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Related Concept Videos

Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
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...
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...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...

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Related Experiment Video

Updated: Jul 20, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Thalidomide-induced toxic epidermal necrolysis.

S B Horowitz1, A L Stirling

  • 1College of Pharmacy and Allied Health Professions, St. John's University, Jamaica, New York 11439, USA.

Pharmacotherapy
|October 8, 1999
PubMed
Summary

Toxic epidermal necrolysis (TEN) is a severe skin reaction. This case highlights a rare instance of TEN caused by thalidomide in a glioblastoma patient, emphasizing the need for vigilance in immunosuppressed individuals.

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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
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A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis
07:22

A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis

Published on: March 14, 2025

Area of Science:

  • Dermatology
  • Oncology
  • Pharmacology

Background:

  • Toxic epidermal necrolysis (TEN) is a severe, life-threatening dermatologic disorder with high mortality rates.
  • Identifying and withdrawing the causative agent is paramount for effective TEN management.
  • Thalidomide, while known for hypersensitivity reactions in HIV-positive patients, is increasingly used in other immunosuppressed populations, including cancer patients.

Observation:

  • A 62-year-old female patient was treated with thalidomide for glioblastoma.
  • The patient developed toxic epidermal necrolysis (TEN) after approximately five weeks of therapy.

Findings:

  • This case presents a rare occurrence of thalidomide-induced TEN.
  • The patient's glioblastoma diagnosis and immunosuppressed state are relevant factors.

Implications:

  • Increased use of thalidomide in immunosuppressed patients, such as those with malignancies, may lead to a higher incidence of severe dermatologic reactions like TEN.
  • Clinicians should maintain a high index of suspicion for TEN in patients receiving thalidomide, particularly those who are immunosuppressed.
  • Further research is warranted to understand the risk factors and mechanisms of thalidomide-induced TEN in diverse patient populations.