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Related Concept Videos

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

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Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
536
Peptic Ulcer Disease I: Introduction01:30

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

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

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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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Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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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...
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Related Experiment Video

Updated: Jan 15, 2026

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

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Helicobacter pylori Infection, Metabolomic Signature and Extra-gastric Cancer Risk: A Mediation and Mendelian

Yan Chen1,2, Yuhui Yu1,2, Qiufen Sun1,2

  • 1Department of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.

Molecular Carcinogenesis
|October 7, 2025
PubMed
Summary

Helicobacter pylori infection increases colorectal cancer (CRC) risk, particularly in males. This risk is mediated by sex-specific metabolomic changes, including methionine sulfone, suggesting new prevention strategies.

Keywords:
H. pylori infectionMendelian randomizationcolorectal cancermetabolomic signatureplasma metabolites

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Rapid Detection of Fecal Antigen of Helicobacter pylori Infection Based on Double Antibody Sandwich Detection Technology
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Area of Science:

  • Metabolomics and Cancer Epidemiology
  • Microbiome-Host Interactions

Background:

  • Helicobacter pylori (H. pylori) infection is linked to gastric diseases, with emerging evidence suggesting a role in extra-gastric malignancies.
  • The precise mechanisms connecting H. pylori infection to cancers beyond the stomach remain largely unelucidated.

Purpose of the Study:

  • To investigate the association between H. pylori infection and the risk of major extra-gastric cancers using metabolomic profiling.
  • To identify H. pylori-associated metabolic signatures and explore their mediating role in cancer development, with a focus on sex-specific effects.

Main Methods:

  • Untargeted metabolomics data from 1800 participants in two Chinese cohorts were analyzed to create an H. pylori-associated metabolomic signature.
  • Conditional logistic regression was used in 1:1 matched case-control studies for lung, colorectal (CRC), esophageal, and hepatocellular carcinoma.
  • Mediation and Mendelian randomization (MR) analyses were employed to assess the mediating effects of metabolites and causal relationships.

Main Results:

  • H. pylori infection was significantly associated with increased CRC risk (OR=1.80), predominantly in males (OR=3.01), but not other studied cancers.
  • An H. pylori-associated metabolomic signature (26 metabolites) and methionine sulfone were positively linked to CRC risk in males.
  • Mediation analysis revealed partial mediation by the metabolomic signature (12.08%) and methionine sulfone (16.79%) in males.

Conclusions:

  • H. pylori infection is linked to an elevated risk of colorectal cancer, particularly in males, through sex-specific metabolomic alterations.
  • Methionine sulfone emerges as a key metabolite mediating the association between H. pylori and CRC risk in males.
  • These findings provide insights into CRC pathogenesis and may guide the development of targeted prevention strategies for H. pylori-infected individuals.