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Related Concept Videos

Peptic Ulcer01:27

Peptic Ulcer

23
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...
23
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...
2.0K
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

1.0K
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...
1.0K
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

1.5K
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...
1.5K
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

1.7K
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
1.7K
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

1.5K
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.
1.5K

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Related Experiment Video

Updated: Mar 25, 2026

Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
03:47

Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography

Published on: November 1, 2024

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Association between Helicobacter Pylori and Gastric Cancer.

B Kafle1, R S Bhandari2, P J Lakhey2

  • 1Department of Medicine, Tribhuvan University Teaching Hospital, Kathmandu, Nepal.

JNMA; Journal of the Nepal Medical Association
|February 25, 2016
PubMed
Summary

This study found no significant association between Helicobacter pylori infection and gastric cancer in the studied population. Further prospective trials are needed to explore combined risk factors for gastric carcinogenesis.

Keywords:
helicobacter pylori; gastric cancer; risk factors.

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Area of Science:

  • Gastroenterology
  • Oncology
  • Microbiology

Background:

  • Helicobacter pylori infection is a suspected risk factor for gastric cancer.
  • Gastric carcinogenesis is a complex process influenced by multiple factors.

Purpose of the Study:

  • To investigate the correlation between Helicobacter pylori infection and gastric cancer.
  • To analyze the prevalence of H. pylori in patients with gastric carcinoma.

Main Methods:

  • A case-control study was conducted with 37 gastric cancer patients and 50 healthy controls.
  • H. pylori presence was assessed using ELISA and biopsy methods.
  • Histopathological examination confirmed gastric carcinoma in all cases.

Main Results:

  • H. pylori incidence was 54% in gastric cancer cases and 64% in controls.
  • No statistically significant difference in H. pylori prevalence was observed between cases and controls.
  • Distal tumors showed a significant association with H. pylori positivity.

Conclusions:

  • The study did not establish a definitive association between H. pylori infection and gastric cancer.
  • Prospective studies are recommended to investigate the interplay of various risk factors in gastric cancer development.