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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...
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...
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.
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...

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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

Helicobacter pylori infection.

Brendan C Delaney1, Paul Moayyedi, David Forman

  • 1Department of Primary Care and General Practice, University of Birmingham, Birmingham, UK.

BMJ Clinical Evidence
|May 21, 2009
PubMed
Summary

This systematic review examines treatments for acute gastroenteritis, finding that clear fluids and enteral rehydration solutions are key for managing dehydration. Loperamide and lactose-free feeds were also evaluated for effectiveness and safety.

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Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
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Area of Science:

  • Gastroenterology
  • Clinical Medicine
  • Evidence-Based Practice

Background:

  • Diarrhoea is characterized by frequent, unformed, liquid stools.
  • Effective management of acute gastroenteritis primarily involves fluid replacement to prevent or treat dehydration.
  • The review focuses on interventions for acute gastroenteritis, a common condition often managed with supportive care.

Purpose of the Study:

  • To systematically review the effects of various treatments for acute gastroenteritis.
  • To answer the clinical question regarding the efficacy and safety of interventions for acute gastroenteritis.
  • To synthesize evidence from multiple databases and include safety alerts.

Main Methods:

  • A systematic review was conducted, searching major medical databases up to August 2006.
  • Inclusion criteria encompassed systematic reviews, randomized controlled trials (RCTs), and observational studies.
  • The GRADE system was utilized to evaluate the quality of evidence for interventions.

Main Results:

  • Sixteen studies met the inclusion criteria for the review.
  • The review assessed interventions including clear fluids, enteral rehydration solutions (oral/gastric), lactose-free feeds, and loperamide.
  • GRADE methodology was applied to determine the quality of evidence for each intervention.

Conclusions:

  • The systematic review provides information on the effectiveness and safety of key interventions for acute gastroenteritis.
  • Clear fluids and enteral rehydration solutions are highlighted as primary management strategies.
  • The safety and efficacy of loperamide and lactose-free feeds were also evaluated within the scope of the review.