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Related Concept Videos

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: 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...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
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...
Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...

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Electrophoretic Delivery of γ-aminobutyric Acid (GABA) into Epileptic Focus Prevents Seizures in Mice
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Anticonvulsant hypersensitivity syndrome: an update.

Sandra R Knowles1, Norman Dewhurst, Neil H Shear

  • 1Department of Pharmacy, Sunnybrook Health Sciences Centre, University of Toronto, 2075 Bayview Ave, Toronto, Ontario, M4N 3M5, Canada. Sandra.knowles@sunnybrook.ca

Expert Opinion on Drug Safety
|July 17, 2012
PubMed
Summary

Anticonvulsant hypersensitivity syndrome (AHS) is a severe drug reaction. Genetic testing may help predict AHS risk and guide safer anticonvulsant selection.

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Area of Science:

  • Pharmacology
  • Toxicology
  • Immunology

Background:

  • Anticonvulsant hypersensitivity syndrome (AHS) is a rare, severe adverse drug reaction.
  • It is linked to aromatic anticonvulsants like phenytoin, phenobarbital, and carbamazepine.
  • AHS presents with fever, rash, and organ involvement weeks after starting medication.

Purpose of the Study:

  • To review the incidence, epidemiology, and pathogenesis of AHS.
  • To provide recommendations for AHS diagnosis and management.
  • To explore predictive testing for AHS.

Main Methods:

  • Literature review on AHS incidence and epidemiology.
  • Discussion of AHS pathogenesis.
  • Analysis of diagnostic and predictive testing methods.

Main Results:

  • AHS incidence is estimated between 1:1000 and 1:10,000, but true rates are unknown.
  • High cross-reactivity exists among aromatic anticonvulsants, necessitating avoidance.
  • No universal predictive tests for AHS currently exist.

Conclusions:

  • Patients with AHS should avoid all aromatic anticonvulsants due to cross-reactivity.
  • Genetic testing shows promise for predicting AHS risk and guiding anticonvulsant choice.
  • Cellular surrogate tests are primarily diagnostic, lacking the practicality of genetic tests.