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Gastritis II: Pathophysiology

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

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...

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

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 Ulcer Disease II: Pathophysiology

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: Pathophysiology

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.

Peptic Ulcer Disease I: Introduction

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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.
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Updated: Jul 5, 2026

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

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

Published on: March 7, 2025

Chronic urticaria and Helicobacter pylori.

Mukesh K Yadav¹, Jai P Rishi, S Nijawan

¹Department of Medicine, SMS Medical College, Jaipur, India. dr_mukesh77@rediffmail.com

Indian Journal of Medical Sciences

|May 1, 2008

Summary

Helicobacter pylori (HP) infection is linked to chronic idiopathic urticaria (CIU). Eradicating HP significantly improves skin lesions in CIU patients, suggesting HP should be part of the diagnostic workup.

Area of Science:

Dermatology
Gastroenterology
Microbiology

Background:

Helicobacter pylori (HP) is a newly identified factor potentially causing chronic urticaria (CU).
HP eradication offers a promising treatment avenue for CU, potentially curing the condition.

Purpose of the Study:

To determine the prevalence of HP infection in chronic idiopathic urticaria (CIU) patients.
To evaluate the impact of HP eradication therapy on skin lesions and quality of life in CIU patients.

Main Methods:

Endoscopy with antral biopsy for urease and histopathology to detect HP-associated gastritis.
HP eradication therapy administered to infected patients, with confirmation via fecal antigen assay.
Response assessed using the Chronic Urticaria Quality-of-Life Questionnaire (CU-Q2oL) and need for rescue medication.

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

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

Published on: July 28, 2023

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Last Updated: Jul 5, 2026

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

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

Published on: March 7, 2025

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

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

Published on: July 28, 2023

Main Results:

HP-associated gastritis was found in 70.58% of CIU patients.
Eradication therapy led to significant improvement in 81.25% of infected patients.
A significant association (P = 0.003) was observed between HP presence and response to eradication therapy.

Conclusions:

HP eradication therapy shows a significant positive response in infected CIU patients.
HP infection should be considered in the diagnostic evaluation of individuals with chronic idiopathic urticaria.