C1 Esterase Inhibitor (Berinert) for ACE Inhibitor-Induced Angioedema: Two Case Reports

Leibfried, Maria; Kovary, Alexandra

doi:10.1177/0897190016677427

Cited by 17 publications

(4 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After a gift of 1500 units of C1 inhibitor concentrate, improvement was seen within 20 min. Several other case reports confirmed successful treatment with C1 inhibitor concentrate [35][36][37][38]. Patients showed improvement on average 88 min and complete resolution in 10.1 h, without the need for other treatment such as intubation or corticosteroids or a second gift of C1 inhibitor concentrate.…”

Section: C1 Inhibitor Concentratementioning

confidence: 67%

Current Treatment of Angioedema Induced by ACE Inhibitors

Terreehorst

Reitsma

Cohn

2019

Curr Treat Options Allergy

View full text Add to dashboard Cite

Purpose of Review Angioedema is a well-known side effect of ACE inhibitors. Current knowledge shows that the underlying pathophysiological mechanism is an excess of bradykinin, most likely due to ineffective breakdown pathways. Since C1 inhibitor deficiency has the same pathophysiological background, it would be logical to assume that C1 inhibitor deficiency treatments could be of use in ACE inhibitor-induced angioedema. The objective of this review was to evaluate the evidence for treatment of ACE inhibitorinduced angioedema by means of drugs intervening in the bradykinin system. Recent Findings We searched in the literature for double-blind placebo-controlled trials using either inhibitors of production of kallikrein, bradykinin receptor antagonists, C1 inhibitor concentrate, or fresh frozen plasma as treatment for ACE inhibitor-induced angioedema. The reference list of retrieved articles was checked for articles with the same subject (snowballing). The evidence for each treatment was evaluated by IT and DMC. Summary Double-blind placebo-controlled trials were only found for ecallantide and icatibant. Both treatments did not show superiority over conventional treatment with histamine receptor antagonists and steroids. No double-blind placebo-controlled trials were found of fresh frozen plasma or C1 inhibitor concentrate. To date, there is insufficient evidence for the use of bradykinin receptor antagonists and kallikrein production inhibitors. Although case reports regarding the use of fresh frozen plasma and C1 inhibitor concentrate are positive, well-designed trials are lacking. Drug Allergy (L Mayorga, Section Editor)

show abstract

Section: C1 Inhibitor Concentratementioning

confidence: 67%

Current Treatment of Angioedema Induced by ACE Inhibitors

Terreehorst

Reitsma

Cohn

2019

Curr Treat Options Allergy

View full text Add to dashboard Cite

show abstract

“…Symptoms resolved in 13 patients. One patient, who experienced a relapse 4 h after treatment, underwent tracheotomy [ 38 ]. None of the 10 patients treated with C1-INH from the same case series required intubation or tracheotomy compared to the historical control group who received standard treatment at the same institution (3/47, 6.38% required tracheotomy; 5/47, 10.64% required intubation) [ 37 ].…”

Section: Methodsmentioning

confidence: 99%

Bradykinin-induced angioedema in the emergency department

et al. 2022

View full text Add to dashboard Cite

Background Acute airway angioedema commonly occurs through two distinct mechanisms: histamine- and bradykinin-dependent. Although they respond to distinct treatments, these two potentially life-threatening states present similarly. Poor recognition of the bradykinin-dependent pathway leads to treatment errors in the emergency department (ED), despite the availability of multiple pharmacologic options for hereditary angioedema (HAE) and other forms of bradykinin-induced angioedema. Here, we consider the pathophysiology and clinical features of bradykinin-induced angioedema, and we present a systematic literature review exploring the effectiveness of the available therapies for managing such cases. Methods PubMed searches using ‘emergency’, ‘bradykinin’ and various therapeutic product names identified studies reporting the efficacy of treatments for bradykinin-induced angioedema in the ED setting. In all, 22 studies met prespecified criteria and are analysed here. Findings Whereas histamine-induced angioedema has a faster onset and often presents with urticaria, bradykinin-induced angioedema is slower in onset, with greater incidence of abdominal symptoms. Acute airway angioedema in the ED should initially be treated with anaphylactic protocols, focusing on airway management and treatment with epinephrine, antihistamine and systemic steroids. Bradykinin-induced angioedema should be considered if this standard treatment is not effective, despite proper dosing and regard of beta-adrenergic blockade. Therapeutics currently approved for HAE appear as promising options for this and other forms of bradykinin-induced angioedema encountered in the ED. Conclusion Diagnostic algorithms of bradykinin-induced angioedema should be followed in the ED, with early use of approved therapies to improve patient outcomes.

show abstract

“…67,68 Although rare, serious cases of ACEi-A can require intensive care, including tracheal intubation, and may lead to death. 66,[71][72][73] Bradykinin receptor 2 antagonist (icatibant)-a drug approved for HAE-has also been proposed to treat ACEi-A and has been shown in one study to quicken resolution of angioedema. As described above, time to onset for ACEi-A varies from days to years and has also been reported to occur after discontinuation of the ACEi.…”

Section: Clinical Featuresmentioning

confidence: 99%

“…70 Rather, fresh frozen plasma, C1 esterase inhibitor or tranexamic acid had been found to be effective in several case series and are often utilized in real-life practice when first-line treatment fails. 66,[71][72][73] Bradykinin receptor 2 antagonist (icatibant)-a drug approved for HAE-has also been proposed to treat ACEi-A and has been shown in one study to quicken resolution of angioedema. 73 However, two further studies, one of which was a large multi-centre trial, were unable to replicate this finding.…”

Section: Clinical Featuresmentioning

confidence: 99%

Pharmacogenetics of angiotensin‐converting enzyme inhibitor‐induced angioedema

Liau

Chua

Kennedy

et al. 2019

Clin Experimental Allergy

View full text Add to dashboard Cite

Angioedema is a rare adverse effect of the commonly used angiotensin-converting enzyme inhibitors (ACEi) and is reported to occur with a prevalence of 0.1%-0.7%.Although most ACEi-induced angioedema (ACEi-A) cases are mild, severe cases requiring intensive care and even resulting in death have been reported in the literature. The mechanisms underlying ACEi-A are not yet fully understood, but bradyki-

show abstract

C1 Esterase Inhibitor (Berinert) for ACE Inhibitor-Induced Angioedema: Two Case Reports

Abstract: C1INH (human) was a successful addition to the traditional management of 2 patients with angioedema due to ACEI.

Cited by 17 publications

References 12 publications

Current Treatment of Angioedema Induced by ACE Inhibitors

Current Treatment of Angioedema Induced by ACE Inhibitors

Bradykinin-induced angioedema in the emergency department

Pharmacogenetics of angiotensin‐converting enzyme inhibitor‐induced angioedema

Contact Info

Product

Resources

About