Inmaculada Doña1,2, Raquel Jurado-Escobar3, James R Perkins3, Pedro Ayuso3, María Carmen Plaza-Serón3, Natalia Pérez-Sánchez1, Paloma Campo1,2, Gador Bogas-Herrera1, Joan Bartra4,5,6, María José Torres1,2, Marek Sanak7, José Antonio Cornejo-García2,3. 1. Allergy Unit, IBIMA, Regional University Hospital of Malaga, UMA, Malaga, Spain. 2. ARADyAL Network RD16/0006/0001, Carlos III Health Institute, Madrid, Spain. 3. Research Laboratory, IBIMA, Regional University Hospital of Malaga, UMA, Malaga, Spain. 4. ARADyAL Network RD16/0006/0007, Carlos III Health Institute, Madrid, Spain. 5. Unitat d'Allergia, Servei de Pneumologia, Hospital Clinic, Universitat de Barcelona, Barcelona, Spain. 6. Institut d'Investigacions Biomediques August Pi I Sunyer (IDIBAPS), Barcelona, Spain. 7. Department of Medicine, Jagiellonian University Medical College, Krakow, Poland.
Abstract
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.
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 NIUApatients, 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.
Authors: Milena Sokolowska; G Enrico Rovati; Zuzana Diamant; Eva Untersmayr; Jürgen Schwarze; Zuzanna Lukasik; Florentina Sava; Alba Angelina; Oscar Palomares; Cezmi A Akdis; Liam O'Mahony; Milos Jesenak; Oliver Pfaar; María José Torres; Marek Sanak; Sven-Erik Dahlén; Grzegorz Woszczek Journal: Allergy Date: 2022-02-25 Impact factor: 14.710