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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 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...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
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...

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Related Experiment Video

Updated: Jun 3, 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 and Arteriosclerosis].

Teruaki Matsui1

  • 1Division of Gastroenterology and Hepatology, Dept. of Internal Medicine, Nihon University School of Medicine, Japan.

Gan to Kagaku Ryoho. Cancer & Chemotherapy
|March 16, 2011
PubMed
Summary

Helicobacter pylori infection may lead to arteriosclerosis by reducing vitamin B12 and folic acid levels, increasing homocysteine. Eradicating H. pylori may help prevent this lifestyle-related disease.

Area of Science:

  • Gastroenterology
  • Cardiovascular Medicine
  • Nutritional Science

Background:

  • Helicobacter pylori (H. pylori) infection is linked to various diseases, including gastritis and gastric cancer.
  • Increased homocysteine levels are associated with arteriosclerosis and lifestyle-related diseases.
  • Vitamin B12 (VB12) and folic acid are crucial for homocysteine metabolism, requiring activation by gastric acid and intrinsic factors.

Purpose of the Study:

  • To investigate the relationship between H. pylori infection and homocysteine levels, a potential trigger for arteriosclerosis.
  • To evaluate the impact of H. pylori-induced gastric mucosal atrophy on vitamin B12 and folic acid levels.
  • To assess the effectiveness of H. pylori eradication therapy in preventing arteriosclerosis.

Main Methods:

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Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
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Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

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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

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
05:23

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

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  • Comparison of homocysteine, vitamin B12, and folic acid levels in H. pylori-positive and negative individuals across different age groups.
  • Measurement of arteriosclerosis using pulse wave velocity (PWV).
  • Assessment of gastric mucosal atrophy via gastrointestinal endoscopy.

Main Results:

  • Significantly higher homocysteine and lower vitamin B12 and folic acid levels were observed in elderly individuals and those with H. pylori infection.
  • Pulse wave velocity (PWV) positively correlated with gastrin and homocysteine levels, and inversely with vitamin B12 and folic acid.
  • H. pylori-negative individuals exhibited lower arteriosclerosis; eradication therapy showed a trend towards improvement in H. pylori-positive individuals.

Conclusions:

  • H. pylori infection may induce arteriosclerosis through mechanisms involving gastric mucosal atrophy, leading to deficiencies in vitamin B12 and folic acid.
  • The severity of gastric mucosal atrophy correlates with the severity of arteriosclerosis.
  • H. pylori eradication therapy shows potential in mitigating arteriosclerosis associated with the infection.