icatibant and Laryngeal-Edema

ACE-inhibitor induced angioedema is a non-allergic drug-related side effect. Inhibited bradykinin degradation leads to an unphysiological enhanced bradykinin plasma level with vascular leakage and, consequently, to angioedema. ACE-inhibitor induced angioedema develop rapidly in the head and neck region. Typical sites of manifestation are lips, tongue, and larynx. Novel pharmacotherapies may allow a causal treatment of the ACE-inhibitor induced angioedema in the future.

Topics: Adrenal Cortex Hormones; Algorithms; Angioedema; Angioedemas, Hereditary; Angiotensin-Converting Enzyme Inhibitors; Bradykinin; Bradykinin Receptor Antagonists; Forecasting; Histamine Antagonists; Humans; Laryngeal Edema; Laryngoscopy; Magnetic Resonance Imaging; Time Factors; Tomography, X-Ray Computed

Hereditary angioedema due to C1-inhibitor deficiency (HAE-C1INH) is a rare genetic disease that runs in the family. As a result of the disease, acute swellings of the subcutaneous tissue and mucous membranes of the digestive and respiratory systems, including the larynx, occur. Any attack of the disease involving the throat and larynx is particularly dangerous and requires knowledge of clinical determinants of the disease and its proper management.. The study included adult consecutive HAE-C1INH patients having follow-up visits in our centre. The group was examined with a structured clinical questionnaire, concerning the last 6 months and focusing particularly on laryngeal swelling attacks.. 55 subjects (F/M - 35/20, age range - 18-76) were included in the study. Laryngeal attacks occurred in 19 individuals (34.5%): 1-3, 4-6, and ≥7 attacks in 9, 8 and 2 patients, respectively, two of whom required intubation. In comparison to other patients, subjects with laryngeal attacks were characterised by significantly more frequent: (1) facial attacks, (2) severe disease activity, (3) the occurrence of female patients, (4) mental stress as a trigger of attacks. All patients with laryngeal attacks had a rescue medication at home and 15/19 (78%) patients could use it at home. Most of them used plasma-derived C1-inhibitor 17/19 (89.5%) and icatibant, 8/19 (42.1%).. HAE-C1INH patients with laryngeal attacks require particular attention. Proper training regarding the identification of these patients, adequate management, access to emergency services and emergency drugs are essential to ensure the safety of subjects with this localization of HAE-C1INH attacks.

Topics: Adolescent; Adult; Aged; Angioedemas, Hereditary; Bradykinin; Female; Humans; Laryngeal Edema; Male; Middle Aged; Surveys and Questionnaires; Vasodilator Agents; Young Adult

Angioedema is a localized, sudden, transient, and often recurrent swelling of the deeper layers of the skin or mucosa with no epidermal component. It is caused by vasoactive substances that produce a transient increase in endothelial permeability. Angioedema involving the laryngeal components is a life-threatening situation for the patient,and it is a challenge for the emergency medicine physician to rapidly achieve a safety airway. Most cases of laryngeal angioedema are induced by histamine release; but 10% are bradykinin induced, which does not respond to the conventional algorithm of treating allergic induced angioedema. We present a case report of an angiotensin converting enzyme (ACE) inhibitor–induced laryngeal angioedema alleviated only after treatment with the new bradykinin receptor inhibitor medication icatibant which was licensed only for use in hereditary angioedema. We reviewed the literature for the use of icatibant in acquired drug-induced angioedema; and because of the similar pathogenesis between the hereditary angioedema and the ACE inhibitor–induced angioedema,we propose an algorithm for careful use of icatibantin life-threatening angioedema in the emergency department.

Topics: Aged; Angioedema; Angiotensin-Converting Enzyme Inhibitors; Bradykinin; Bradykinin B2 Receptor Antagonists; Female; Humans; Laryngeal Edema

Hereditary angio-oedema (HAE) is a rare genetic disease caused by deficiency of complement C1 inhibitor. It is characterised by recurrent episodes of subcutaneous or submucosal oedema typically involving the extremities, bowel, face or larynx. Within the latest years it has become evident that the active mediator of HAE attacks is an increased level of bradykinin and various new treatment modalities have been developed. The aim of this paper is to give an update from the Danish HAE Comprehensive Care Centre on current treatment possibilities and address some of the challenges when diagnosing HAE.

Topics: Adult; Angioedemas, Hereditary; Bradykinin; Bradykinin B2 Receptor Antagonists; Complement C1 Inactivator Proteins; Complement C1 Inhibitor Protein; Complement Inactivating Agents; Diagnosis, Differential; Erythema; Female; Humans; Kallikreins; Laryngeal Edema; Peptides; Receptor, Bradykinin B2; Recombinant Proteins