A 56-year-old woman comes to the emergency department with facial swelling and difficulty breathing. She woke up today with a "feeling of fullness" in her lips, and 2 hours later her husband said that her lips looked puffy. There is no itching or skin rash. The patient has had no similar symptoms before. She has a history of gastroesophageal reflux disease and takes lansoprazole daily. She also began taking lisinopril 2 months ago for hypertension. The patient's blood pressure is 135/75 mm Hg. On examination, there is moderate swelling of her lips and tongue. Mild audible stridor without wheezing is present. Which of the following is the most likely mechanism responsible for this patient's symptoms?

Question

A 56-year-old woman comes to the emergency department with facial swelling and difficulty breathing.  She woke up today with a "feeling of fullness" in her lips, and 2 hours later her husband said that her lips looked puffy.  There is no itching or skin rash.  The patient has had no similar symptoms before.  She has a history of gastroesophageal reflux disease and takes lansoprazole daily.  She also began taking lisinopril 2 months ago for hypertension.  The patient's blood pressure is 135/75 mm Hg.  On examination, there is moderate swelling of her lips and tongue.  Mild audible stridor without wheezing is present.  Which of the following is the most likely mechanism responsible for this patient's symptoms?

Quizplus · Accepted Answer

11ec160b_3798_ba2f_9249_4b5847bdc919_MD0001_00 Angioedema is a rare and potentially serious adverse effect of ACE inhibitor therapy. Symptoms typically appear within days of initiation but can also occur after weeks to years of therapy. Although angioedema can affect any tissue, it most commonly involves the tongue, lips, or eyelids. Laryngeal edema and difficulty breathing may also occur. ACE inhibitor-induced angioedema is due to bradykinin accumulation. Normally, ACE is responsible for bradykinin breakdown. ACE inhibitors prevent bradykinin degradation, leading to increased levels. Bradykinin is a potent vasodilator that ultimately increases vascular permeability, causing significant angioedema. ACE inhibitors should be discontinued in patients who develop angioedema. (Choice B) Hereditary C1-esterase inhibitor deficiency also causes bradykinin-mediated angioedema, but it usually presents in childhood and early adolescence. This patient's age and history make ACE inhibitor-induced bradykinin accumulation more likely. (Choice C) Even though IgE-dependent mast cell degranulation can cause angioedema, it is more commonly associated with urticaria and pruritus. True hypersensitivity or an allergy to ACE inhibitors is very rare and not likely in this patient. (Choice D) ACE inhibitors decrease production of angiotensin II, which reduces negative feedback on the renin-angiotensin-aldosterone system, thereby promoting renin release. Increased renin levels are a natural compensatory response to ACE inhibitor therapy and have no role in causing angioedema. (Choice E) In nonimmune mediated mast cell degranulation, there is direct activation of mast cells independent of IgE cross-linking. These pseudoallergic reactions can be caused by chemicals, heat, and certain drugs (eg, opiates, vancomycin) and are clinically similar to hypersensitivity and allergic reactions. Educational objective: Angioedema is a rare and serious adverse effect of ACE inhibitor therapy. ACE inhibition increases bradykinin levels, which increase vascular permeability and lead to angioedema. Symptoms include tongue, lips, or eyelid swelling and, less frequently, laryngeal edema and difficulty breathing. ACE inhibitors should be discontinued in affected patients. __________ References: Bradykinin and the pathophysiology of angioedema. (http://www.ncbi.nlm.nih.gov/pubmed/12639808) Angioedema from angiotensin-converting enzyme (ACE) inhibitor treated with complement 1 (C1) inhibitor concentrate. (http://www.ncbi.nlm.nih.gov/pubmed/16451161)

A 56-Year-Old Woman Comes to the Emergency Department with Facial