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

Allergic Drug Reactions01:27

Allergic Drug Reactions

Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing numerous...
Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation. 
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...

You might also read

Related Articles

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

Sort by
Same author

Bullous Fixed Drug Eruption to Metformin Following a DRESS Syndrome to Allopurinol: What's the Link?

Dermatitis : contact, atopic, occupational, drug·2025
Same author

<i>Letter:</i> Urticarial Vasculitis Triggered by Sulodexide in an Elderly Patient with Renal Impairment: A Case Report.

Dermatitis : contact, atopic, occupational, drug·2025
Same author

Rituximab-induced subcutaneous sarcoidosis in a patient with refractory pemphigus vulgaris.

Therapie·2025
Same author

Carbamazepine-Induced DRESS Syndrome During Epstein-Barr Virus Reactivation in an Adolescent.

The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG·2025
Same author

Caffeine-induced fixed drug eruption: evidence from a positive patch test.

The British journal of dermatology·2024
Same author

Teratogenic effect of Misoprostol following failure of elective abortion: A case of femoral agenesis and review of the literature.

Radiology case reports·2024

Related Experiment Video

Updated: Jul 8, 2026

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

24.5K

Certolizumab-Induced Urticarial Vasculitis: A Case Report.

Bouraoui Ouni1, Ferdaous Chahed1, Raoudha Slim1

  • 1Department of Pharmacology. Faculty of Medicine, University of Sousse, Sousse, Tunisia.

Current Drug Safety
|March 27, 2025
PubMed
Summary

Certolizumab (CZ), a TNF-α blocker for rheumatoid arthritis, can rarely cause urticarial vasculitis (UV). Discontinuation of CZ led to rapid symptom resolution in a patient, highlighting awareness needs.

Keywords:
Certolizumabcase report.rheumatoid arthritistumour necrosis factor-αvasculitis

More Related Videos

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.4K
A Metadata Extraction Approach for Clinical Case Reports to Enable Advanced Understanding of Biomedical Concepts
07:50

A Metadata Extraction Approach for Clinical Case Reports to Enable Advanced Understanding of Biomedical Concepts

Published on: September 20, 2018

15.7K

Related Experiment Videos

Last Updated: Jul 8, 2026

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

24.5K
Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.4K
A Metadata Extraction Approach for Clinical Case Reports to Enable Advanced Understanding of Biomedical Concepts
07:50

A Metadata Extraction Approach for Clinical Case Reports to Enable Advanced Understanding of Biomedical Concepts

Published on: September 20, 2018

15.7K

Area of Science:

  • Rheumatology
  • Dermatology
  • Immunology

Background:

  • Certolizumab (CZ) is a widely used TNF-α inhibitor for rheumatoid arthritis (RA).
  • While effective, rare adverse events associated with biologic therapies require careful monitoring.
  • Urticarial vasculitis (UV) is an uncommon but recognized potential side effect of TNF-α blocking agents.

Observation:

  • A 33-year-old female with RA developed urticarial lesions one week after initiating CZ therapy.
  • Differential diagnoses including infections and autoimmune conditions were excluded through comprehensive testing.
  • The clinical presentation and temporal association strongly suggested CZ-induced UV, supported by a Naranjo score of 5.

Findings:

  • Withdrawal of Certolizumab resulted in the rapid and complete resolution of urticarial skin lesions.
  • This case confirms a probable causal link between CZ treatment and the development of urticarial vasculitis.
  • Microbiological and autoimmunity tests ruled out alternative etiologies for the vasculitis.

Implications:

  • Healthcare providers should consider urticarial vasculitis in patients presenting with characteristic skin lesions during Certolizumab therapy.
  • Increased clinical awareness of this rare side effect is crucial for timely diagnosis and management.
  • Prompt discontinuation of CZ may lead to favorable outcomes and resolution of UV symptoms.