Related Experiment Video

Updated: Aug 26, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
09:05

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

Helicobacter pylori seropositivity is associated with enhanced platelet activation in patients with intermittent

Kevin Cassar1, Paul Bachoo, Isobel Ford

  • 1Department of Vascular Surgery, the health Services Research Unit, University of Aberdeen, Aberdeen, Scotland, UK. k.cassar@abdn.ac.uk

Journal of Vascular Surgery
|February 26, 2004
PubMed

Insights

Helicobacter pylori infection is linked to increased platelet activation in patients with intermittent claudication. This enhanced platelet activity in H pylori-positive individuals is not associated with endothelial injury.

Area of Science:

  • Vascular Medicine
  • Infectious Diseases
  • Hematology

Background:

  • Intermittent claudication (IC) patients face elevated cardiovascular and cerebrovascular mortality risks.
  • Helicobacter pylori (H pylori) infection and abnormal platelet function are implicated in atherosclerosis and ischemic events.

Purpose of the Study:

  • To investigate the relationship between H pylori serology, platelet activation, and endothelial injury in patients with IC.

Main Methods:

  • Prospective observational study of 125 IC patients.
  • Assessed H pylori serology via ELISA.
  • Measured platelet activation using P-selectin expression and fibrinogen binding via flow cytometry.
  • Quantified endothelial injury using von Willebrand factor levels.

Main Results:

  • H pylori serology was positive in 49.6% of patients.
  • Significantly increased P-selectin expression (platelet activation marker) in H pylori-positive patients (P=.039).
  • No significant difference in platelet fibrinogen binding or von Willebrand factor levels between groups.

Conclusions:

  • H pylori-positive patients with IC exhibit heightened platelet activation.
  • Endothelial cell injury does not appear to be the mechanism driving this enhanced platelet activation.
Abstract

Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...