Name:
A 37-Year-Old with Swollen Lips
Description:
A 37-Year-Old with Swollen Lips
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Duration:
T00H04M55S
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Upload Date:
2022-02-28T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
♪ (music) ♪
CATHY: [Handy] Hi, welcome to Harrison's Podclass, where we discuss important concepts in internal medicine. I'm Cathy Handy.
CHARLIE: And I'm Charlie Wiener
CHARLIE: and we're coming to you from the Johns Hopkins School of Medicine. ♪ (music) ♪ Welcome to Episode 42: A 37-Year-Old with Swollen Lips. I'll start the question. A 37-year-old man has recently been diagnosed with systemic hypertension. He's prescribed lisinopril as initial monotherapy. He takes this medication as prescribed for three days, and on the third day notes that his right hand is swollen and it is also itching mildly and has diffuse tingling. Later that same evening, his lips become swollen and he has difficulty breathing.
CHARLIE: Cathy, do you see where we're going with this?
CATHY: Well, it sounds like angioedema that's probably caused by the ACE inhibitor. Although I'll also note that it is a bit curious, but obviously not unheard of, that a 37-year-old was diagnosed with systemic hypertension. I'm going to assume that he had an appropriate workup and that he failed non-pharmacologic therapy, which would be the first-line recommendation for a treatment of hypertension. An ACE inhibitor, though, is a very reasonable first-choice line treatment once pharmacotherapy is started, and the most recent guidelines on the management of hypertension from 2017 would support this as well.
CHARLIE: Okay, so the question's going to ask about mechanisms, and it says: "Which of the following statements accurately describes this condition? Option A. His symptoms are due to direct activation of mast cells by lisinopril; Option B. His symptoms are due to impaired bradykinin degradation by lisinopril; Option C. His symptoms are unlikely to recur if he is switched to enalapril; Option D. Peripheral blood analysis will show a deficiency of C1 inhibitor; and Option E. Plasma IgE levels are likely to be elevated.
CATHY: Okay, so like you mentioned, the question's really asking about the mechanism behind the angioedema that's associated with ACE inhibitors. So, the answer here is B, that his symptoms are due to impaired bradykinin degradation by lisinopril. So, remember that these medications inhibit angiotensin-converting enzyme which converts angiotensin I to the vasoactive angiotensin II. However, ACE inhibitors also inhibit the enzyme that breaks down bradykinin, thus causing increased levels which in a predisposed individual can result in angioedema.
CATHY: This is also the mechanism for ACE inhibitor-induced cough. Now the angioedema, it usually does occur within the first few months after starting treatment, but it can occur at any time, and it's not always present when a patient first starts the medication. Although, in this case, there obviously is a temporal relationship since he just started it about three days ago. It's also important to note that usually this doesn't present with severe itching or hives, and it's not an allergic reaction; it's really a manifestation of the enzymatic inhibitor in susceptible individuals.
CHARLIE: Any comments on the management?
CATHY: It is usually self-resolving, and you have to stop the ACE inhibitor, and the patient should be switched to a different class of medications and shouldn't be retried with the other ACE inhibitors.
CHARLIE: So, that rules out Option C, because enalapril is in the same class as lisinopril. In what situations would you be concerned about the other manifestations of the angioedema?
CATHY: In someone with low levels of C1 inhibitor, which is in Option D, I'd be thinking about hereditary angioedema. IgE-mediated angioedema, which is Option E, occurs due to specific antigen sensitivity. This is the classic type of allergic reaction that causes anaphylaxis, and usually this airway obstruction is also accompanied by urticaria and itching. Now, lisinopril is not a medication that causes direct activation of mast cells.
CATHY: Opiates and NSAIDs are associated with this, and the direct activation of mast cells is usually also accompanied by urticaria, but IgE is not involved in those scenarios.
CHARLIE: So, that rules out Option A also, obviously.
CATHY: Yeah.
CHARLIE: So what would you use to treat his hypertension now that he can't use ACE inhibitors?
CATHY: A thiazide diuretic or a calcium channel blocker would also be reasonable first-line approaches in this patient.
CHARLIE: What about ARBs, such as losartan?
CATHY: So ARBs, or angiotensin II receptor blockers, do have a much lower rate of angioedema and are not absolutely contraindicated in someone who wasn't able to tolerate an ACE inhibitor. But you have lots of options for first-line treatment of hypertension, so, it wouldn't be my first choice in this case.
CHARLIE: So, the teaching point is that ACE inhibitors are a good first-line treatment for hypertension but can be complicated by angioedema and cough, which is thought to be mediated by increased levels of bradykinin.
CATHY: To learn more, you can read about angioedema and the many causes in the Rheumatology and Immunology chapters of Harrison's. And the most recent guidelines on the management of hypertension can be found in the Journal of the American College of Cardiology, and that was published in 2017. ♪ (music) ♪