[Bradykinin mediated angioedema]

Rev Med Interne. 2011 Apr;32(4):225-31. doi: 10.1016/j.revmed.2009.11.021. Epub 2010 Jun 9.
[Article in French]

Abstract

Bradykinin angioedema (AE) are characterized by acute recurrent episodes of localized swelling. They are not associated with pruritus or erythema, and are short-lived (24 to 72 hours), disappearing without any sequelae. Corticosteroids are useless. Skin or mucous membranes (upper respiratory and intestinal) could be affected. Bradykinin AE can be secondary to: (1) AE associated with C1 inhibitor deficiency (hereditary or acquired); (2) drug-induced AE (converting enzyme inhibitors…); (3) type III AE type (oestrogen dependant) without C1 inhibitor deficiency. These type III AE can be associated with a gain of function mutation that markedly increases factor XII activity. Prognosis depends on the laryngeal attacks (resulting in 25 % of death in the absence of specific treatment). In case of severe attacks, icatibant (bradykinin receptor antagonist) or C1 inhibitor concentrate can be used. In case of frequent attacks, long-term therapy with danazol or tranexamic acid is effective.

Publication types

  • English Abstract

MeSH terms

  • Angioedema / drug therapy
  • Angioedema / genetics*
  • Angioedema / physiopathology
  • Angioedemas, Hereditary / genetics
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Antifibrinolytic Agents / therapeutic use
  • Bradykinin / genetics*
  • Complement C1 Inhibitor Protein / genetics
  • Complement Inactivating Agents / metabolism
  • Estrogen Antagonists / therapeutic use
  • Genetic Markers / genetics
  • Humans
  • Prognosis
  • Treatment Outcome
  • Vasodilator Agents / metabolism*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antifibrinolytic Agents
  • Complement C1 Inhibitor Protein
  • Complement Inactivating Agents
  • Estrogen Antagonists
  • Genetic Markers
  • Vasodilator Agents
  • Bradykinin