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Related Concept Videos

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: 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...
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...
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...
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...
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...

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Related Experiment Video

Updated: Jul 7, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
05:46

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

Abacavir hypersensitivity reaction: an update.

Christine A Hughes1, Michelle M Foisy, Norman Dewhurst

  • 1Faculty of Pharmacy & Pharmaceutical Sciences, HIV, Northern Alberta HIV Program and Regional Pharmacy Services, Capital Health Region, Edmonton, Alberta, Canada. hughes@ualberta.ca

The Annals of Pharmacotherapy
|February 28, 2008
PubMed
Summary

Abacavir hypersensitivity reaction (HSR) is a serious immune-mediated event. Genetic screening for HLA-B(*)5701 before starting abacavir significantly reduces HSR risk and avoids unnecessary drug discontinuation.

Related Experiment Videos

Last Updated: Jul 7, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
05:46

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

Area of Science:

  • Pharmacogenomics
  • Immunology
  • Infectious Diseases

Background:

  • Abacavir is an important antiretroviral medication for HIV treatment.
  • Abacavir hypersensitivity reaction (HSR) is a significant adverse event associated with its use.
  • HSR onset is typically within the first 6 weeks of therapy, presenting with nonspecific symptoms.

Purpose of the Study:

  • To review the clinical features, risk factors, diagnosis, and management of abacavir HSR.
  • To evaluate the role of genetic screening in preventing abacavir-induced hypersensitivity.

Main Methods:

  • Comprehensive literature search of MEDLINE and EMBASE databases (1950-2007).
  • Inclusion of studies on clinical and immunogenetic risk factors, genetic screening benefits, and HSR management.
  • Review of conference abstracts and article bibliographies for relevant information.

Main Results:

  • Abacavir HSR is immune-mediated with nonspecific signs and symptoms, complicating diagnosis.
  • Patch testing may aid diagnosis but remains experimental.
  • Genetic screening for human leukocyte antigen (HLA) HLA-B(*)5701 demonstrates 100% negative predictive value for abacavir HSR.
  • Pharmacogenetic testing for HLA-B(*)5701 appears cost-effective.

Conclusions:

  • Early recognition and management of abacavir HSR are crucial to avoid serious adverse events.
  • Screening for HLA-B(*)5701 before abacavir initiation is a valuable tool to decrease HSR risk.
  • Genetic screening can also prevent the unnecessary discontinuation of abacavir in patients who do not have the risk allele.