Eicosanoid mediator profiles in different phenotypes of nonsteroidal anti-inflammatory drug-induced urticaria
| Autor: | Maria del Carmen Plaza-Serón, Raquel Jurado-Escobar, Pedro Ayuso, Joan Bartra, Jose A. Cornejo-Garcia, Natalia Pérez-Sánchez, Inmaculada Doña, Gador Bogas-Herrera, María José Torres, Marek Sanak, Paloma Campo, James R. Perkins |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Adult
Male 0301 basic medicine Adolescent Nerd Immunology Administration Oral Prostaglandin Pharmacology Dinoprost Drug Hypersensitivity Young Adult 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Humans Immunology and Allergy Cyclooxygenase Inhibitors Angioedema skin and connective tissue diseases Anaphylaxis Leukotriene E4 Leukotriene Aspirin business.industry Anti-Inflammatory Agents Non-Steroidal Middle Aged medicine.disease digestive system diseases Phenotype 030104 developmental biology 030228 respiratory system Eicosanoid chemistry Drug-induced urticaria Cyclooxygenase 1 Eicosanoids Female Arachidonic acid medicine.symptom business |
| Popis: | Background The role of arachidonic acid metabolites in NSAID-induced hypersensitivity 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 inhibition in NIUA. Patients with this entity show a similar pattern eicosanoid levels following ASA challenge to those with NECD. Further studies will help ascertain the cell populations involved and the underlying molecular mechanisms. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|