A 59-year-old woman developed sudden dyspnea after taking non-steroidal anti-inflammatory drugs (NSAIDs) for epigastralgia. She had a history of bronchial asthma after childbirth. Computed tomography showed bilateral peripheral bronchial wall thickening, lumen narrowing, obstruction, and circumferential lower esophageal mucosal edema. The patient was diagnosed with aspirin-exacerbated respiratory disease (AERD), a hypersensitivity reaction. Respiratory symptoms improved with intravenous dexamethasone. Endoscopy confirmed lower esophageal mucosal edema; mucosal biopsy detected eosinophilic infiltration, suggesting eosinophilic esophagitis (EoE). Although EoE is often diagnosed after AERD, the patient was simultaneously diagnosed with AERD and EoE after taking NSAIDs. Thus, EoE should be considered as a potential comorbidity when AERD develops after NSAID administration for abdominal symptoms.
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http://dx.doi.org/10.7759/cureus.74384 | DOI Listing |
Allergy
December 2024
2nd Department of Internal Medicine, Jagiellonian University Medical College, Kraków, Poland.
J Clin Med
December 2024
Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, 08907 Barcelona, Spain.
In patients with aspirin-exacerbated respiratory disease (AERD), there is disparate regulation of prostaglandin E2 (PGE) and prostaglandin D (PGD). Both prostanoids are synthesised by cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2). However, while the basal synthesis of PGE tends to decrease, that of PGD increases in patients with AERD.
View Article and Find Full Text PDFFront Allergy
November 2024
IAPA 's Clinic, Department of Otorhinolaryngology-Head and Neck Surgery, Instituto Nacional de Enfermedades Respiratorias, Ismael Cosío Villegas, Ciudad de México, México.
It has been estimated that Nonsteroidal Anti-inflammatory drug (NSAID) Exacerbated Respiratory Disease (N-ERD) previously named as Aspirin Exacerbated Respiratory Disease (A-ERD) affects around 1.4 million persons in the United States. Its prevalence in asthmatic patients has widely been underestimated, as a considerable number of patients would need an aspirin provocation test to confirm the diagnosis.
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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