Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

44
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...
44
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

3.0K
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.
3.0K
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

807
Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
807
Peptic Ulcer Disease I: Introduction01:25

Peptic Ulcer Disease I: Introduction

28
Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...
28
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

1.2K
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...
1.2K
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

1.7K
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
1.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Microsatellite instability in gastric intestinal metaplasia in patients with and without gastric cancer.

The American journal of pathology·2000
Same author

Helicobacter pylori and gastric cancer: both primary and secondary preventive measures are required.

Archives of internal medicine·2000
Same author

Proinflammatory activation of neutrophils and monocytes by Helicobacter pylori is not associated with cagA, vacA or picB genotypes.

APMIS : acta pathologica, microbiologica, et immunologica Scandinavica·2000
Same author

Modified Genta triple stain for identifying Helicobacter pylori.

Journal of clinical pathology·2000
Same author

Furazolidone combination therapies for Helicobacter pylori infection in the United States.

Alimentary pharmacology & therapeutics·2000
Same author

H. pylori in the pathogenesis of duodenal ulcer: interaction between duodenal acid load, bile, and H. pylori.

The American journal of gastroenterology·2000

Related Experiment Video

Updated: May 4, 2026

Chinese Herbal Retention Enema for the Treatment of Ulcerative Colitis
06:19

Chinese Herbal Retention Enema for the Treatment of Ulcerative Colitis

Published on: May 16, 2025

2.5K

NSAID ulcers: prevalence and prevention.

D Y Graham1

  • 1Rm 3A-320 (111D), Veterans Affairs Medical Center , 2002 Holcombe Blvd., Houston, TX 77030 , USA.

Modern Rheumatology
|January 4, 2014
PubMed
Summary

Misoprostol is the only proven agent to prevent serious ulcers from nonsteroidal anti-inflammatory drug (NSAID) use. Combining proton pump inhibitors with misoprostol may offer better ulcer prevention than either alone in NSAID users.

Area of Science:

  • Gastroenterology
  • Pharmacology

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used but associated with serious gastrointestinal complications, including ulcers.
  • Effective prevention strategies for NSAID-induced ulcers are crucial due to their epidemic nature.

Purpose of the Study:

  • To critique recent clinical trials on endoscopic ulcer prevention in NSAID users.
  • To evaluate the efficacy of different agents and H. pylori status in preventing NSAID-related gastroduodenal ulcers.

Main Methods:

  • Review and critique of results from clinical trials on endoscopic ulcer prevention.
  • Analysis of outcomes based on drug doses, outcome measures, and Helicobacter pylori (H. pylori) status.

Main Results:

  • Misoprostol is the only agent definitively proven to prevent life-threatening ulcer complications in NSAID users.

More Related Videos

Author Spotlight: Liujunzi Decoction as a Traditional Chinese Treatment for Coloproctitis Cancer
06:24

Author Spotlight: Liujunzi Decoction as a Traditional Chinese Treatment for Coloproctitis Cancer

Published on: October 13, 2023

1.9K
Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
08:58

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

Published on: January 5, 2017

12.0K

Related Experiment Videos

Last Updated: May 4, 2026

Chinese Herbal Retention Enema for the Treatment of Ulcerative Colitis
06:19

Chinese Herbal Retention Enema for the Treatment of Ulcerative Colitis

Published on: May 16, 2025

2.5K
Author Spotlight: Liujunzi Decoction as a Traditional Chinese Treatment for Coloproctitis Cancer
06:24

Author Spotlight: Liujunzi Decoction as a Traditional Chinese Treatment for Coloproctitis Cancer

Published on: October 13, 2023

1.9K
Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
08:58

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

Published on: January 5, 2017

12.0K
  • Proton pump inhibitor (PPI) therapy was not superior to a low dose of misoprostol for gastroduodenal ulcer prevention in chronic NSAID users.
  • PPIs were significantly inferior to misoprostol in patients with H. pylori-negative ulcers, while antisecretory therapy accelerated gastritis in H. pylori-positive patients.
  • Combination therapy with an antisecretory drug and low-dose misoprostol may be more effective than monotherapy for preventing NSAID ulcer complications.

    • Conclusions:

    • H. pylori status is a critical factor in managing NSAID-induced ulcers.
    • Consideration of H. pylori eradication is prudent for patients requiring long-term co-therapy with antisecretory agents.
    • Omeprazole alone may provide a false sense of security regarding NSAID ulcer prevention.