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Related Concept Videos

Allergic Reactions02:06

Allergic Reactions

Overview
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...
Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs

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.
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
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 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),...
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...

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Related Experiment Video

Updated: Jun 14, 2026

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity
10:22

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity

Published on: September 16, 2011

Progesterone-responsive urticaria and eosinophilia.

R J Mittman1, D I Bernstein, D R Steinberg

  • 1Department of Medicine, University of Cincinnati Medical Center, Ohio 45267.

The Journal of Allergy and Clinical Immunology
|September 1, 1989
PubMed
Summary

This study details a unique case of chronic cyclic urticaria and hypereosinophilia in a woman, finding that progesterone levels influence hive activity and eosinophil counts.

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Last Updated: Jun 14, 2026

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Area of Science:

  • Immunology
  • Endocrinology
  • Dermatology

Background:

  • A 30-year-old black albino woman presented with a 4-year history of monthly urticarial episodes linked to hypereosinophilia.
  • Urticaria consistently began at the end of menses, lasting 1-2 weeks, with no evidence of malignancy, infection, or visceral involvement.

Observation:

  • A 30-year-old woman experienced monthly urticarial episodes linked to hypereosinophilia, starting at menses.
  • Symptoms correlated with eosinophil counts and urinary histamine levels.
  • Hives and eosinophilia decreased as serum progesterone levels rose.

Findings:

  • Progesterone demonstrated in vitro inhibition of histamine release from patient basophils.
  • Oral medroxyprogesterone treatment led to urticaria remission and reduced eosinophil counts.
  • This case suggests progesterone modulates urticaria and hypereosinophilia.

Implications:

  • Progesterone may play a key role in cyclic urticaria and hypereosinophilia.
  • Hormonal therapy could be a potential treatment avenue for similar cases.
  • Further research into sex hormone-immune interactions in urticaria is warranted.