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Related Concept Videos

Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

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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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Allergic Drug Reactions01:27

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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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Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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Extrinsic and Intrinsic Pathways of Hemostasis01:20

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
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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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A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
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Factor XII-Driven Inflammatory Reactions with Implications for Anaphylaxis.

Lysann Bender1, Henri Weidmann1, Stefan Rose-John2

  • 1Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Frontiers in Immunology
|October 3, 2017
PubMed
Summary
This summary is machine-generated.

Anaphylaxis and hereditary angioedema involve factor XII (FXII) activation, leading to inflammation and bradykinin release. Targeting FXII and the kallikrein-kinin system offers potential treatments for these severe conditions.

Keywords:
anaphylaxisbradykinincontact systemfactor XIIheparinkallikrein–kinin systemmast cellspolyP

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Area of Science:

  • Immunology
  • Hematology
  • Allergy

Background:

  • Anaphylaxis is a severe allergic reaction driven by mast cell mediators.
  • Factor XII (FXII) activation initiates contact system pathways, including coagulation and inflammation.
  • The kallikrein-kinin system, producing bradykinin (BK), is implicated in anaphylaxis severity.

Purpose of the Study:

  • To review the integration of FXII with inflammation and complement systems in anaphylaxis and hereditary angioedema (HAE).
  • To highlight diagnostic and therapeutic strategies for bradykinin-related diseases.

Main Methods:

  • Literature review focusing on the role of FXII in anaphylaxis and HAE.
  • Analysis of the interplay between complement and kallikrein-kinin systems.
  • Examination of current treatment approaches for BK-mediated disorders.

Main Results:

  • Mast cell activation releases heparin and polyphosphate, promoting FXII activation.
  • FXII activation triggers the kallikrein-kinin system, leading to bradykinin release and inflammation.
  • C1 esterase inhibitor links complement and kallikrein-kinin systems; its deficiency causes HAE.

Conclusions:

  • FXII plays a central role in integrating inflammation and complement pathways in anaphylaxis and HAE.
  • Understanding FXII's role is crucial for developing targeted therapies for BK-related conditions.
  • Therapeutic strategies targeting FXII and bradykinin pathways show promise for managing severe allergic and swelling disorders.