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Related Concept Videos

Allergic Drug Reactions01:27

Allergic Drug Reactions

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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...
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Inhaled corticosteroids (ICS) are anti-inflammatory drugs used primarily in treating persistent asthma and providing long-term maintenance. They target the bronchial mucosa, the lining of the airways, to control inflammation, a critical factor in asthma progression and exacerbation.
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Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

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Asthma is a chronic respiratory condition for which new therapeutic avenues, including anti-inflammatory drugs like mast cell stabilizers and anti-IgE treatments, continue to be developed.
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Hypersensitivities01:30

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Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
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Drug Toxicity: Allergic Reactions01:30

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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...
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Allergic Reactions: Anaphylaxis01:30

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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,...
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Related Experiment Video

Updated: May 7, 2026

An Ex vivo Mast Cell Degranulation Assay using Crude Peritoneal Exudate Cells and Natural Antigen Stimulation
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Modulation of the atopy patch test reaction by topical corticosteroids and tar.

E G Langeveld-Wildschut1, H Riedl, T Thepen

  • 1Department of Dermatology/Allergology, University Medical Center Utrecht, Utrecht, The Netherlands.

The Journal of Allergy and Clinical Immunology
|October 14, 2000
PubMed
Summary
This summary is machine-generated.

Topical glucocorticosteroids (GCSs) and tar reduce allergic inflammation in atopic eczema (AE) by inhibiting T cell and eosinophil influx. The atopy patch test (APT) effectively evaluates these anti-inflammatory treatment effects.

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Area of Science:

  • Dermatology
  • Immunology
  • Pharmacology

Background:

  • Standardizing pharmacologic studies in atopic eczema (AE) is challenging due to disease variability.
  • Assessing topical treatments for AE requires reliable methods to evaluate inflammatory responses.

Purpose of the Study:

  • To evaluate the effects of topical glucocorticosteroids (GCSs) and tar on the atopy patch test (APT) reaction in AE patients.
  • To assess both macroscopic and microscopic changes following pretreatment with GCSs and tar.

Main Methods:

  • Nonlesional skin of AE patients was pretreated with GCSs, tar, or vehicle for 3 weeks.
  • Atopy patch tests (APTs) were conducted, and skin biopsy specimens were collected for immunohistochemical analysis.

Main Results:

  • Both GCSs and tar significantly reduced the macroscopic APT reaction.
  • GCSs and tar equally inhibited the influx of T cells, eosinophils, and specific inflammatory markers.
  • Expression of adhesion molecules like VCAM-1 and E-selectin was reduced by both treatments.

Conclusions:

  • Topical GCSs and tar effectively reduce allergic inflammation in AE, though cellular components persist.
  • The APT serves as a valuable tool for assessing the efficacy of topical anti-inflammatory treatments in AE.