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Contact System Activation and Bradykinin Generation in Angioedema: Laboratory Assessment and Biomarker Utilization

Sandra C Christiansen1, Bruce L Zuraw2

  • 1Department of Medicine, University of California San Diego, 9500 Gilman Drive, Mail Code 0732, La Jolla, CA 92093, USA.

Immunology and Allergy Clinics of North America
|June 27, 2024
PubMed

The role of contact system activation has been clearly established in the pathogenesis of hereditary angioedema due to C1 inhibitor deficiency (HAE-C1INH). C1 inhibitor (C1INH)-protease complexes, levels of functional C1INH, plasma kallikrein activation, and cleavage of high-molecular-weight kininogen have each been associated with disease activity. More recently, HAE with normal levels of C1INH (HAE-nl-C1INH) has been recognized. Six genetic mutations have been identified which are linked to HAE-nl-C1INH phenotypes. The majority of individuals with HAE-nl-C1INH fall into the unknown category. There is substantial evidence that bradykinin generation underlies the recurrent attacks of swelling in some of these cohorts.

Keywords:
BiomarkerBradykininC1 inhibitorC1 inhibitor complexesC4Contact systemHereditary angioedemaVascular permeability

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