*; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000096:biosynthesis / Q000097:blood; D015539:Platelet Activation / Q000276:immunology*; D011446:Prospective Studies; D014841:von Willebrand Factor / Q000032:analysis / Q000096:biosynthesis*
D015415:Biomarkers; D019007:P-Selectin; D014841:von Willebrand Factor; D005340:Fibrinogen