Background: Over 30% of local allergic rhinitis (LAR) patients self-report bronchial symptoms suggestive of asthma, but the relationship between the allergen exposure and the bronchial symptoms has not been studied.Objective: To investigate whether a bronchial counterpart of LAR exists.Methods: Patients were classified by clinical history, skin prick test/serum specific IgE (sIgE), and nasal allergen provocation test (NAPT) into the LAR, allergic rhinitis (AR), and nonallergic rhinitis (NAR) phenotypes. Twenty-eight LAR, 18 AR, and 19 NAR patients self-reporting bronchial symptoms suggestive of asthma and 8 healthy controls (HC) were subjected to a methacholine test (MT) before (Visit 1) and 24 hours after (Visit 3) a bronchial provocation test with Dermatophagoides pteronyssinus (BPT-DP) (Visit 2). Induced sputum and peripheral blood obtained after each MT were analyzed for immune cell populations, tryptase, ECP, and sIgE. Results:A positive MT was found in 50% of LAR, 83.3% of AR, 57.89% of NAR, and 0% of HC individuals (P = 0.022 AR vs LAR) at V1. BPT-DP was positive in 8 LAR and 15 AR patients (28% vs 83.3%, P < 0.001), with no positive responses in NAR and HC.All BPT-DP+ patients experienced a significant decrease of PC 20 at V3 vs V1 (P = 0.016 LAR, P ≤ 0.001 AR). BPT-DP+ patients also showed a significant increase of eosinophils, monocytes, and ECP in induced sputum at V3 compared with V1. Conclusion:The results suggest the existence of a new asthma phenotype (local allergic asthma) defined by absence of systemic atopy and positivity to BPT with allergen. K E Y W O R D Sallergic, asthma, IgE, local, rhinitis | 1503 CAMPO et Al.

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.Abbreviatons: ASA, acetyl salicylic acid; COX-1, cyclooxygenase 1; LTE4, leukotriene E4; NECD, NSAID-exacerbated cutaneous disease; NIUA, NSAID-induced urticaria/angioedema; NSAIDs, nonsteroidal anti-inflammatory drugs; PGE2, prostaglandin E2; 9a,11b-PGF2, 9α,11β-prostaglandin F2.Inmaculada Doña and Raquel Jurado-Escobar contributed equally to this work.

Allergic rhinitis is associated with elevated serum IgE levels. IgE response is mediated by the high-affinity IgE receptor (FcεRI), which is polymorphic. Studies analyzing the association between allergic rhinitis and FcεRI variants have been conducted with controversial results. The objective of this study is to analyze, in 1,041 individuals, the putative clinical association of allergic rhinitis with common polymorphisms in FcεRI subunits genes. These SNPs included FECR1A rs2494262, rs2427837 and rs2251746; FECR1B rs1441586, rs569108 and rs512555; FCER1G rs11587213, rs2070901 and rs11421. Statistically significant differences were observed for the FCER1B rs569108 and rs512555 polymorphisms frequencies when comparing patients with allergic rhinitis without asthma and controls. The OR (95% CI) value for the 237Gly allele (rs569108) is equal to 0.26 (0.08–0.86, P = 0.017) and for the G allele (rs512555) it is equal to 0.27 (0.08–0.88, P = 0.020). These two SNPs are linked (D’ = 1.0, LOD = 56.05). Also observed was a statistically significant trend towards lower IgE values among allergic rhinitis patients with variant alleles for both SNPs. In conclusion, in patients with allergic rhinitis without asthma, the FCER1B rs569108 and rs512555 polymorphisms are associated with increased risk of developing allergic rhinitis and with lower IgE levels.