Canis ISSN: 2398-2942

Urticaria and angioedema

Synonym(s): Hives, angioneurotic edema

Contributor(s): Michael Day, Rosanna Marsella

Introduction

  • Urticaria is an acute onset, transient, cutaneous inflammatory reaction pattern characterized by edema, erythema and pruritus.
  • The classical lesion is an elevated wheal of 1-5 cm in diameter, which may be localized or generalized over the body. In humans the equivalent lesions are referred to as hives.
  • In urticaria these lesions are restricted to the dermis and may become confluent.
  • In angioedema the subcutaneous tissue becomes involved and there may be a progression to systemic anaphylaxis.
  • Urticaria and angioedema are generally immunological reactions, and most cases presumptively involve classical type I hypersensitivity. They are localized forms of anaphylactic reaction Anaphylaxis, urticaria and angioedema.
  • A wide range of allergenic substances may trigger urticarial reactions including environmental allergens Skin: allergic contact dermatitis , insect bites Skin: external parasite bite reaction Skin: flea bite hypersensitivity , incompatible blood transfusions, food Skin: food hypersensitivity or drugs (including vaccines Suspected adverse reactions to vaccination ).

Pathogenesis

Etiology

  • Drugs, infectious organisms, foods, pollens, and insects can be responsible for urticaria.
  • In humans antibodies against the high affinity high IgE receptors may be found.

Predisposing factors

General
  • Prior exposure to the causative allergen.

Pathophysiology

  • Urticaria and angioedema are generally immunological reactions to a wide variety of causative agents including environmental allergens, insect bites, incompatible blood transfusion, food, drugs and vaccines.
  • These are classical type I immediate hypersensitivity reactions.
  • The pathogenesis of both lesions would theoretically require the dog to be sensitized to the causative allergen by (repeated) prior exposure. However in the case of incompatible blood transfusions and in some cases of vaccine-induced reactions, urticaria occurs on the administration of the first dose of vaccine. In such cases it is possible that there is sensitization to a cross-reactive environmental allergen that permits the reaction, or that non-IgE-mediated mast cell degranulation occurs but this has been poorly investigated.
  • The pathogenesis of type I hypersensitivity involves the production of allergen-specific IgE (and subtypes of IgG) antibody following sensitization. These antibodies attach to specific receptor molecules on the surface of cutaneous or mucosal mast cells, circulating basophils and epidermal Langerhans dendritic cells. On subsequent exposure to the sensitizing allergen, there is mast cell degranulation with ensuing vasodilation, tissue edema and inflammation, smooth muscle contraction (bronchoconstriction) and pruritus.
  • The urticarial reaction that may occur with incompatible blood transfusion is a type I hypersensitivity reaction, and the causative allergen is most likely protein within the donor blood. By contrast, the hemolytic transfusion reactions involve type II hypersensitivity with sensitization to a cell-associated antigen (eg blood group antigen) and the production of IgG and IgM antibodies. This might occur by prior incompatible blood transfusion, or alternatively in the case of some blood group antigens, spontaneously occurring alloantibodies are present (presumptively due to prior exposure to cross-reactive environmental antigens). Exposure to the causative antigen permits binding of the IgG/IgM antibodies, with activation of the classical complement pathway and generation of the anaphylactic mediators C3a and C5a. These may directly cause mast cell degranulation and mediate a similar anaphylactic-type response.
  • In some cases Type III hypersensitivity may be responsible for recurrent urticaria.

Timecourse

  • These are acute onset reactions following exposure to the inciting allergen.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • Day M J & Shaw S E (1999)Immune-mediated skin disease.In: M J DayClinical Immunology of the Dog and Cat.Manson Publishing, London. pp 88-125.


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