Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10662/20196
Títulos: Eicosanoid mediator profiles in different phenotypes of nonsteroidal anti‐inflammatory drug‐induced urticaria
Autores/as: Doña, Inmaculada
Jurado Escobar, Raquel
Perkins, James R.
Ayuso Parejo, Pedro
Plaza Serón, María Carmen
Pérez Sánchez, Natalia
Campo Mozo, Paloma
Bogas Herrera, Gádor
Bartra, Joan
Torres Jaén, María José
Sanak, Marek
Cornejo García, José Antonio
Palabras clave: Hipersensibilidad a fármacos;Drug hypersensitivity;Eicosanoids;Antiinflamatorios no esteroideos;Non-steroidal antiinflammatory;Eicosanoides
Fecha de publicación: 2019
Editor/a: John Wiley and Sons Ltd.
Resumen: Background: The role of arachidonic acid metabolites in NSAID‐induced hypersensi- tivity has been studied in depth for NSAID‐exacerbated respiratory disease (NERD) and NSAID‐exacerbated cutaneous disease (NECD). However, no information is available for NSAID‐induced urticarial/angioedema (NIUA), despite it being the most frequent clinical entity induced by NSAID hypersensitivity. We evaluated changes in leukotriene and prostaglandin metabolites for NIUA patients, using patients with NECD and single‐NSAID‐induced urticaria/angioedema or anaphylaxis (SNIUAA) for comparison. Methods: Urine samples were taken from patients with confirmed NSAID‐induced urticaria and healthy controls, at baseline and at various time intervals after ASA administration. Eicosanoid measurement was performed using high‐performance liquid chromatography‐tandem mass spectrometry and gas chromatography‐mass spectrometry. Results: No differences were found between groups at baseline. Following ASA administration, LTE4 and 9α,11β‐PGF2 levels were increased in both NIUA and NECD patients compared to baseline, rising initially, before decreasing toward initial levels. In addition, the levels of these metabolites were higher in NIUA and NECD when compared with the SNIUAA and control groups after ASA administration. No changes were found with respect to baseline values for SNIUAA and control groups. Conclusions: We present for the first time data regarding the role of COX‐1 inhibi- tion in NIUA. Patients with this entity show a similar pattern eicosanoid levels fol- lowing ASA challenge to those with NECD. Further studies will help ascertain the cell populations involved and the underlying molecular mechanisms.
URI: http://hdl.handle.net/10662/20196
ISSN: 0105-4538
1398-9995
DOI: 10.1111/all.13725
Colección:DTMQU - Artículos

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