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

Ostenfeld, Sarah; Bygum, Anette; Rasmussen, Eva Rye

doi:10.1136/bcr-2015-212891

Cited by 8 publications

(7 citation statements)

References 16 publications

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“…A 75-year-old female was reported to have presented with lingual angioedema secondary to ACE inhibitor use. She was unresponsive to antihistamines, steroids and adrenaline but was successfully treated with one dose of icatibant (bradykinin receptor antagonist) and hence avoided intubation or mechanical ventilation [22].…”

Section: Discussionmentioning

confidence: 99%

Management of acute tongue swelling

Min¹,

Mohammad²,

Vallamkondu³

et al. 2020

Heighpubs Otolaryngol Rhinol

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Acute tongue swelling can present as an upper airway obstruction. There are a number of pathologies which potentially can cause tongue swelling include angioedema, anaphylaxis, drug rash with eosinophilia and systemic symptom (DRESS) syndrome, local allergic reaction, trauma resulting in tongue haematoma or lingual abscess, viral infections (herpes simplex virus, herpes zoster virus, Coxsackie virus), bacterial infection, foreign body and neoplasia. Aim To present a case series of patients presenting with an acute tongue swelling sharing our experience in managing these patients.

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Section: Discussionmentioning

confidence: 99%

Management of acute tongue swelling

Min¹,

Mohammad²,

Vallamkondu³

et al. 2020

Heighpubs Otolaryngol Rhinol

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“…C1q, MBL, and FXII are known to recognize apoptotic and necrotic cells that can trigger the CP and LP of complement ultimately leading to cleavage of C3/C5 into C3a/C5a and C3b/C5b. BK generated by the KK system activation can cause dry cough ( 74 ) and pulmonary inflammation with edema ( 75 ) by binding to BKR2. C3a and C5a bind to the anaphylatoxin receptors: C3aR, C5aR1, and C5aR2 and C5a is also able to activate endothelial cells in COVID-19 patients leading to von Willebrand Factor (vWF) and p-selectin exposure on the endothelial lining thereby contributing to the thrombotic phenotype ( 76 ).…”

Section: Conceptual Mechanisms Inducing Covid-19-triggered Ardsmentioning

confidence: 99%

How the Innate Immune System of the Blood Contributes to Systemic Pathology in COVID-19-Induced ARDS and Provides Potential Targets for Treatment

et al. 2022

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Most SARS-CoV-2 infected patients experience influenza-like symptoms of low or moderate severity. But, already in 2020 early during the pandemic it became obvious that many patients had a high incidence of thrombotic complications, which prompted treatment with high doses of low-molecular-weight heparin (LMWH; typically 150-300IU/kg) to prevent thrombosis. In some patients, the disease aggravated after approximately 10 days and turned into a full-blown acute respiratory distress syndrome (ARDS)-like pulmonary inflammation with endothelialitis, thrombosis and vascular angiogenesis, which often lead to intensive care treatment with ventilator support. This stage of the disease is characterized by dysregulation of cytokines and chemokines, in particular with high IL-6 levels, and also by reduced oxygen saturation, high risk of thrombosis, and signs of severe pulmonary damage with ground glass opacities. The direct link between SARS-CoV-2 and the COVID-19-associated lung injury is not clear. Indirect evidence speaks in favor of a thromboinflammatory reaction, which may be initiated by the virus itself and by infected damaged and/or apoptotic cells. We and others have demonstrated that life-threatening COVID-19 ARDS is associated with a strong activation of the intravascular innate immune system (IIIS). In support of this notion is that activation of the complement and kallikrein/kinin (KK) systems predict survival, the necessity for usage of mechanical ventilation, acute kidney injury and, in the case of MBL, also coagulation system activation with thromboembolism. The general properties of the IIIS can easily be translated into mechanisms of COVID-19 pathophysiology. The prognostic value of complement and KKsystem biomarkers demonstrate that pharmaceuticals, which are licensed or have passed the phase I trial stage are promising candidate drugs for treatment of COVID-19. Examples of such compounds include complement inhibitors AMY-101 and eculizumab (targeting C3 and C5, respectively) as well as kallikrein inhibitors ecallantide and lanadelumab and the bradykinin receptor (BKR) 2 antagonist icatibant. In this conceptual review we discuss the activation, crosstalk and the therapeutic options that are available for regulation of the IIIS.

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“…First, the nosology of anaphylaxis has changed, and almost 17 years ago, the World Allergy Organization recommended dropping the term anaphylactoid reaction due to confusion of its implications and instead, classifying anaphylaxis into two major groups, allergic and nonallergic, with kinin and complement-mediated reactions falling into the nonallergic category, as pointed out in my review (4).…”

Section: The Author Repliesmentioning

confidence: 99%

Refractory Anaphylaxis Needing Emergency Intubation Supported by Expert Opinion and Published Guidelines: Could We Use Off-Label Drugs to Avoid It?

Honoré

Redant

Préseau

et al. 2022

Critical Care Medicine

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I n a recently issue of Critical Care Medicine, Krishaswamy (1) discussed about refractory cases of anaphylaxis and states that if angioedema does not respond to epinephrine, prompt endotracheal intubation is indicated and is supported by published guidelines (2). The situation of "epinephrine resistant" might be the first clue to the suspicion of bradykinin angioedema or anaphylactoid reaction. The resemblance of this condition to the much more common picture of histamine-induced angioedema means that many patients have been treated as such with epinephrine, corticosteroids, and antihistaminic (1). In a few cases, treatment failure will occur and bradykinin-mediated angioedema may become a valid alternative diagnosis (2). In recent years, new medical treatments have been introduced in the treatment of hereditary angioedema (HAE), a genetic disease characterized by bradykinin-mediated recurrent angioedema. Selective bradykinin B2 receptor antagonists and complement C1-esterase inhibitors are the most promising medical alternatives (2). Angiotensin-converting enzyme inhibitors (ACEIs) are common drugs widely used for renal and cardiovascular disorders (2). Acquired angioedema related to the use of an ACEI is an uncommon adverse reaction that can lead to life-threatening airway obstruction. The onset of angioedema is not due to a classical allergic reaction mediated by histamine but, rather, a symptom of an increased level of bradykinin (2). In a large patient series from Tai et al (3), 367 patients presented to a hospital because of angioedema during a 11-year period. Of those, nearly 50% were prescribed an ACEI. Twelve patients needed intubation but only one required tracheostomy (3). While histamine-induced angioedema treated with epinephrine, corticosteroids, and antihistaminic drugs will improve (1), bradykinin-mediated angioedema will not. A case report described a patient with angioedema who was treated IV with antihistamine and glucocorticoid in combination with epinephrine inhalations (4). After 6 hours, the swelling progressed, and the patient was admitted to the ICU and treated with icatibant, and the swelling resolved within 2 hours avoiding intubation (4) Icatibant is a bradykinin receptor antagonist, treatment of choice instead of anti-allergic medications, which have no proven efficacy in this condition (4). In HAE, the abnormal elevated production of bradykinin is caused by dysregulation of kallikrein activity due to an inherited C1-inhibitor deficiency or mutation in patients with HAE (5). In case of life-threatening airway obstruction due to HAE, plasma-derived C1-inhibitor (or recombinant C1-inhibitor-ruconest) and icatibant (plus ecallantide-recombinant plasma kallikrein inhibitor; CSL Behring, King of Prussia, PA) could be used to avoid

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

Cited by 8 publications

References 16 publications

Management of acute tongue swelling

Management of acute tongue swelling

How the Innate Immune System of the Blood Contributes to Systemic Pathology in COVID-19-Induced ARDS and Provides Potential Targets for Treatment

Refractory Anaphylaxis Needing Emergency Intubation Supported by Expert Opinion and Published Guidelines: Could We Use Off-Label Drugs to Avoid It?

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