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Related Concept Videos

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...
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Pharmacological management
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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...
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Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
Peptic Ulcer Disease II: Pathophysiology01:24

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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...
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Peptic Ulcer Disease II: Pathophysiology

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Updated: Jun 8, 2026

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

Published on: March 7, 2025

Sequential therapy for Helicobacter pylori eradication.

Mustafa Yakut1, Kubilay Çinar, Gülseren Seven

  • 1Department of Gastroenterology, Ankara University, School of Medicine, Ankara. musyakut@gmail.com

The Turkish Journal of Gastroenterology : the Official Journal of Turkish Society of Gastroenterology
|October 9, 2010
PubMed
Summary

Sequential therapy for Helicobacter pylori achieved 88% eradication initially, persisting in 77% after one year. This offers a viable alternative to declining triple therapy success rates.

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Area of Science:

  • Gastroenterology
  • Infectious Diseases
  • Microbiology

Background:

  • Helicobacter pylori eradication rates with standard triple therapy are declining.
  • Naive H. pylori-positive patients require effective treatment alternatives.

Purpose of the Study:

  • To compare the efficacy of sequential therapy versus ranitidine bismuth citrate-based triple therapy for H. pylori eradication.
  • To assess the long-term persistence of H. pylori eradication achieved with sequential therapy.

Main Methods:

  • Prospective study comparing sequential therapy (pantoprazole, amoxicillin, metronidazole, tetracycline) with ranitidine bismuth citrate-based triple therapy.
  • Invasive H. pylori tests used for diagnosis and one-month post-treatment evaluation.
  • One-year follow-up using H. pylori stool antigen test for sequential therapy group.

Main Results:

  • Initial eradication rates: 88% for sequential therapy vs. 95% for ranitidine bismuth citrate group.
  • One-year follow-up showed sustained eradication in 77% of patients treated with sequential therapy.
  • Both treatments were well-tolerated with minimal side effects.

Conclusions:

  • Sequential therapy demonstrates high initial H. pylori eradication rates.
  • Sustained eradication with sequential therapy is achieved in a significant majority of patients at one year.
  • Sequential therapy is a promising option for H. pylori eradication, especially given the decline in triple therapy effectiveness.