China
Africa
Explore chapters and articles related to this topic
Principles of Heart Failure Pharmacotherapy
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Erika L. Hellenbart, Stephanie Dwyer Kaluzna, Robert J. DiDomenico
Angioedema, swelling of the lips, tongue, nose, or throat, can occur in 0.1–0.7% of patients taking an ACEI at any time during a course of therapy.14 Although rare, angioedema can cause life-threatening asphyxia. Therefore, the offending agent should be discontinued immediately. Risk of ACEI-induced angioedema is five times higher in Black patients.20 Other risk factors for ACEI-induced angioedema include female gender, age greater than 65 years, drug hypersensitivity, seasonal allergies, and NSAID use.14 Since ARBs do not affect bradykinin levels, they have a lower risk of angioedema than ACEIs. ARBs can be considered in patients with a history of angioedema on ACEI but angioedema has been reported in 2–17% of patients upon rechallenge with an ARB.21,22 Therefore, ARBs should be used cautiously in patients with a history of ACEI-induced angioedema and should be avoided in those with a history of life-threatening angioedema from an ACEI.9,15 ARNI use is contraindicated in patients with a history of angioedema, regardless of severity, to either an ACEI or ARB.10
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
Angioedema is non-pitting edema that affects deeper tissue layers and is associated with approximately 40% of urticaria cases. The edema occurs in the deep dermis and subcutaneous tissues. Areas of angioedema may be of normal skin coloration or erythematous. Angioedema is not typically accompanied with pruritus, but can be associated with sensations of pressure, aching or burning. The distribution of angioedema may vary, although it often affects the lips, face or hands. Angioedema can also occur in areas of pressure, such as under clothing waistbands or straps. Angioedema is sometimes asymmetrical, such as swelling of only one half of an upper lip. When angioedema affects the upper airway, difficulty speaking, shortness of breath and even death from asphyxia may occur.
Clinical Manifestations and Histological Characteristics
Published in Kirsti Kauppinen, Kristiina Alanko, Matti Hannuksela, Howard Maibach, Skin Reactions to Drugs, 2020
Kirsti Kauppinen, Arja-Leena Kariniemi
Angioedema is a deep inflammatory skin lesion. It is characterized by localized swelling which may develop on a few skin sites only. Edema is usually asymmetrical. Predilection areas for angioedema are the lips, eyelids, external genitals, and external parts of the extremities. Laryngeal and lingual edemas are the most serious types of the edema reaction and without first aid they can result in suffocation.
Angiotensin-converting enzyme inhibitor induced angioedema: not always a class effect? A case report and short narrative review
Published in Current Medical Research and Opinion, 2021
Guillaume Becker, Fabien Rougerie, Amelia-Naomi Sabo, Marie-Caroline Dalmas, Estelle Ayme-Dietrich, Laurent Monassier
Many pathophysiological mechanisms for the onset of angioedema have been proposed. Understanding these mechanisms is crucial, as it provides a classification and leads to effective diagnosis and therapeutic approaches. Angioedema is usually classified according to the mediator involved and the presence of skin symptoms. Because of increased vascular permeability, various vasoactive mediators such as histamine or bradykinin have been suggested1. These mediators can be released by basophils or mast cells, generated during the activation of the kinin–kallikrein system, or produced by still unknown mechanisms. Whatever the mechanism, it results in plasma extravasation to the surrounding tissues. Three main categories of angioedema can be identified: (i) angioedema with urticaria (histamine- or immune-mediated); (ii) angioedema mediated by bradykinin without urticaria; and (iii) so-called idiopathic angioedema2. Consequently, angioedema caused by the activation of the immune system and the release of vasoactive mediators by mast cells responds to treatments based on antihistamines, glucocorticoids and epinephrine.
The importance of recognizing and managing a rare form of angioedema: hereditary angioedema due to C1-inhibitor deficiency
Published in Postgraduate Medicine, 2021
International and US guidelines recommend that all patients suspected of having HAE should undergo prompt laboratory evaluation to support diagnosis [1,17,61]. Laboratory evaluation for patients suspected of having HAE include blood levels of complement C4, C1-INH protein, and C1-INH function; these tests should be repeated to confirm diagnosis of HAE 1 or 2 if any of these levels are abnormally low [1]. Table 1 outlines laboratory findings typical of the various types of angioedema. C1q levels are typically normal in most types of bradykinin-mediated angioedema; however, low levels can be indicative of AAE, especially in the patient presenting with symptoms after the age of 40 or those with lymphoproliferative or autoimmune disease [61]. Laboratory analysis of complement levels C1q and C4 can be affected by handling of samples, giving spuriously low levels. C1-inhibitor function can be assayed by a commonly available enzyme-linked immunosorbent assay (ELISA) or by a chromogenic method. The ELISA may tend to overestimate function giving a “gray zone” result, a problem not present with the chromogenic assay. The chromogenic assay is unfortunately not as readily available as the ELISA [65]. Laboratory values may also be altered by recent use of C1-INH or 17-alpha alkylated androgenic steroids. Genetic testing for SERPING1 mutations is not essential for the diagnosis of HAE-C1-INH types 1 and 2 [66].
Safety and tolerability of sacubitril-valsartan: a systematic review and meta-analysis
Published in Expert Opinion on Drug Safety, 2021
Gonçalo Martins e Pereira, Gonçalo S. Duarte, Vasyl Katerenchuk, João Costa, Cláudio David, Joaquim J. Ferreira, Fausto J. Pinto, Daniel Caldeira
Regarding angioedema, there was an increased risk with sacubitril-valsartan when compared with ARB. This higher risk can be explained by the association of the sacubitril component, given the fact that both drugs act via its ARB part on bradykinin metabolism, the causal metabolite in angioedema’s pathogenesis [33]. However, this subgroup difference was not statistically significant. We should highlight that almost all the angioedema events were mild episodes, without airway compromise [2,10]. However, this may be a consequence of selection bias given the fact that patients with a history of angioedema or angioedema during the active run-in were excluded. The administration of sacubitril-valsartan for extended periods increased the risk of angioedema compared to active controls. This might be explained by the prolonged exposition to the drug, being suggested by comparing the event rate of sacubitril-valsartan for shorter and longer follow-ups (0.12% vs. 0.49%), while the event rate with active controls was similar between follow-ups (0.28 vs. 0.20). Thus, angioedema is an adverse event that can be potentially serious, so it should be closely monitored and identified.