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 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
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 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
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

52
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...
52
Peptic Ulcer01:27

Peptic Ulcer

48
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...
48

You might also read

Related Articles

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

Sort by
Same author

A Multicenter Analysis of Patients with Bullous Pemphigoid: Clinical Characteristics and Insights into Drug-Associated Disease.

International journal of molecular sciences·2026
Same author

Response to Barnawi et al., "Bullous pemphigoid in the era of immunotherapy: Implications for treatment algorithms".

Journal of the American Academy of Dermatology·2026
Same author

Bidirectional association between immunobullous diseases and obsessive-compulsive disorder including excoriation disorder.

Archives of dermatological research·2026
Same author

Diagnosis of immunobullous diseases in underrepresented groups: an all of us database study.

Archives of dermatological research·2026
Same author

International development of Investigator Global Assessment scores for pemphigus.

Journal of the European Academy of Dermatology and Venereology : JEADV·2026
Same author

US expert opinions on the treatment of bullous pemphigoid based on guidelines from the European Academy of Dermatology and Venereology.

Journal of the American Academy of Dermatology·2026

Related Experiment Video

Updated: May 3, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

9.9K

Pemphigus herpetiformis: from first description until now.

Michael Kasperkiewicz1, Cezary Kowalewski2, Stefania Jabłońska2

  • 1Department of Dermatology, University of Lübeck, Lübeck, Germany.

Journal of the American Academy of Dermatology
|January 30, 2014
PubMed
Summary
This summary is machine-generated.

Pemphigus herpetiformis is a rare autoimmune blistering disease. It presents with features of dermatitis herpetiformis but has the immune markers of pemphigus, often targeting desmoglein 1.

Keywords:
autoantibodyautoantigenautoimmunitybullous diseasedesmogleinpemphigus

More Related Videos

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
05:05

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid

Published on: June 17, 2025

1.7K
Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
10:27

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Published on: December 15, 2011

23.9K

Related Experiment Videos

Last Updated: May 3, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

9.9K
Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
05:05

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid

Published on: June 17, 2025

1.7K
Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
10:27

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Published on: December 15, 2011

23.9K

Area of Science:

  • Dermatology
  • Immunology
  • Autoimmune Diseases

Background:

  • Pemphigus herpetiformis (PH) is a rare autoimmune blistering disease.
  • It clinically resembles dermatitis herpetiformis but immunologically aligns with pemphigus.
  • First described by Jabłońska et al. in 1975.

Purpose of the Study:

  • To summarize reported cases of pemphigus herpetiformis.
  • To consolidate current knowledge on PH epidemiology, clinical, histologic, and immunopathologic features.
  • To review pathophysiologic concepts, associated diseases, and treatment strategies for PH.

Main Methods:

  • Literature review of pemphigus herpetiformis cases.
  • Synthesis of data on clinical presentation, histology, and immunopathology.
  • Analysis of epidemiological trends, associated conditions, and therapeutic outcomes.

Main Results:

  • PH typically targets desmoglein 1, with occasional desmoglein 3 involvement.
  • Autoantibodies against desmocollin are increasingly recognized in PH patients.
  • The disorder presents a unique combination of clinical and immunological characteristics.

Conclusions:

  • Pemphigus herpetiformis represents a distinct entity within the pemphigus spectrum.
  • Understanding its specific autoantigen targets is crucial for diagnosis and management.
  • Further research is needed to fully elucidate the pathophysiology and optimize treatment.