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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...
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 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.
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
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...

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Related Experiment Video

Updated: Jun 27, 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 Chronic ITP.

Roberto Stasi1, Drew Provan

  • 1Department of Medical Sciences, Ospedale Regina Apostolorum, Albano Laziale, Italy. roberto.stasi@uniroma2.it

Hematology. American Society of Hematology. Education Program
|December 17, 2008
PubMed
Summary

Eradicating Helicobacter pylori infection can improve platelet counts in about half of immune thrombocytopenic purpura (ITP) patients. This simple treatment is recommended, especially in areas with high H. pylori prevalence.

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One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
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Last Updated: Jun 27, 2026

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

Published on: November 21, 2014

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
10:44

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

Published on: June 18, 2016

Area of Science:

  • Hematology
  • Gastroenterology
  • Immunology

Background:

  • Immune thrombocytopenic purpura (ITP) is an autoimmune disorder characterized by low platelet counts.
  • Helicobacter pylori (H. pylori) infection is implicated in ITP pathogenesis, with eradication showing variable platelet responses.
  • High prevalence of H. pylori infection in certain regions correlates with increased ITP response rates.

Purpose of the Study:

  • To investigate the association between H. pylori eradication and platelet response in ITP patients.
  • To identify factors influencing the effectiveness of H. pylori eradication therapy in ITP.
  • To explore potential mechanisms linking H. pylori infection to immune-mediated platelet destruction.

Main Methods:

  • Observational studies analyzing platelet count changes post-H. pylori eradication.
  • Comparison of response rates across different geographic regions and patient subgroups.
  • Review of proposed pathogenetic mechanisms, including molecular mimicry and immune responses.

Main Results:

  • H. pylori eradication therapy leads to a platelet response in approximately 50% of infected ITP patients.
  • Response rates are higher in specific populations (e.g., Japan, Italy) and less effective in severe or chronic ITP.
  • Predictive clinical features for treatment response remain inconsistently identified.

Conclusions:

  • H. pylori eradication is a simple, inexpensive, and low-toxicity treatment option for ITP patients.
  • Routine screening for H. pylori in ITP patients is advisable, particularly in high-prevalence areas.
  • Further research is needed to elucidate the precise mechanisms of H. pylori's role in ITP and identify response predictors.