Bradykinin-mediated angioedema

Obtułowicz, Krystyna

doi:10.20452/pamw.3273

Cited by 42 publications

(41 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The severity of anaphylaxis is correlated with the intensity of CSA and BK formation 20 . The abnormal production of BK leads to anaphylaxis and angioedema via its ability to increase inflammation and vessel permeability 21 , 45 . There are common triggers for anaphylactic reactions such as food, medications or insect venom, of which 44–57% of the fatal anaphylaxis was triggered by medications, far more than other inducements 3 , 46 – 48 .…”

Section: Discussionmentioning

confidence: 99%

“…For example, penicillin-induced IHR was much more likely with parenteral administration than oral administration 58 . Angioedema, BK-mediated swelling 45 , is also common in penicillin-induced IHR 59 , 60 . Perhaps, not coincidentally, Caucasians, whose FXII levels are significantly higher than Japanese 61 , suffer from more penicillin-induced IHR compared with Asians including Japanese 60 .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Penicillin causes non-allergic anaphylaxis by activating the contact system

Gao

Han

Zhang

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Immediate hypersensitivity reaction (IHR) can be divided into allergic- and non-allergic-mediated, while “anaphylaxis” is reserved for severe IHR. Clinically, true penicillin allergy is rare and most reported penicillin allergy is “spurious”. Penicillin-initiated anaphylaxis is possible to occur in skin test- and specific IgE-negative patients. The contact system is a plasma protease cascade initiated by activation of factor XII (FXII). Many agents with negative ion surface can activate FXII to drive contact system. Our data showed that penicillin significantly induced hypothermia in propranolol- or pertussis toxin-pretreated mice. It also caused a rapid and reversible drop in rat blood pressure, which did not overlap with IgE-mediated hypotension. These effects could be countered by a bradykinin-B2 receptor antagonist icatibant, and consistently, penicillin indeed increased rat plasma bradykinin. Moreover, penicillin not only directly activated contact system FXII-dependently, but also promoted bradykinin release in plasma incubated-human umbilical vein endothelial cells. In fact, besides penicillin, other beta-lactams also activated the contact system in vitro. Since the autoactivation of FXII can be affected by multiple-factors, plasma from different healthy individuals showed vastly different amidolytic activity in response to penicillin, suggesting the necessity of determining the potency of penicillin to induce individual plasma FXII activation. These results clarify that penicillin-initiated non-allergic anaphylaxis is attributed to contact system activation, which might bring more effective diagnosis options for predicting penicillin-induced fatal risk and avoiding costly and inappropriate treatment clinically.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Penicillin causes non-allergic anaphylaxis by activating the contact system

Gao

Han

Zhang

et al. 2020

Sci Rep

View full text Add to dashboard Cite

show abstract

“…1 The deficiency of C1INH 1,2 disturbs the complement cascade, coagulation, kinins, and fibrinolysis and results in an uncontrolled release of bradykinin, the main mediator in C1INH -HAE. 3 Previous studies supported the involvement of blood coagulation and fibrinolysis in the pathophysiology of C1INH -HAE despite the absence of clinically relevant thrombosis and hemostatic disorders. 4,5 To our knowledge, there have been no reports on the properties of plasma fibrin clot in relation to thrombin formation in this disease despite evidence on their role in several pathologies.…”

mentioning

confidence: 88%

Elevated thrombin generation and factor VIII activity during angioedema attack in patients with hereditary C1 inhibitor deficiency

Obtułowicz¹,

Dyga²,

Natorska³

et al. 2019

Polish Archives of Internal Medicine

Self Cite

View full text Add to dashboard Cite

The ethics committee of Jagiellonian University in Kraków approved the study and patients signed a written informed consent form. The study was carried out in accordance with the Declaration of Helsinki and its amendments. Laboratory investigations Blood samples (vol/vol, 9:1 of 3.2% trisodium citrate) were spun at 2000 g for 10 minutes, and the supernatants were aliquoted and stored at a temperature of-80ºC. Plasma levels of the C1INH antigen (aC1INH) were measured using nephelometry (Siemens Healthcare Diagnostics GmbH, Marburg, Germany). The functional activity of C1INH was determined using the functional chromogenic assay Berichrom C1INH (Siemens Healthcare Diagnostics). All patients had reduced serum C1INH levels (mean, 0.07 g/l; reference range, 0.21-0.39 g/l) and functional activity of C1INH (mean functional activity of C1INH, 26.0%; reference range, 70%-130%). Plasma levels of factor VIII (FVIII; based on activated partial thromboplastin time) were evaluated using the Behring Coagulation System (Siemens Healthcare Diagnostics). ELI-SA test kits were used to measure thrombin-antithrombin complexes (TAT; Enzygnost TAT micro, Siemens Healthcare Diagnostics). Fibrin clot analysis Plasma fibrin clot permeability was determined as described previously. 7 The permeation coefficient (K s), which indicates the average size of pores formed in the fibrin network (with low values indicating a tightly packed fibrin structure), was calculated from the equation: K s = Q × L × η/t × A × Δp, where Q is the flow rate in time, L is the length of a fibrin gel, η is the viscosity of liquid (in poise), t is percolating time, A is the cross-sectional area (in cm 2), and Δp is a differential pressure (in dyne/cm 2).

show abstract

“…Tratando-se de uma doença genética autossômica dominante, de deficiência congênita funcional, qualitativa ou quantitativa determinada pela ausência do inibidor de C1 esterase (C1NH), o AEH também entra no quadro de doenças imunológicas e inflamatórias. Esta Research, Society and Development, v. 9, n. 10, e099107858, 2020 (CC BY 4.0) | ISSN 2525-3409 | DOI: http://dx.doi.org/10.33448/rsd-v9i10.7858 7 A bradicinina se liga ao receptor B2 expresso nas células endoteliais, reduzindo assim as junções endoteliais, fazendo com que ocorra um aumento na permeabilidade vascular induzindo ao edema (Obtulowicz, 2016;Marceau et al 2020).…”

Section: Fisiopatologia Do Aehunclassified

“…Níveis de bradicinina elevados no sangue coletado de locais com edemas, quando comparados com outros locais não afetados por AEH, demonstram que a via de bradicinina desempenha um papel importante no diagnóstico da doença (Obtulowicz, 2016;Marceau et al 2020;Giavina-Bianchi et al, 2017;Maurer et al 2017). e mecanismos que levam a doença (30) .…”

Section: Fisiopatologia Do Aehunclassified

Investigação genética relacionada a fisiopatologia e sintomas clínicos do Angioedema Hereditário

Kruk

Fortunato

Moraes

et al. 2020

RSD

View full text Add to dashboard Cite

Angioedema Hereditário (AEH) é uma doença pouco conhecida por profissionais da saúde, portanto subdiagnosticada. O objetivo do estudo, foi analisar artigos referentes à temática abordada dos últimos 5 anos. AEH é uma doença genética rara e grave do sistema imunológico, de caráter autossômico dominante, causada pela deficiência de inibidor de C1 esterase (C1-INH). Classificada em 3 fenótipos: deficiência quantitativa do inibidor de C1-INH, disfunção de C1-INH e C1-INH normal. Mutações em diversos genes estão associadas ao fenótipo do AEH, pacientes com deficiência e disfunção da proteína C1-INH possuem mutações no gene SERPING1 e pacientes com C1-INH normal, podem apresentar mutações nos genes F12, angiopoietina (ANGPT1), plasminogênio (PLG) ou cininogênio (KNG1). Os sintomas do AEH são caracterizados por edemas recorrentes em várias partes do corpo, tanto em pele como órgãos internos. Para a elaboração deste estudo realizou-se uma revisão integrativa da literatura, os artigos foram pesquisados em três bases de dados eletrônicas, Google Scholar, PubMed e Scielo, utilizando os descritores “angioedema hereditário”, “mutações”, “bradicinina”, “C1-INH”, “SERPING1”, “plasminogênio”, “angiopoietina”, “F12” e “cininogênio”, conectados por operadores boleanos AND e OR. A pesquisa no banco de dados revelou um total de 874 artigos, após triagem, 32 artigos foram avaliados. Com a pesquisa tornou-se possível compreender não somente os mecanismos percursores que levam ao desenvolvimento da doença, mas também as mutações genéticas responsáveis pelas diversas formas de manifestações clínicas do AEH, corroborando a construção de conhecimento dos profissionais envolvidos no diagnóstico e tratamento da patologia.

show abstract

Bradykinin-mediated angioedema

Cited by 42 publications

References 35 publications

Penicillin causes non-allergic anaphylaxis by activating the contact system

Penicillin causes non-allergic anaphylaxis by activating the contact system

Elevated thrombin generation and factor VIII activity during angioedema attack in patients with hereditary C1 inhibitor deficiency

Investigação genética relacionada a fisiopatologia e sintomas clínicos do Angioedema Hereditário

Contact Info

Product

Resources

About