Drug-Induced Angioedema

Classification	ICD-10: T78.3; OMIM: 300909;
External resources	Orphanet: 91385;

Drug-induced angioedema
Drug-induced angioedema
Other names: Acquired angioedema
	ACE-I induced angioedema
Specialty	Dermatology

Drug-induced angioedema is a known complication of the use of angiotensin-converting enzyme (ACE) inhibitors, angiotensin II antagonists (ARBs), and Angiotensin-Neprilysin Inhibitor LCZ969.^[1]^: 120 The angioedema appears to be dose dependent as it may resolve with decreased dose.^[1]^: 120

Signs and symptoms[edit | edit source]

Angioedema presents itself as an abrupt onset of non-pitting, non-itchy swelling that involves the mucosal layers. Some common locations of angioedema are the face, particularly the lips and around the eyes, hands and feet, and genitalia.^[2] A rare, yet serious complication is one inside the abdomen, the symptom usually being severe stomach upset, which is much less obvious than the other locations.^[3]

Risk factor[edit | edit source]

Some common ACE Inhibitors are:

Benazepril (Lotensin)
Captopril (Capoten)
Enalapril (Vasotec)
Lisinopril (Prinivil, Zestril)
Ramipril (Altace)

Some common ARBs are:

Candesartan (Atacand)
Losartan (Cozaar)
Olmesartan (Benicar)
Valsartan (Diovan)

Diagnosis[edit | edit source]

The diagnosis of drug-induced angioedema is done via, but not limited to:^[4]

Analysis of complement factors
Tryptase levels
Specific allergy test

Management[edit | edit source]

The treatment for this induced condition may include emergency medication as well as epinephrine.^[4]

Incidence[edit | edit source]

The chance of drug-induced angioedema is extremely uncommon, however, as studies show incidence of less than 1%.^[5] The reason this adverse effect may occur is due to the build-up of bradykinin, a vasodilator. This causes blood vessels to dilate and allow for fluid buildup in the mucosal surfaces.

References[edit | edit source]

↑ ^1.0 ^1.1 James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0.
↑ Winters, Michael. “Clinical Practice Guideline: Initial Evaluation and Management of Patients Presenting
↑ J Community Hosp Intern Med Perspect. 2014; 4(4): 10.3402/jchimp.v4.25260
↑ ^4.0 ^4.1 Lerch, Marianne (2012). "Drug-induced angioedema". Chemical Immunology and Allergy. 97: 98–105. doi:10.1159/000335621. ISSN 1662-2898. Archived from the original on 15 April 2022. Retrieved 14 April 2022.
↑ Banerji, Aleena. “Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department.” Annals of Allergy, Asthma & Immunology (2008); 100: 327-332. Web. 2 Nov 2014

2. Angiotensin-Neprilysin Inhibition versus Enalapril in Heart Failure (PARADIGM-HF Investigators); NEJM.org, September 11, 2014; Vol.371, No.11.

External links[edit | edit source]

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[Andrews-1] 1.0 ^1.1 James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0.

[2] Winters, Michael. “Clinical Practice Guideline: Initial Evaluation and Management of Patients Presenting

[3] J Community Hosp Intern Med Perspect. 2014; 4(4): 10.3402/jchimp.v4.25260

[ref-4] 4.0 ^4.1 Lerch, Marianne (2012). "Drug-induced angioedema". Chemical Immunology and Allergy. 97: 98–105. doi:10.1159/000335621. ISSN 1662-2898. Archived from the original on 15 April 2022. Retrieved 14 April 2022.

[5] Banerji, Aleena. “Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department.” Annals of Allergy, Asthma & Immunology (2008); 100: 327-332. Web. 2 Nov 2014

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