Eicosanoid mediator profiles in different phenotypes of nonsteroidal anti‐inflammatory drug‐induced urticaria

Abstract

Background

The role of arachidonic acid metabolites in NSAIDs‐induced hypersensitivity has been studied in depth for NSAIDs‐exacerbated respiratory disease (NERD) and NSAIDs‐exacerbated cutaneous disease (NECD). However, no information is available for NSAIDs‐induced urticarial/angioedema (NIUA), despite it being the most frequent clinical entity induced by NSAIDs‐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 NSAIDs‐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 towards 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.

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