Analysis of daily aspirin intake on platelet-associated factors and aggregation in nonsteroidal anti-inflammatory drug exacerbated respiratory disease: A cross-sectional study.

Abstract

Background: Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by chronic rhinosinusitis with nasal polyposis (CRSwNP), adult-onset asthma and hypersensitivity to NSAIDs. Long-term aspirin treatment after desensitization (ATAD) is used for clinical improvement in N-ERD patients. However, information on the potential effect of ATAD on the platelet-neutrophil aggregates (PNA) level in N-ERD patients is highly limited.

Objective: This study aimed to explore the impact of PNA on the pathogenesis of N-ERD and the potential effect of ATAD on N-ERD patient profiles from a platelet point-of-view.

Methods: Sixty-one individuals were enrolled, including 16 N-ERD patients with ATAD (ATAD+), 15 N-ERD patients without ATAD (ATAD-), 15 aspirin-tolerant asthma (ATA) patients, and 15 healthy controls (HCs). Lipid mediators classical in N-ERD, including urinary-LTE4 (uLTE4), prostaglandin-D2 (PGD2), and prostaglandin-E2 (PGE2) were assessed by ELISA. Platelet activation was estimated based on expression levels of sP-selectin, CD40L, Platelet Factor-4 (PF4), RANTES, Thromboxane-A2 (TXA2), PAF, 12-HETE in plasma levels by ELISA; and PNA percentage by flow cytometry.

Results: ATAD+; 12-HETE, and PF4 levels were remarkably low, while higher levels were determined in ATAD- and ATA groups. ATAD+; uLTE4 levels were positively correlated with 12-HETE. Another positive correlation was detected between sP-selectin and 12-HETE in ATAD-. Compared to HCs, it was found that among all N-ERD patients, significant increase in PNA.

Conclusions: Plasma levels of PGE2, PF4, and 12-HETE appear to be affected by aspirin treatment. We believe that 12-HETE could play a significant role in the N-ERD pathogenesis by contributing to platelet activation.