Angioedema

Abstract

Angioedema can be caused by either mast cell degranulation or activation of the kallikrein-kinin cascade. In the former case, angioedema can be caused by allergic reactions caused by immunoglobulin E (IgE)-mediated hypersensitivity to foods or drugs that can also result in acute urticaria or a more generalized anaphylactic reaction. Nonsteroidal anti-inflammatory drugs (cyclooxygenase 1 inhibitors, in particular) may cause angioedema with or without urticaria, and leukotrienes may have a particular role as a mediator of the swelling. Reactions to contrast agents resemble allergy with basophil and mast cell degranulation in the absence of specific IgE antibody and can be generalized, that is, anaphylactoid. Angioedema accompanies chronic urticaria in 40% of patients, and approximately half have an autoimmune mechanism in which there is IgG antibody directed to the subunit of the IgE receptor (40%) or to IgE itself (5%-10%). Bradykinin is the mediator of angioedema in hereditary angioedema types I and II (C1 inhibitor [INH] deficiency) and the newly described type III disorder some of which are caused by a mutation involving factor XII. Acquired C1 INH deficiency presents in a similar fashion to the hereditary disorder and is due either to C1 INH depletion by circulating immune complexes or to an IgG antibody directed to C1 INH. Although each of these causes excessive bradykinin formation because of activation of the plasma bradykinin-forming pathway, the angioedema due to angiotensin-converting enzyme inhibitors is caused by excessive bradykinin levels due to inhibition of bradykinin degradation. Idiopathic angioedema (ie, pathogenesis unknown) may be histaminergic, that is, caused by mast cell degranulation with histamine release, or nonhistaminergic. The mediator pathways in the latter case are yet to be defined. A minority may be associated with the same autoantibodies associated with chronic urticaria. Angioedema that is likely to be life threatening (laryngeal edema or tongue/pharyngeal edema that obstructs the airway) is seen in anaphylactic/anaphylactoid reactions and the disorders mediated by bradykinin.

Adverse drug reactions to ibuprofen: a case report

“…1,7,12 This patient developed allergic bronchial asthma & angioedema after taking one tablet of ibuprofen. He presented with swelling over lip, orbital area, throat and severe breathing difficulty.…”

“…Cysteinyl leukotrienes are 3-4 times potent than histamine in causing contraction of airway smooth muscles, increased secretion of bronchial mucus and increased vascular permeability leading to bronchoconstriction and angioedema. [5][6][7]15 Involvement of respiratory system may be life threatening, hence immediate detection of severity of ADR and its management is essential.…”

Angioedema 2 months after Administration of Rivaroxaban (Xarelto)

“…Neither Endotracheal intubateion, trachestomy nor epinephrine were required. As part of the management of angioedema all her previous medications were stopped including rivaroxaban which was replaced with Tinzaparin for a short period and the patient was observed for resolution of the angioedema [1,2]. Few days after the treatment of angioedema the symptoms resolved completely with the swelling in the lower lip and tongue disappearing.…”

“…Pulmonary embolism is a common disease, with an estimated annual incidence of 70 cases per 100,000 population [1][2][3]. The condition usually leads to hospitalisation and may be fatal.…”

Risperidone induced angioedema with concurrent EPS symptoms: a case report and review of literature

“…Swelling of the tongue, larynx, and pharynx can potentially be life threatening by compromising the airway. Lip and periorbital swelling are the most common sites for angioedema to occur [5]. Though a wide range of medications have been found to cause angioedema, the angiotensin-converting enzyme inhibitors are the most frequently reported.…”