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Related Concept Videos

Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

64
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...
64
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

64
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...
64
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

77
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,...
77
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

69
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...
69
Allergic Reactions02:06

Allergic Reactions

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Overview
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Allergic Drug Reactions01:27

Allergic Drug Reactions

1.5K
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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Related Experiment Video

Updated: Feb 28, 2026

An Ex vivo Mast Cell Degranulation Assay using Crude Peritoneal Exudate Cells and Natural Antigen Stimulation
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[The anaphylactoid reaction after colloid infusion]

J Ring

    Fortschritte Der Medizin
    |November 3, 1977
    PubMed
    Summary

    Colloidal volume substitutes can cause rare but severe anaphylactoid reactions. Different colloids involve distinct mechanisms, with protein aggregates and antibodies playing key roles in patient reactions.

    Area of Science:

    • Anesthesiology
    • Immunology
    • Pharmacology

    Background:

    • Colloidal volume substitutes are widely used for fluid resuscitation.
    • These agents carry a risk of anaphylactoid reactions, although the general incidence is low (0.03%).
    • Severe complications can arise from these reactions, necessitating a deeper understanding of their mechanisms.

    Purpose of the Study:

    • To elucidate the distinct pathomechanisms underlying anaphylactoid reactions induced by various colloidal volume substitutes.
    • To identify specific components and immunological factors contributing to these adverse events.
    • To correlate clinical symptom severity with immunological markers in dextran-induced reactions.

    Main Methods:

    • Review of existing literature on anaphylactoid reactions to colloidal volume substitutes.

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  • Analysis of pathomechanisms involving protein aggregates in human serum albumin incompatibility.
  • Investigation of the role of stabilizers in altering protein immunogenicity.
  • Examination of antibody classes (IgG, IgM) in dextran incompatibility.
  • Correlation analysis between clinical symptoms and anti-dextran-antibody titers.

    • Main Results:

    • Anaphylactoid reactions to colloids, though infrequent, can lead to severe outcomes.
    • Protein aggregates are implicated in human serum albumin incompatibility reactions.
    • Stabilizers can modify the immunogenicity of plasma proteins.
    • IgG and IgM antibodies are involved in severe dextran incompatibility.
    • A direct correlation exists between clinical symptom severity and anti-dextran-antibody titers.

    Conclusions:

    • Understanding the specific pathomechanisms of anaphylactoid reactions to different colloids is crucial for patient safety.
    • Immunological factors, including protein aggregates and specific antibodies, are key determinants of reaction severity.
    • Monitoring anti-dextran-antibody titers may help predict the intensity of clinical symptoms in dextran-related reactions.