Aspirin hypersensitivity continues to be a major clinical challenge in patients with coronary artery disease (CAD), particularly in those requiring percutaneous coronary intervention (PCI) in the absence of a validated alternative antiplatelet regimen. Although true aspirin allergies are uncommon, they can manifest with severe reactions such as angioedema or anaphylaxis, highlighting the critical role of diagnostic challenge tests and tolerance induction strategies. Here, a 61-year-old female with end-stage renal disease (ESRD) on hemodialysis presented with new-onset heart failure and elevated troponins in the setting of a hypertensive emergency. A subsequent left heart catheterization revealed severe multivessel disease, but PCI was deferred due to her history suggestive of aspirin-induced angioedema and the absence of a known optimal approach in this scenario. Given the feasibility of completing a desensitization protocol, aspirin desensitization was pursued, facilitating the successful placement of a drug-eluting stent. This case highlights the need for validated protocols to manage aspirin hypersensitivity, as the current treatment paradigm necessitates a highly individualized approach by the treating clinician.
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http://dx.doi.org/10.14740/jmc4239 | DOI Listing |
Cochrane Database Syst Rev
January 2025
Department of Otorhinolaryngology, Amsterdam University Medical Centre, Amsterdam, Netherlands.
Background: NSAID-exacerbated respiratory disease (N-ERD) is a hypersensitivity to non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen, accompanied by chronic rhinosinusitis (with or without nasal polyps) or asthma. The prevalence of hypersensitivity to NSAIDs is estimated to be 2%. The first line of treatment is the avoidance of NSAIDs.
View Article and Find Full Text PDFAllergy
December 2024
2nd Department of Internal Medicine, Jagiellonian University Medical College, Kraków, Poland.
Clin Transl Allergy
December 2024
2nd Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Background: Nonsteroidal anti-inflammatory drugs-exacerbated respiratory disease (NSAIDs-ERD) is characterized by altered arachidonic acid (AA) metabolism. Aspirin hypersensitivity is diagnosed using aspirin challenge, while induced sputum is collected to perform cell counts and to identify local biomarkers in induced sputum supernatant (ISS). This study aimed to assess the levels of a newly identified eicosanoid, 15-oxo-eicosatetraenoic acid (15-oxo-ETE), in ISS at baseline and during aspirin-induced bronchospasm in patients with NSAIDs-ERD.
View Article and Find Full Text PDFImmunol Invest
December 2024
Clinic of Otorhinolaryngology and Maxillofacial Surgery, University Clinical Center of Serbia, Belgrade, Serbia.
Background: In this review article, we aimed to discuss the pathogenesis of sensorineural hearing loss (SNHL) in patients with different forms of chronic rhinosinusitis (CRS), with special reference to the connection of the immune response of the nasal and middle ear mucosa and inner ear structures.
Methods: Articles for this review were identified using PubMed and Google© Scholar databases.
Results: Different phenotypes of CRS may be associated with impaired function of the inner and outer cells of the organ of Corti.
Curr Opin Allergy Clin Immunol
February 2025
Ellsworth and Mabel Simmons Professor of Allergy and Immunology, Section Chief, Allergy/Immunology James A. Haley VA Hospital, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Purpose Of Review: This review provides the current understanding on the mechanism, diagnosis, and treatment of aspirin exacerbated respiratory disease (AERD) with chronic rhinosinusitis (CRS).
Recent Findings: Updates focus on the current understanding of type 2 inflammation as a disease driver, alterations in gene expression in nasal polyps, and use of biologics in treating aspirin exacerbated respiratory disease. Recent findings include altered expression of GATA binding protein 3 (GATA3), interleukin (IL)-4, IL-5, and IL-17 in nasal polyps supports the current understanding that type 2 inflammation predominantly drives the pathophysiology of AERD with CRS.
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