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The skin clinical phenotypes of nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity (NH) are very heterogeneous with several syndromes after NSAID intake, which include different symptoms, different organ involvement and different associated concomitant diseases and possibly different underlying pathophysiology and mechanisms. Making a correct diagnosis in NH is an exciting journey for any allergist. Thus, to classify these diseases properly will be pivotal for appropriate diagnostic and management strategy. Treatment modalities are depending on the clinical phenotypes of NH and they will embrace for each patient: the avoidance of culprit NSAID, the finding of well-tolerated NSAID and in certain cases, desensitization procedures when the NSAID treatment was absolutely needed as well as the control of associated diseases such as spontaneous chronic urticarial or allergic respiratory diseases. This review updates the recent evidence of classification, diagnostic strategies, and management of skin NSAID hypersensitivity reactions.

This article contains information related to the research article entitled "Biomarkers associated with disease severity in allergic and nonallergic asthma" (S. Baos, D. Calzada, L. Cremades, J. Sastre, J. Quiralte, F. Florido, C. Lahoz, B. Cárdaba, In press). Specifically, the clinical criteria stablished for selecting the study population (n=104 subjects) are described. Moreover, this article describes the criteria for selecting the 94 genes to be analyzed in PBMCs (peripheral blood mononuclear cells), it is provided a description of these genes and a Table with the genes most differentially expressed by clinical phenotypes and, finally it is detailed the experimental methodology followed for studying the protein expression of MSR1 (macrophage scavenger receptor 1), one of the genes evaluated in the research. This work was supported in part by research grants PI13/01730 co-supported by FEDER, CIBERES (ISCIII, 0013) and Biobank (PT13/0010/0012) from the Fund for Health Research (Spanish Ministry of Economy and Competitiveness). S. Baos was supported by CIBERES (ISCIII, 0013) and Conchita Rábago Foundation. D. Calzada by Conchita Rábago Foundation, Madrid, Spain. L. Cremades was supported by a contract from MINECO (PEJ-2014-A-31609, Sistema de Garantía Juvenil), cofinanced by European Social Fund (ESF) and Youth Employment Initiative (YEI). Yes

Background Eosinophilic esophagitis (EoE) is an antigen-driven disease mediated by an abnormal immune Th2 response. Objective The objective of this article is to investigate genes associated with regulating immune responses leading to disease susceptibility. Methods Twenty-seven tag single nucleotide polymorphisms (tSNPs) selected in five candidate genes ( TLR3, TLR4, FOXP3, FLG and TSLP) were genotyped in 218 EoE patients and 376 controls. Skin prick tests were carried out in EoE patients with a panel of 17 aeroallergens and 22 plant- and animal-derived foods. Results Five tSNPs located in the TSLP locus and one tSNP located in the TLR3 locus were significantly associated with EoE. The interactions between TLR3 and TSLP loci were analyzed. TLR3+/TSLP– and TLR3–/TSLP+ individuals showed a significantly reduced susceptibility to EoE compared to TLR3–/TSLP– individuals (OR = 0.66, p = 0.036 and OR = 0.23, p = 0.00014, respectively). Likewise, TLR3+/TSLP+ individuals showed the most decreased susceptibility of developing EoE (OR = 0.16, p = 0.0001). However, the interaction gain attributed to the combination of both genes was negative (IG = –4.52%), which indicated redundancy or independent effect. Additionally, TLR3 locus was found to be associated with aeroallergen and food sensitization in EoE patients (OR = 9.67, pc = 0.025 and OR = 0.53, pc = 0.048, respectively). Conclusion TLR3 constitutes a novel genetic susceptibility locus for developing EoE, and the effects would be independent of TSLP.