There do not appear to be consistent genetic markers to reliably predict features of or the presence hypersensitivity reactions. Recent evidence continues to alleviate early concerns cross-reactivity between sulfonamide antibiotics and non-antibiotics. Sulfonamide drug allergy is frequently encountered by the practicing clinician. For sulfonamide antibiotics, delayed rash is the most common clinical manifestation. There is no current evidence to support avoidance of all non-antibiotic sulfonamides in those with a reported allergy to sulfonamide antibiotics, although certain scenarios require caution. Available evidence supports the cautious reintroduction of sulfonamide antibiotics via desensitization, which is usually well tolerated and should be considered in those with strong indications for trimethoprim-sulfamethoxazole and a reported sulfonamide allergy.
Background: For patients with peanut allergy, there are currently no methods to predict who will develop sustained unresponsiveness (SU) after oral immunotherapy (OIT).Objective: Assess IgE binding to peanut (PN), Ara h 2, and specific linear epitopes of Ara h 2 as predictors of the important clinical parameters: eliciting dose threshold and attainment of SU following OIT. Methods: Samples and clinical data were collected from children undergoing OIT. PN-and Ara h 2-sIgE were quantified by ImmunoCAP ® . IgE binding to linear peptides of Ara h 2 and Ara h 6 was measured with peptide microarrays.Results: Values of PN-sIgE correlated with eliciting dose (P = .001) and with a higher likelihood of achieving SU (P < .0001), but these relationships were lost at higher values for PN-sIgE (≥14 kIU for eliciting dose and ≥35 kIU/L for SU). In subjects with PN-sIgE ≥ 14 kIU/L, binding of IgE to epitopes 5 and 6 of Ara h 2 was associated with a lower eliciting dose at baseline challenge (P < .001; P c < .02). In subjects with PN-sIgE ≥ 35 kIU/L, a combined model of IgE binding to epitopes 1, 5, and 6 with PN-sIgE was highly predictive of attainment of SU (AUC of 0.86; P = .0067).
Conclusion:In young patients with peanut allergy, measurement of PN-sIgE and IgE binding to specific linear epitopes of Ara h 2 in baseline samples may allow stratification of patients regarding sensitivity to challenge and outcome of OIT.
K E Y W O R D Sallergens, food allergy, IgE, immunotherapy, oral immunotherapy, peanut allergy, tolerance induction
RATIONALE: The interaction between chronic inflammation and neural dysfunction points to an involvement linking the nervous and the immune system in the airways. In particular, environmental exposure to nanoparticles has been associated with an enhanced risk of asthma. But the impact of nanoparticles on neurogenic mechanism remains to be determined. The aim of this study was to identify the impact of nanoparticles on neuro inflammation in a mouse model of allergic asthma. METHODS: Using mice sensitized with ovalbumin (OVA) and OVA challenged (OVA sensitized/challenged mice) as well as mice treated with saline and challenged with air, and mice exposed to nanoparticles 200 ug/m 3 on days 21-23. The effect of nanoparticles on P2X3, TRPV1, and neuropeptides was estimated using ELISA, immunoblotting, and immunohistochemical stain. RESULTS: Nanoparticles exposure more increased in airway inflammation, and airway obstruction in OVA mice, and those were augumented in nanoparticles exposed mice. TRPV1 protein increased and P2X3 protein decreased in OVA and nanoparticles exposed mice. Substance P, ATP, and CGRP increased in BAL fluid of OVA and nanoparticles exposed mice. CONCLUSIONS: These results indicate that nanoparticles might be involved in the pathogenesis of bronchial asthma through neurogenic mechanism.
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