A 38-year-old woman on lisinopril develops recurrent episodes of painless, non-pruritic facial angioedema without urticaria. Which mechanism explains this ACE inhibitor-induced angioedema?

• A IgE-mediated degranulation of mast cells
• B Bradykinin accumulation due to ACE inhibition — bradykinin-mediated angioedema ✓
• C C1-inhibitor deficiency unmasked by ACE inhibition
• D Complement activation causing C3a and C5a release

Explanation

ACE (kininase II) normally degrades bradykinin. ACE inhibition leads to bradykinin accumulation, causing increased vascular permeability via bradykinin B2 receptors on endothelial cells, producing painless, non-pruritic angioedema without urticaria. This is non-histaminergic and does NOT respond to antihistamines or adrenaline. Treatment requires stopping the ACE inhibitor; acute attacks may respond to icatibant (B2 receptor antagonist) or C1-INH concentrate. Switching to ARBs reduces but does not eliminate risk.

Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.