Lack of Major Involvement of Common Gene Polymorphisms in the Risk of Developing Cross-Hypersensitivity to NSAIDs.

Cross-hypersensitivity to non-steroidal anti-inflammatory drugs (NSAIDs) is a relatively common, non-allergic, adverse drug event triggered by two or more chemically unrelated NSAIDs. Current evidence point to COX-1 inhibition as one of the main factors in its etiopathogenesis. Evidence also suggests that the risk is dose-dependent.

Deep sequencing of prostaglandin-endoperoxide synthase (PTGE) genes reveals genetic susceptibility for cross-reactive hypersensitivity to NSAID.

Background And Purpose: Cross-reactive hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) is a relatively common adverse drug event caused by two or more chemically unrelated drugs and that is attributed to inhibition of the COX activity, particularly COX-1. Several studies investigated variations in the genes coding for COX enzymes as potential risk factors. However, these studies only interrogated a few single nucleotide variations (SNVs), leaving untested most of the gene sequence.

Outcomes and Laboratory and Clinical Findings of Asthma and Allergic Patients Admitted With Covid-19 in a Spanish University Hospital.

Individual susceptibility and clinical outcome of Covid-19 are variable and mortality is also very variable across countries, being particularly high in Spain. Comorbidities might increase the risk for less favourable outcomes, but it has been reported that patients with antecedents of asthma or allergic diseases were under-represented among hospitalized Covid-19 patients. Aiming to compare the clinical evolution of patients with antecedents of asthma or allergic diseases and patients without these antecedents, we analyzed a series of 113 consecutive patients with Covid-19 in a regional hospital in Spain.

Pharmacogenetic Factors Affecting Asthma Treatment Response. Potential Implications for Drug Therapy.

Asthma is a frequent disease, mainly characterized by airway inflammation, in which drug therapy is crucial in its management. The potential of pharmacogenomics testing in asthma therapy has been, to date, little explored. In this review, we discuss pharmacogenetic factors affecting asthma treatment, both related to drugs used as controller medications for regular maintenance, such as inhaled corticosteroids, anti-leukotriene agents, long-acting beta-agonists, and the new biologic agents used to treat severe persistent asthma.

Asthma and allergic rhinitis associate with the rs2229542 variant that induces a p.Lys90Glu mutation and compromises AKR1B1 protein levels.

Asthma and rhinitis are two of the main clinical manifestations of allergy, in which increased reactive oxygen or electrophilic species can play a pathogenic role. Aldose reductase (AKR1B1) is involved in aldehyde detoxification and redox balance. Recent evidence from animal models points to a role of AKR1B1 in asthma and rhinitis, but its involvement in human allergy has not been addressed.

FCERI and Histamine Metabolism Gene Variability in Selective Responders to NSAIDS.

The high-affinity IgE receptor (Fcε RI) is a heterotetramer of three subunits: Fcε RIα, Fcε RIβ, and Fcε RIγ (α2) encoded by three genes designated as (), and , respectively. Recent evidence points to FCERI gene variability as a relevant factor in the risk of developing allergic diseases. Because Fcε RI plays a key role in the events downstream of the triggering factors in immunological response, we hypothesized that FCERI gene variants might be related with the risk of, or with the clinical response to, selective (IgE mediated) non-steroidal anti-inflammatory (NSAID) hypersensitivity.

A Nonsynonymous FCER1B SNP is Associated with Risk of Developing Allergic Rhinitis and with IgE Levels.

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.

Genetic determinants of metamizole metabolism modify the risk of developing anaphylaxis.

Metamizole is a NSAID that has been banned in several countries because of its toxicity. It is often involved in selective hypersensitivity reactions and most hypersensitivity patients develop anaphylaxis. Metamizole is rapidly metabolized, and metabolic profiles are related to genetic factors.

Type IV reaction due to phenylephrine administered nasally with cross-reactivity with ethylephrine.

Type IV hypersensitivity eye reactions have been described after the administration of the sympathomimetic agent phenylephrine. We report the case of an atopic woman who developed nasal congestion and discharge, dysphagia, and dyspnea 1 hour after the administration of Stopcold pills and Disneumon Pernasal nasal spray for otitis. The same symptoms reappeared after the accidental administration of Rinobanedif ointment in the nasal mucosa.

Variability of the L-Histidine decarboxylase gene in allergic rhinitis.

Background: Nonsynonymous polymorphisms in genes coding for histamine-metabolizing enzymes, diamine oxidase and histamine N-methyltransferase are related to the risk of developing allergic diseases. The role of polymorphisms in the histidine decarboxylase gene remains unexplored. The objective of this study is to identify novel polymorphisms in the human histidine decarboxylase gene and to analyse the clinical association of nonsynonymous polymorphisms with rhinitis.

Polymorphisms of histamine-metabolizing enzymes and clinical manifestations of asthma and allergic rhinitis.

Background: Polymorphisms of enzymes involved in histamine biodisposition may affect clinical symptoms in diseases related to histamine, such as asthma or allergic rhinitis (AR).

Objective: This study aims to analyse two common polymorphisms in genes coding for histamine-metabolizing enzymes in patients with allergic diseases.

Methods: Five-hundred and sixty-five individuals participated in the study, including 270 unrelated patients with asthma and/or AR recruited from a single centre and 295 healthy volunteers.