Angioedema can occur in isolation, accompanied by urticaria, or as a feature of anaphylaxis in mast cell-mediated disorders, bradykinin-mediated disorders, as well as in others with unknown mechanisms, such as infections, rare disorders, or idiopathic angioedema.
Standard agents for anaphylactic reactions have limited efficacy for bradykinin-mediated angioedema and, therefore, agents approved for hereditary angioedema are increasingly prescribed for these patients.
The severity of anaphylaxis was associated with mast cell degranulation, increased plasma heparin levels, the intensity of contact system activation, and bradykinin formation.
The drug effect may be compromised by an elicited immune response, resulting in the production of anti-asparaginase antibodies causing an anaphylactic reaction or silent inactivation of the enzyme.
Two NLRP3 SNPs (rs4612666 and rs10754558) were significantly associated with susceptibility to food-induced anaphylaxis (P = .00086 and P = .00068, respectively).
It is a clinical diagnosis, although measurement of serial serum total mast cell tryptase (MCT) is gold standard and may help differentiate anaphylaxis from its mimics.
Relationship Between Anaphylaxis and Use of Beta-Blockers and Angiotensin-Converting Enzyme Inhibitors: A Systematic Review and Meta-Analysis of Observational Studies.
We aimed to identify knowledge gaps among Internal Medicine residents and students in the diagnosis and treatment of anaphylaxis and angiotensin-converting enzyme (ACE)-inhibitor-induced angioedema through their participation in a simulation course.
Some studies show an increased risk of anaphylaxis in patients who are taking ACE inhibitors and beta-blockers, whereas others studies do not show an increased risk.
Drugs like beta-blockers, angiotensin converting enzyme-inhibitors, antihistamines or steroids may hide or blunt initial clinical manifestations of anaphylaxis.