Acquired angioedema may also be associated with the use of angiotensin-converting enzyme (ACE) inhibitors. Risk factors for ACE inhibitor–induced angioedema include history of smoking, increasing age, and female gender.3 African-American race has been correlated with increased incidence of angioedema, with rates 4 to 5 times that of Whites,1 but race is now identified as a social and not a biological construct and should not be relied on to make medical decisions about prescribing.
The rate of occurrence for ACE inhibitor–induced angioedema is highest within the first 30 days of medication use2; however, it can occur anytime. The absolute risk has been estimated as 0.3% per year.4
Patient age. Histaminergic angioedema can occur at any age. The hereditary subtype of nonhistaminergic angioedema is more common in younger individuals, typically occurring in infancy to the second decade of life, and tends to run in families, while the acquired subtype often manifests in adults older than 40.2
Physical exam findings. The typical manifestation of nonhistaminergic angioedema is firm, nonpitting, nonpruritic swelling resulting from fluid shifts to the reticular dermis and subcutaneous or submucosal tissue. In comparison, histaminergic reactions commonly involve deeper dermal tissue.
Commonly affected anatomic sites also vary by angioedema type but do not directly distinguish a cause. Allergic and ACE inhibitor–induced subtypes more commonly involve the lips, tongue, larynx, and face, whereas hereditary and other acquired etiologies are more likely to affect the periphery, abdomen, face, larynx, and genitourinary systems.2 So the way that this patient presented was a bit unusual.
Continue to: Symptom history