Language
English
Publication Date
1-1-2020
Journal
TH Open
DOI
10.1055/s-0040-1701238
PMID
31984307
PMCID
PMC6978173
PubMedCentral® Posted Date
1-23-2020
PubMedCentral® Full Text Version
Post-print
Abstract
Angiotensin-converting enzyme (ACE) inhibitors are extensively prescribed to treat patients with hypertension, congestive heart failure, and diabetic nephropathy. A small fraction of these patients (approximately 0.7%) develop angioedema, manifested by swelling of the lips and oropharynx. Angioedema of oropharynx is a medical emergency that can lead to asphyxiation and death. The angioedema is due to bradykinin generated from high molecular weight kininogen by kallikrein, which is derived from plasma prekallikrein by action of the factor XIIa, factor Xia, or prolylcarboxypeptidase. Bradykinin induces vasodilation and increased vascular permeability. ACE is the major degrading enzyme of bradykinin in the intravascular department. ACE inhibitors inhibit the proteolytic inactivation of bradykinin. We report a patient with oropharyngeal angioedema associated with an ACE inhibitor with complete absence of plasma prekallikrein due to homozygous mutation (Ser97PhefsTer173).
Keywords
bradykinin, prekallikrein, kininogen
Published Open-Access
yes
Recommended Citation
, "Lisinopril-Induced Angioedema in a Patient with Plasma Prekallikrein Deficiency" (2020). Faculty, Staff and Students Publications. 1064.
https://digitalcommons.library.tmc.edu/baylor_docs/1064