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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 Reactions02:06

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Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

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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...
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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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Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

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Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
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Apixaban-induced anaphylaxis.

Jessica Hyunji Park1, Brett James Schuchardt2, Che Mathew Harris2

  • 1Division of Hospital Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA hpark73@jh.edu.

BMJ Case Reports
|March 31, 2026
PubMed
Summary
This summary is machine-generated.

Anaphylaxis, a severe allergic reaction, is a rare but potentially fatal side effect of apixaban. This case highlights the importance of considering this adverse event in patients experiencing allergic symptoms after apixaban use.

Keywords:
AnaphylaxisDrugs and medicinesImmunologyUnwanted effects / adverse reactions

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Area of Science:

  • Pharmacology
  • Clinical Medicine
  • Allergy and Immunology

Background:

  • Apixaban is a widely used anticoagulant for venous thromboembolism.
  • Adverse drug reactions, including anaphylaxis, can occur with anticoagulants.
  • Rarely reported cases of apixaban-induced anaphylaxis necessitate clinical awareness.

Purpose of the Study:

  • To report a case of anaphylaxis following therapeutic apixaban administration.
  • To emphasize the clinical presentation and management of apixaban-induced anaphylaxis.
  • To raise awareness among healthcare providers about this rare adverse effect.

Main Methods:

  • A case report of a patient experiencing anaphylaxis after apixaban initiation.
  • Clinical assessment including vital signs, physical examination, and laboratory tests (serum tryptase).
  • Review of literature on apixaban-associated anaphylaxis.

Main Results:

  • The patient presented with deep vein thrombosis and subsequently developed anaphylaxis symptoms including dyspnea, hypoxia, hypotension, and urticarial rash within an hour of apixaban ingestion.
  • Elevated serum tryptase levels confirmed anaphylaxis.
  • Prompt treatment with epinephrine, diphenhydramine, and methylprednisolone led to clinical improvement.

Conclusions:

  • Anaphylaxis is a rare but potentially life-threatening adverse effect of apixaban.
  • Healthcare providers should maintain a high index of suspicion for anaphylaxis in patients presenting with allergic symptoms after apixaban initiation.
  • Early recognition and prompt management are crucial for favorable outcomes in apixaban-induced anaphylaxis.