Life-Threatening ACE Inhibitor-Induced Angioedema After Eleven Years on Lisinopril

Norman, Johanna L.; Holmes, Whitney L.; Bell, William A.; Finks, Shannon W.

doi:10.1177/0897190012465990

Cited by 16 publications

(15 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A literature search using PubMed and the keywords “angiotensin‐converting enzyme inhibitor” and “angioedema” revealed multiple cases of ACEI‐induced angioedema that developed more than 1 year after the initiation of the drug. One case described the development of visceral angioedema after 9 years of enalapril therapy, while another described two episodes of angioedema occurring 11 years after the initiation of therapy with lisinopril . A separate case report noted the development of ACEI‐induced angioedema 23 years after the initiation of enalapril in a patient without any known risk factors, which, per our review, is the longest reported time from the initiation of ACEI therapy to the development of angioedema in the literature.…”

Section: Timingmentioning

confidence: 76%

Angiotensin‐converting enzyme inhibitor–induced angioedema: A review of the literature

Brown

Gonzalez

Monteleone

2017

J of Clinical Hypertension

View full text Add to dashboard Cite

According to the National Health and Nutrition Examination Survey 2012, one third of antihypertensive prescriptions in the United States in the past decade were for angiotensin-converting enzyme inhibitors (ACEIs). An important and serious side effect of ACEIs is angioedema caused by a reduction in bradykinin degradation. In a national medical chart abstraction study conducted at the US Veterans Affairs Health Care System in 2008, 0.20% of ACEI initiators developed angioedema while on the medication. The angiotensin-converting enzyme is a part of the renin-angiotensin system that converts angiotensin I to angiotensin II. It is additionally responsible for the degradation of bradykinin, which is generated from high molecular weight kininogen by kallikrein. Via bradykinin 2 receptors, bradykinin affects vascular permeability and stimulates the release of substance P, which is a peptide that causes vasodilation and fluid extravasation into tissues. Inhibition of the angiotensin-converting enzyme and subsequent blockade of bradykinin degradation is thought to be a likely explanation for ACEI-induced angioedema. Studies have shown that blacks, women, and smokers are at an increased risk for ACEI-induced angioedema. A 2005 study identified black race, history of drug rash, age older than 65 years, and seasonal allergies as independent risk factors for angioedema related to enalapril. Angioedema may occur at any time during treatment with ACEIs and may continue after the medication is discontinued. The degree of ACEI-angiotensin receptor blocker angioedema cross-reactivity is difficult to determine from the literature. However, multiple studies have reported relatively low rates of native angioedema with angiotensin receptor blockers (approximately half that of ACEIs, or 0.1%) and a low incidence of cross-reactivity (<10%).Common treatments for angioedema, such as antihistamines and glucocorticoids, have not been shown to be effective in ACEI-induced angioedema. However, medications that have been used for acute treatment of hereditary angioedema and target the factors that cause ACEI-mediated angioedema are being explored.

show abstract

Section: Timingmentioning

confidence: 76%

Angiotensin‐converting enzyme inhibitor–induced angioedema: A review of the literature

Brown

Gonzalez

Monteleone

2017

J of Clinical Hypertension

View full text Add to dashboard Cite

show abstract

“…The development of ACEI-AAE can present itself within a few hours of the first ACEI intake, as in our case, and as late as after 20 years of regular use 9 10. With corticosteroid and antihistamine treatment, the mean time until complete resolution is 27.1 hours, and with the use of icatibant (a specific bradykinin receptor antagonist), 8.0 hours 6.…”

Section: Discussionmentioning

confidence: 50%

Life-threatening angio-oedema after the first dose of an ACE inhibitor—not an anaphylactic reaction

Nielsen

Bygum²,

Rasmussen

2016

BMJ Case Reports

View full text Add to dashboard Cite

We present a case of a 60-year-old Caucasian woman, with no prior history of swellings, who was admitted to a hospital due to life-threatening angio-oedema. She had, the previous day, been prescribed an ACE inhibitor for her essential hypertension. She had taken one tablet at night-time, and awoke in the morning with a swollen face progressing to involve the tongue and throat within a few hours. On arrival at her doctor's office, her voice had altered. Corticosteroids and antihistamine were administered while awaiting an ambulance. Arriving at the emergency department, she had dyspnoea due to increasingly severe angio-oedema of the upper airways. Neither adrenaline inhalations, intravenously administrated corticosteroids, atropine nor furosemide were effective and the patient soon become bradycardic. A tracheotomy was performed and the patient was placed on a ventilator. She eventually made a full recovery. It was concluded that she had suffered from life-threatening angio-oedema due to her new medication.

show abstract

“…A number of cases of ACEi-induced angio-oedema have been successfully treated with complement C1-esterase inhibitor concentrate, which in Denmark is approximately 25% cheaper per dose compared to icatibant (ie, Berinert 1000 U=€1400) 8 9 16 17…”

Section: Discussionmentioning

confidence: 99%

Life-threatening ACE inhibitor-induced angio-oedema successfully treated with icatibant: a bradykinin receptor antagonist

Ostenfeld

Bygum²,

Rasmussen

2015

BMJ Case Reports

View full text Add to dashboard Cite

SUMMARYWe present a case of a 75-year-old woman treated with an ACE inhibitor, who presented with angio-oedema of the tongue and had difficulty speaking. No symptoms of anaphylaxis or urticaria were present. The patient was treated intravenously with antihistamine and glucocorticoid in combination with adrenaline inhalations. After 6 h in the hospital the swelling progressed, and the patient was admitted to the intensive care unit and treated with one injection of icatibant-a bradykinin receptor antagonist. The patient reported subjective relief after 20-30 min and the swelling resolved within 2 h. Although the angiooedema was potentially life threatening, the patient avoided intubation and mechanical ventilation. ACE inhibitor-induced angio-oedema is most likely caused by an accumulation of bradykinin and substance P. Consequently, a bradykinin receptor antagonist is the rational treatment of choice instead of antiallergic medications, which have no proven efficacy in this condition. BACKGROUND

show abstract

Life-Threatening ACE Inhibitor-Induced Angioedema After Eleven Years on Lisinopril

Cited by 16 publications

References 38 publications

Angiotensin‐converting enzyme inhibitor–induced angioedema: A review of the literature

Angiotensin‐converting enzyme inhibitor–induced angioedema: A review of the literature

Life-threatening angio-oedema after the first dose of an ACE inhibitor—not an anaphylactic reaction

Life-threatening ACE inhibitor-induced angio-oedema successfully treated with icatibant: a bradykinin receptor antagonist

Contact Info

Product

Resources

About