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In conjunction with BMJ Case Reports, DTB will feature occasional drug-related cases that are likely to be of interest to readers. These will include cases that involve recently marketed drugs for which there is limited knowledge of adverse effects and cases that highlight unusual reactions to drugs that have been marketed for several years.
Summary
Angioedema is potentially life-threating swelling of integument and mucosa that has multiple potential aetiologies with varying mechanisms. Drug-induced angioedema is often easily correlated with the offending agent and can be prevented with discontinuation of the medication. Many medications have now been implicated in drug-induced angioedema but the two most common are ACE inhibitors and non-steroidal anti-inflammatory drugs (NSAIDs). This case highlights severe angioedema secondary to celecoxib and reviews varying aetiologies of angioedema and NSAID hypersensitivity reactions.
Background
Angioedema is defined as localised swelling involving the subcutaneous, submucosal and/or deep dermal tissues that can involve any area of the body. It has the potential to be life threatening with upper airway mucosal involvement that can lead to airway obstruction.1 2 Many medications have been identified as causative agents of angioedema. The most often implicated pharmacological categories include ACE inhibitors (ACE-i) and non-steroidal anti-inflammatory drugs (NSAIDs).3 NSAIDs are one of the most widely available medications worldwide and are a mainstay of treatment for pain and inflammation. NSAIDs provide these benefits by inhibiting cyclooxygenase (COX) 1 and 2 and reducing proinflammatory cytokines, mediated by the conversion of arachidonic acid to prostaglandin H2. Selective COX-2 inhibitors were developed to reduce side effects and intolerance of COX-1 inhibition.4 Hypersensitivity reactions to NSAIDs, including angioedema, are known, but the pathophysiology is not well understood and very few cases describe hypersensitivity reactions with COX-2 inhibitor use. The prevalence of NSAID hypersensitivity, including angioedema and urticaria, in the general population is 0.1%–0.3%. …
Footnotes
Contributors All authors made substantial contributions to conception and design. VVJ collected patient data, performed literature review, and drafted the manuscript. JA and IA assisted with critical revisions. VVJ obtained patient consent. All authors gave final approval of the version to be published and agreed to be accountable for aspects of the work.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.