A 40-year-old man on ACE inhibitor for hypertension presents with recurrent episodes of massive swelling of lips, tongue, and periorbital tissue without urticaria or pruritus. The mechanism underlying this drug-induced angioedema is:

• A IgE-mediated mast cell degranulation causing histamine release
• B Complement C1 esterase inhibitor deficiency triggered by the drug
• C Bradykinin accumulation due to inhibition of ACE (kininase II) ✓
• D Leukotriene-mediated increase in vascular permeability

Explanation

ACE inhibitor-induced angioedema is bradykinin-mediated. ACE (kininase II) normally degrades bradykinin; when ACE is inhibited, bradykinin accumulates, causing vasodilation and increased vascular permeability particularly in the deep dermis and submucosa, producing non-pruritic angioedema without urticaria. Unlike histamine-mediated angioedema, it does not respond to antihistamines or epinephrine. Mast-cell independent mechanism — does not involve IgE or complement. Hereditary angioedema (HAE) involves C1-esterase inhibitor deficiency; ACE inhibitors can exacerbate HAE but the primary mechanism differs. Treatment: discontinue ACE inhibitor; switch to ARB (lower risk). Acute attacks may require icatibant (bradykinin B2 receptor antagonist) or C1-INH concentrate.

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

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Written and medically reviewed by the StethoPrep medical team.