ACE-inhibitor-related angioedema

ACE-inhibitor-related angioedema is not a true allergy but is considered an adverse class effect secondary to the mechanism of action.2 48 The proposed pathophysiologic mechanism is the accumulation of bradykinin secondary to the inhibition of ACE.248 However, this cannot explain how ACE-inhibitor-related angioedema can occur anytime from hours to decades after a patient has started the medication.3411 13 About a quarter of patients with ACE-inhibitor-related angioedema present within 1 week of starting the medication.13 On the other end of the spectrum, approximately half present after having been on the medication for at least a year.13 This may be explained by the fact that in the setting of ACE inhibition, aminopeptidase P (APP) and dipeptidyl peptidase 4 (DPP4) become responsible for breaking down the vasoactive peptides bradykinin and substance P, respectively.14 Factors adversely affecting these enzymes may trigger angioedema.14 Female gender, African-American descent, and tobacco use are risk factors for the development of ACEinhibitor-related angioedema.3467 14 Certain atopic diseases, such as seasonal allergies and asthma, may also be risk factors.5-71314 On the other hand, diabetes mellitus is possibly associated with a decreased risk because diabetic patients appear to have increased DPP4 activity to aid in the breakdown of substance P.5-14-15 Currently, no laboratory test exists to confirm the diagnosis of ACE-inhibitor-related angioedema.13 The diagnosis is made when a patient on an ACE inhibitor presents with nonpruritic, nontender, well-demarcated areas of angioedema and other causes have been ruled out.13 The differential diagnosis includes the different types of hereditary angioedema, acquired angioedema, medication allergy, food sensitivity, reaction to trauma, and exposure to extreme temperatures.'4 Patients with ACE-inhibitor-related angioedema can present with varying levels of respiratory distress, with some requiring an airway intervention.