ACE Inhibitor???Induced Angioedema

Vleeming, W.; Amsterdam, Jan van; Stricker, Bruno H. Ch.; Wildt, Dick J. De

doi:10.2165/00002018-199818030-00003

Cited by 212 publications

(52 citation statements)

References 158 publications

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“…2,8 High levels of circulating bradykinin have been well documented in patients with angioedema. 4 Although multiple vasoactive peptides have been implicated in angioedema, including substance P, 1 bradykinin is arguably the most important in ACE inhibitorrelated angioedema.…”

Section: Discussionmentioning

confidence: 99%

“…4 Acute trauma causes activation of bradykinin through the release of factor XII of the clotting cascade. 2 Bradykinin is then broken down by ACE while passing through the lung. 3 The blockade of this enzyme by ACE inhibitor leads to both the local and systemic accumulation of bradykinin in susceptible individuals by decreasing its catabolism.…”

Section: Discussionmentioning

confidence: 99%

“…However, it most often occurs within the first week after starting therapy. 2 Up to 25% of reported cases of angioedema seem to be a result of ACE inhibitor therapy. 2 The other most common causes include allergic reactions, hereditary angioedema, C1 esterase inhibitor deficiency, and idiopathic angioedema.…”

mentioning

confidence: 99%

“…2 Up to 25% of reported cases of angioedema seem to be a result of ACE inhibitor therapy. 2 The other most common causes include allergic reactions, hereditary angioedema, C1 esterase inhibitor deficiency, and idiopathic angioedema. 2 The mechanism of action of ACE inhibitors includes the blockade of the ACE, which leads to vasodilation.…”

mentioning

confidence: 99%

“…2 The other most common causes include allergic reactions, hereditary angioedema, C1 esterase inhibitor deficiency, and idiopathic angioedema. 2 The mechanism of action of ACE inhibitors includes the blockade of the ACE, which leads to vasodilation. Other actions of ACE inhibitors include blockade of the conversion of substance P to inactive peptides and the blockade of bradykinin degradation.…”

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confidence: 99%

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Angioedema After Local Trauma in a Patient on Angiotensin-Converting Enzyme Inhibitor Therapy

Simmons

Folsom²,

Bryden³

et al. 2008

The Journal of the American Board of Family Medicine

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Angioedema is a side effect that is often associated with the use of angiotensin-converting enzyme (ACE) inhibitor medications. These medications result in increased levels of circulating bradykinins. This case illustrates the result of a local traumatic event to the upper lip, presumably causing marked bradykinin release in a patient who was taking an ACE inhibitor. The local release of bradykinin from trauma, in addition to decreased bradykinin catabolism secondary to ACE inhibitor therapy, resulted in angioedema predominantly in the upper lip. The angioedema resolved with discontinuation of the ACE inhibitor. (J Am Board Fam Med 2008;21:577-9.)As the indications and usage of angiotensin-converting enzyme (ACE) inhibitor therapy increases, one of its potential side effects, angioedema, is becoming commonly encountered in primary care. Angioedema is a potentially life-threatening side effect of ACE inhibitor therapy, which has an estimated incidence of 0.1% up to 6%. 1 Angioedema resulting secondary to ACE inhibitor use may occur many years after therapy has been initiated. However, it most often occurs within the first week after starting therapy. 2 Up to 25% of reported cases of angioedema seem to be a result of ACE inhibitor therapy. 2 The other most common causes include allergic reactions, hereditary angioedema, C1 esterase inhibitor deficiency, and idiopathic angioedema. 2 The mechanism of action of ACE inhibitors includes the blockade of the ACE, which leads to vasodilation. Other actions of ACE inhibitors include blockade of the conversion of substance P to inactive peptides and the blockade of bradykinin degradation. The increase in circulating substance P and bradykinin, histamine release, and other mechanisms lead to vasodilatation and increased vascular permeability. 1-3 Angioedema does not resemble other forms of edema in that it does not appear in dependent areas and is often very transient and localized. 4 The most important risk factor for developing ACE inhibitor angioedema seems to be African-American race. The mechanism of this increased risk is not clear but may include bradykinin metabolism. Other risk factors include history of angioedema, allergies to seafood, and recent head or neck surgery. 2

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Angioedema After Local Trauma in a Patient on Angiotensin-Converting Enzyme Inhibitor Therapy

Simmons

Folsom²,

Bryden³

et al. 2008

The Journal of the American Board of Family Medicine

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Comparative Risk for Angioedema Associated With the Use of Drugs That Target the Renin-Angiotensin-Aldosterone System

Toh¹,

Reichman²,

Houstoun³

et al. 2012

Arch Intern Med

187

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Background: Although certain drugs that target the renin-angiotensin-aldosterone system are linked to an increased risk for angioedema, data on their absolute and comparative risks are limited. We assessed the risk for angioedema associated with the use of angiotensinconverting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), and the direct renin inhibitor aliskiren.Methods: We conducted a retrospective, observational, inception cohort study of patients 18 years or older from 17 health plans participating in the Mini-Sentinel program who had initiated the use of an ACEI (n=1 845 138), an ARB (n=467 313), aliskiren (n=4867), or a ␤-blocker (n = 1 592 278) between January 1, 2001, and December 31, 2010. We calculated the cumulative incidence and incidence rate of angioedema during a maximal 365-day follow-up period. Using ␤-blockers as a reference and a propensity score approach, we estimated the hazard ratios of angioedema separately for ACEIs, ARBs, and aliskiren, adjusting for age, sex, history of allergic reactions, diabetes mellitus, heart failure, or ischemic heart disease, and the use of prescription nonsteroidal antiinflammatory drugs.Results: A total of 4511 angioedema events (3301 for ACEIs, 288 for ARBs, 7 for aliskiren, and 915 for ␤-blockers) were observed during the follow-up period. The cumulative incidences per 1000 persons were 1.79 (95% CI, 1.73-1.85) cases for ACEIs, 0.62 (95% CI, 0.55-0.69) cases for ARBs, 1.44 (95% CI, 0.58-2.96) cases for aliskiren, and 0.58 (95% CI, 0.54-0.61) cases for ␤-blockers. The incidence rates per 1000 person-years were 4.38 (95% CI, 4.24-4.54) cases for ACEIs, 1.66 (95% CI, 1.47-1.86) cases for ARBs, 4.67 (95% CI, 1.88-9.63) cases for aliskiren, and 1.67 (95% CI, 1.56-1.78) cases for ␤-blockers. Compared with the use of ␤-blockers, the adjusted hazard ratios were 3.04 (95% CI, 2.81-3.27) for ACEIs, 1.16 (95% CI, 1.00-1.34) for ARBs, and 2.85 (95% CI, 1.34-6.04) for aliskiren.Conclusions: Compared with ␤-blockers, ACEIs or aliskiren was associated with an approximately 3-fold higher risk for angioedema, although the number of exposed events for aliskiren was small. The risk for angioedema was lower with ARBs than with ACEIs or aliskiren.

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Angioedema Associated With Angiotensin-Converting Enzyme Inhibitor Use

Cicardi¹,

Zingale²,

et al. 2004

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A 71-year-old woman presented with a sudden onset of shortness of breath and difficulty speaking. She was a former smoker and had no known allergies. During assessment, she experienced periorbital swelling without pruritus (Figure 1). She was immediately given antihistamine and cortisone treatment, and the swelling slowly resolved and her speech improved. On further enquiry, we found that she had been taking acetylsalicylic acid (ASA) and bisoprolol for hypertension and coronary artery disease for about 10 years, but she had started coughing after perindopril had been added to her medication several days earlier. We believed that perindopril alone or in combination with ASA was the most likely cause of the angioedema, and we changed her medication to amlodipine and clopidogrel. 1 During three months of follow-up, neither angioedema nor cough recurred, and the laboratory results were not indicative of hereditary angioedema. Adverse reactions after short-and long-term intake of angiotensin-converting enzyme (ACE) inhibitors alone or in combination with ASA are common. 1-3 Of those who use ACE inhibitors, angioedema occurs in about 0.5% of white people and up to 5% of black people. 1 About one-quarter of episodes occur during the first month of therapy. 1 There are no known modifiable risk factors, but the risk appears to be higher for women than men and those with C1 esterase inhibitor deficiency, as well as for people of black and Asian descent. 1,4 A history of asthma or urticaria may also be associated with increased risk, especially in combination with ASA use. 1 After acute treatment of angioedema associated with the use of ACE inhibitors, experts recommend immediate discontinuation of the drug and strict lifetime avoidance of this class of medication. 1-3 Although switching to an angiotensin-receptor blocker may improve ACE inhibitor-associated coughing, 1-3 the high cross-reactivity (up to 17%) between ACE inhibitors and angiotensin-receptor blockers may put those with previous episodes of ACE inhibitor-mediated angioedema at increased risk of further occurrences. 2,3 Clinicians should avoid both classes of drugs for patients susceptible to ACE inhibitor-mediated angioedema to prevent potentially life-threatening complications. 2,3 References 1. Vasekar M, Craig TJ. ACE inhibitor-induced angioedema. Curr Allergy Asthma Rep 2012;12:72-8. 2. Beavers CJ, Dunn SP, Macaulay TE. The role of angiotensin receptor blockers in patients with angiotensin-converting enzyme inhibitor-induced angioedema. Ann Pharmacother 2011; 45:520-4. 3. Kanani A, Schellenberg R, Warrington R. Urticaria and angioedema. Allergy Asthma Clin Immunol 2011;7(Suppl 1):S9. 4. Hoover T, Lippmann M, Grouzmann E, et al. Angiotensin converting enzyme inhibitor induced angio-oedema: a review of the pathophysiology and risk factors. Figure 1: Several days after starting perindopril, a 71-year-old woman experienced shortness of breath and periorbital edema. She was also taking acetyl-salicylic acid and bisoprolol.

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ACE Inhibitor???Induced Angioedema

Cited by 212 publications

References 158 publications

Angioedema After Local Trauma in a Patient on Angiotensin-Converting Enzyme Inhibitor Therapy

Angioedema After Local Trauma in a Patient on Angiotensin-Converting Enzyme Inhibitor Therapy

Comparative Risk for Angioedema Associated With the Use of Drugs That Target the Renin-Angiotensin-Aldosterone System

Angioedema Associated With Angiotensin-Converting Enzyme Inhibitor Use

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