Related Experiment Video

Updated: Jun 27, 2026

Quantitative Polymerase Chain Reaction (qPCR)-Based Rapid Diagnosis of Helicobacter pylori Infection and Antibiotic Resistance
06:40

Quantitative Polymerase Chain Reaction (qPCR)-Based Rapid Diagnosis of Helicobacter pylori Infection and Antibiotic Resistance

Published on: July 28, 2023

Henoch-Schönlein purpura associated with Helicobacter pylori infection in a child

John R Mytinger1, James W Patterson, Erin S Thibault

  • 1Department of Pediatrics, University of Virginia Health System, Charlottesville, VA 22908, USA.

Pediatric Dermatology
|December 11, 2008
PubMed

Insights

Henoch-Schönlein purpura, a vasculitis affecting children, can be linked to infections. This case shows successful treatment of Helicobacter pylori infection leading to Henoch-Schönlein purpura resolution.

Area of Science:

  • Pediatric Rheumatology
  • Infectious Diseases
  • Dermatology

Background:

  • Henoch-Schönlein purpura (HSP) is a common childhood vasculitis.
  • Infections are frequently implicated in HSP pathogenesis.
  • Leukocytoclastic vasculitis affects small blood vessels.

Observation:

  • A pediatric case of Henoch-Schönlein purpura is presented.
  • The patient had a concurrent Helicobacter pylori infection.
  • HSP symptoms were observed in the child.

Findings:

  • A direct association between Helicobacter pylori infection and Henoch-Schönlein purpura was identified.
  • Eradication of H. pylori infection led to symptom resolution.
  • This suggests a causal link in this pediatric case.

Implications:

  • Helicobacter pylori should be considered in the differential diagnosis of childhood HSP.
  • Targeting H. pylori infection may be an effective treatment strategy for HSP.
  • Further research into infectious triggers of childhood vasculitis is warranted.

More Related Videos

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode10:44

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

Published on: June 18, 2016

Related Concept Videos

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...
Peptic Ulcer Disease I: Introduction01:25

Peptic Ulcer Disease I: Introduction

Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...
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 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.