Treatment of idiopathic nonhistaminergic angioedema with bradykinin B2 receptor antagonist icatibant

Corso, Isabella Del; Puxeddu, Ilaria; Sardano, E; Geraci, Stephen A.; Breggia, M.; Rocchi, Valeria; Migliorini, Paola

doi:10.1016/j.anai.2012.03.013

Cited by 25 publications

(9 citation statements)

References 4 publications

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“…Efficacy of tranexamic acid has been reported in two case series, but no detailed data are available . Case reports indicate that icatibant can relieve symptoms of angioedema in these patients, whereas no data specifically report on the efficacy of corticosteroids .…”

Section: Idiopathic Nonhistaminergic Acquired Angioedemamentioning

confidence: 99%

“… showed that one patient with InH‐AAE had high levels of bradykinin in the venous blood effluent from the swollen arm, while in a similar situation, but with IH‐AAE, bradykinin levels were normal. Additional evidence supportive of bradykinin as the mediator in this situation comes from scattered case reports showing efficacy of the bradykinin receptor antagonist icatibant in reverting angioedema that is not responsive to antihistamine . Until such findings are confirmed in a significant series of patients, we prefer to maintain the term nonhistaminergic for patients with angioedema not prevented by antihistamine.…”

Section: Idiopathic Nonhistaminergic Acquired Angioedemamentioning

confidence: 99%

See 1 more Smart Citation

Classification, diagnosis, and approach to treatment for angioedema: consensus report from the Hereditary Angioedema International Working Group

Cicardi

Aberer

Banerji

et al. 2014

Allergy

623

694

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Angioedema is defined as localized and self-limiting edema of the subcutaneous and submucosal tissue, due to a temporary increase in vascular permeability caused by the release of vasoactive mediator(s). When angioedema recurs without significant wheals, the patient should be diagnosed to have angioedema as a distinct disease. In the absence of accepted classification, different types of angioedema are not uniquely identified. For this reason, the European Academy of Allergy and Clinical Immunology gave its patronage to a consensus conference aimed at classifying angioedema. Four types of acquired and three types of hereditary angioedema were identified as separate forms from the analysis of the literature and were presented in detail at the meeting. Here, we summarize the analysis of the data and the resulting classification of angioedema.

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Section: Idiopathic Nonhistaminergic Acquired Angioedemamentioning

confidence: 99%

Section: Idiopathic Nonhistaminergic Acquired Angioedemamentioning

confidence: 99%

Classification, diagnosis, and approach to treatment for angioedema: consensus report from the Hereditary Angioedema International Working Group

Cicardi

Aberer

Banerji

et al. 2014

Allergy

623

694

View full text Add to dashboard Cite

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“…When this approach is confirmed to be ineffective, bradykinin targeted drugs are considered, this approach being based on several studies [25][26][27][28][29][30][31][32][33]. These drugs have been indicated for C1-INH-HAE and include plasma derived and recombinant C1-INH, a recombinant inhibitor of plasma kallikrein and the antagonist of bradykinin receptors [10,[24][25][26][27][28][29][30][31][32][33][34][35][36][37]. Fresh frozen plasma, used to replace C1-INH when specific concentrates are not available, can also be an option to replace an unidentified deficiency leading to bradykinin release.…”

Section: Management Of Idiopathic Angiooedemamentioning

confidence: 99%

Differential diagnosis and management issues of idiopathic angiooedema and their resolution

Zanichelli

Mansi

et al. 2015

The Journal of Critical Care Medicine

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Angiooedema is a local and self-limiting swelling of the subcutaneous and sub mucosal tissues, produced by vasoactive peptides that temporary increase the vascular permeability. It is recognized that recurrent angiooedema exposes patients to the risk of fatalities and reduced quality of life, being in some circumstances associated with a critical condition. Angiooedema can occur with or without wheals. The first symptom is urticaria, the second is a distinct nosologic entity. In absence of an identifiable cause, recurrent angiooedema without wheals can be defined as idiopathic and marked"idiopathic histaminergic angiooedema" when it is responsive to anti histamine treatment, and "idiopathic non-histaminergic angiooedema" when it is not. Furthermore, idiopathic non-histaminergic angiooedema can be diagnosed as hereditary or sporadic by family history. In this review, we summarize the approaches to diagnose and treat different forms of idiopathic angiooedema.

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“…Observation that the phenotype, clinical symptoms, and swellings, is largely similar among the various HAE types and that pruritic rash is not a typical feature in U‐HAE patients, indicated that histamine is not of critical importance for the pathology of the disease . On the other hand, the efficacy of treatment with bradykinin‐2 (B2) receptor antagonists in many attacks gave the clinical evidence that bradykinin is the mediator responsible for the disease . Very recently, mutations in the plasminogen gene (PLG), in the angiopoietin 1 gene ( ANGPT‐1 ), and in the kininogen gene ( KNG1 ) have been found in a subsetting of U‐HAE patients .…”

Section: History Of a Search For The (Genetic) Pathogenesismentioning

confidence: 99%

“…11 On the other hand, the efficacy of treatment with bradykinin-2 (B2) receptor antagonists in many attacks gave the clinical evidence that bradykinin is the mediator responsible for the disease. 12 Very recently, mutations in the plasminogen gene (PLG), in the angiopoietin 1 gene (ANGPT-1), and in the kininogen gene (KNG1) have been found in a subsetting of U-HAE patients. [13][14][15] Treatment of antihistamines, combined or not with corticosteroid, was not effective, whereas the use of B2 receptor antagonists was effective in a high number of attacks and prophylaxis with oral tranexamic acid reduced the number and severity of acute episodes.…”

mentioning

confidence: 99%

Hereditary angioedema: Looking for bradykinin production and triggers of vascular permeability

Margaglione

D’Apolito

Santocroce

et al. 2019

Clin Experimental Allergy

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Since the Osler's identification of the inherited nature of hereditary angioedema, a huge array of information was collected on pathogenetic mechanisms of the disease. Over the last years, information grew fast, and mutations in different genes, in addition to C1‐inhibitor, were found to be causative. All types are inherited as autosomal‐dominant traits with incomplete penetrance and little or no genotype‐phenotype correlation. As a result, the clinical expression is characterized by a large heterogeneity. The acknowledgement of mechanisms leading to heterogeneity of the clinical phenotype is likely to provide important information not only for a better understanding of the pathogenesis but also for therapy. Regardless of which gene is mutated, similar pathways seem to play a pivotal role, triggering the up‐regulation of contact activation system/kallikrein kinin system and giving rise to an unbalanced increase of bradykinin. However, notwithstanding the increase of bradykinin in bloodstream, the phenomenon is localized and no general vascular leakage and oedema is recognized. Thus, it is conceivable that there exist one or more localized factors that stimulate the production of bradykinin, which does not become a systemically event. Uncovering of these factors may shed lights on the missing part of the pathogenesis of hereditary angioedema. The present review, collecting information on pathogenesis from biochemical and genetics investigations, tries to provide a comprehensive view of the pathogenesis of hereditary angioedema. This can allow for a better understanding of the disease and lead to focused investigations that can further improve our knowledge.

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Treatment of idiopathic nonhistaminergic angioedema with bradykinin B2 receptor antagonist icatibant

Cited by 25 publications

References 4 publications

Classification, diagnosis, and approach to treatment for angioedema: consensus report from the Hereditary Angioedema International Working Group

Classification, diagnosis, and approach to treatment for angioedema: consensus report from the Hereditary Angioedema International Working Group

Differential diagnosis and management issues of idiopathic angiooedema and their resolution

Hereditary angioedema: Looking for bradykinin production and triggers of vascular permeability

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