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Urticaria and Angioedema
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Jenny M Stitt, Stephen C Dreskin
Acute attacks of HAE are most effectively treated with supplemental C1 inhibitor, a bradykinin B2 receptor antagonist (e.g., icatabant), or a kallikrein inhibitor (e.g., ecallantide) (Cicardi et al. 2010, Parikh and Riedl 2011, Zuraw et al. 2010, Antoniu 2011). The choice of medication is often based on availability. When these medications are not available, symptomatic care and airway monitoring for laryngeal edema should be provided. Administration of fresh frozen plasma, which contains C1 inhibitor, can also be considered; however there is significant concern that FFP may worsen ongoing AE in some patients (Dreskin 2012). The patient’s airway should be monitored, and if there is concern for laryngeal edema and stridor or respiratory distress is evident, the patient should undergo endotracheal intubation. If intubation is unsuccessful due to angioedema, emergent cricothyroidotomy may need to be performed. Other supportive care measures may include intravenous fluids and antiemetics for gastrointestinal symptoms, as well as analgesics for pain.
Role of Engineered Proteins as Therapeutic Formulations
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Khushboo Gulati, Krishna Mohan Poluri
Several of the protein therapeutics have already been developed using different protein scaffolds and are under clinical trials. Some of them include: Affibodies® from the synthetic Z domain of staphylococcal protein, Adnectins® from type III fibronectin domains, Avimers® from LDLR-A modules, Anticalins® from lipocalins, engineered Kunitz Domains, and DARPins® from ankyrin repeat proteins. One of the synthetic scaffolds, namely ecallantide (Kalbitor®), is a 60-amino-acid-long protein based on kunitz domain and has been approved as a therapeutic that inhibits plasma kallikrein. It was selected by phage display technology and was grown in Pichia pastoris strain of yeast (Zuraw et al., 2010). Some of these scaffolds are described in detail in the following sections.
Safety of medications for hereditary angioedema during pregnancy and lactation
Published in Expert Opinion on Drug Safety, 2023
Andrew Yeich, Ahmed Elhatw, Zaynab Ashoor, Kristen Park, Timothy Craig
Authors of the USA Hereditary Angioedema Medical Advisory Board 2020 and the recently published WAO HAE Consensus Guideline recommend that LTP should be an individualized decision for each patient according to individual need of patient and their tolerance to various medications [53,63]. They recommended the use of pdC1-INH SC or IV as a first-line therapy for pregnant and lactating females as they have the least reported side effects and have a history of 40 years of safe usage in Europe during pregnancy and lactation despite the lack of approval by the FDA and similar organizations for usage. Although rcC1-INH has much limited data, the available data are so far reassuring, and the guidelines include it as an appropriate therapy during pregnancy and lactation [64]. The use of anabolic androgens is contraindicated in pregnancy as they cross the placental barrier and be secreted into milk of lactating female causing virilization and other adverse events to the fetus and neonate. No recommendations were provided for the usage of ecallantide or lanadelumab due to absence of safety data in pregnancy and lactation. However, secondary to the 3–4% risk of allergic reactions to ecallantide, and the ability of the lanadelumab antibody IgG1 to cross the placenta, both should be avoided during pregnancy.
Biological therapy in hereditary angioedema: transformation of a rare disease
Published in Expert Opinion on Biological Therapy, 2020
Hilary Longhurst, Henriette Farkas
Improvements in the understanding of the etiology of the hereditary angioedemas has enabled development of treatments targeted at bradykinin and the contact pathway. Overactivity of the contact pathway and excess local bradykinin results from inadequate factor XII and kallikrein inhibition by C1 inhibitor, or overactivation of factor XII or plasminogen in some cases of angioedema with normal C1 inhibitor (Figure 1) [51]. Peptides targeting inhibition of bradykinin B2 receptors (icatibant) are effective when given by subcutaneous administration [52–55]. Availability of a subcutaneous product has widened access to home therapy via nurse administration (in case of ecallantide, which is associated with occasional anaphylactoid events) or self-administration (icatibant). Recurrence occurs more frequently with these agents than with the C1 inhibitors. About 10–20% require a second dose or C1 inhibitor treatment to resolve the HAE attack [56]. As with C1 inhibitors, early treatment improves response and reduces requirement for a second treatment [57].
Lanadelumab for the treatment of hereditary angioedema
Published in Expert Opinion on Biological Therapy, 2019
The approved dose is 30 mg, given as three separate subcutaneous injections of 10 mg in the abdomen, upper arm or thigh on demand [23–27]. The efficacy of Ecallantide was tested in two controlled trials, EDEMA3 and EDEMA4 [26] and the drug was approved by the Food and Drug Administration (FDA) for the treatment of acute angioedema attacks in December 2009. Due to safety concerns (reported acute hypersensitivity reactions) [27], the European Medicines Agency (EMA) did not approve the release to the market of Ecallantide for Europe [Withdrawal of the marketing authorization application for Kalbitor (ecallantide) EMA/888,548/2011]. Until the development of lanadelumab, Ecallantide was the only anti kallikrein drug available for the treatment of C1-INH-HAE, with the specific indication as on-demand therapy.