Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/48609
Campo DC Valoridioma
dc.contributor.authorSuárez-Lorenzo, I.en_US
dc.contributor.authorRodríguez-de Castro, Felipeen_US
dc.contributor.authorCruz-Niesvaara, D.en_US
dc.contributor.authorHerrera-Ramos, E.en_US
dc.contributor.authorRodríguez-Gallego, C.en_US
dc.contributor.authorCarrillo-Díaz, T.en_US
dc.date.accessioned2018-11-23T23:20:59Z-
dc.date.available2018-11-23T23:20:59Z-
dc.date.issued2018en_US
dc.identifier.issn2045-7022en_US
dc.identifier.otherWoS-
dc.identifier.urihttp://hdl.handle.net/10553/48609-
dc.description.abstractBackground and objective: Severe alpha1 antitrypsin deficiency has been clearly associated with pulmonary emphysema, but its relationship with bronchial asthma remains controversial. Some deficient alpha 1 antitrypsin (AAT) genotypes seem to be associated with asthma development. The objective of this study was to analyze the distribution of AAT genotypes in asthmatic patients allergic to house dust mites (HDM), and to asses a possible association between these genotypes and severe asthma.MethodsA cross-sectional cohort study of 648 patients with HDM allergic asthma was carried out. Demographic, clinical and analytical variables were collected. PI*S and PI*Z AAT deficient alleles of the SERPINA1 gene were assayed by real-time PCR.ResultsAsthma was intermittent in 253 patients and persistent in 395 patients (246 mild, 101 moderate and 48 severe). One hundred and forty-five asthmatic patients (22.4%) with at least one mutated allele (S or Z) were identified. No association between the different genotypes and asthma severity was found. No significant differences in all clinical and functional tests, as well as nasal eosinophils, IgA and IgE serum levels were observed. Peripheral eosinophils were significantly lower in patients with the PI*MS genotype (p=0.0228). Neither association between deficient AAT genotypes or serum ATT deficiency (AATD) and development of severe asthma, or correlation between ATT levels and FEV1 was observed.ConclusionIn conclusion, the distribution of AAT genotypes in HDM allergic asthmatic patients did not differ from those found in Spanish population. Neither severe ATTD or deficient AAT genotypes appear to confer different clinical expression of asthma.en_US
dc.languageengen_US
dc.relationNeuroprotección por bloqueo de la capacidad de transactivadora Nf-Kb y factores relacionados.en_US
dc.relation.ispartofClinical and Translational Allergyen_US
dc.sourceClinical and Translational Allergy [ISSN 2045-7022], v. 8, 44 (Noviembre 2018)en_US
dc.subject32 Ciencias médicasen_US
dc.subject320508 Enfermedades pulmonaresen_US
dc.subject320701 Alergiasen_US
dc.subject.otherAlpha 1 antitrypsinen_US
dc.subject.otherAlpha 1 antitrypsin deficiencyen_US
dc.subject.otherHouse dust mitesen_US
dc.subject.otherAsthmaen_US
dc.subject.otherAllergyen_US
dc.titleAlpha 1 antitrypsin distribution in an allergic asthmatic population sensitized to house dust mitesen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1186/s13601-018-0231-xen_US
dc.identifier.scopus85056254819-
dc.identifier.isi000449086700001-
dc.contributor.authorscopusid56529544100-
dc.contributor.authorscopusid26425794500-
dc.contributor.authorscopusid55520041500-
dc.contributor.authorscopusid36952964800-
dc.contributor.authorscopusid6602114379-
dc.contributor.authorscopusid6602765567-
dc.identifier.eissn2045-7022-
dc.identifier.issue44-
dc.relation.volume8en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid6523839-
dc.contributor.daisngid464249-
dc.contributor.daisngid12081666-
dc.contributor.daisngid2130906-
dc.contributor.daisngid603384-
dc.contributor.daisngid8257500-
dc.description.numberofpages8en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Suarez-Lorenzo, I-
dc.contributor.wosstandardWOS:de Castro, FR-
dc.contributor.wosstandardWOS:Cruz-Niesvaara, D-
dc.contributor.wosstandardWOS:Herrera-Ramos, E-
dc.contributor.wosstandardWOS:Rodriguez-Gallego, C-
dc.contributor.wosstandardWOS:Carrillo-Diaz, T-
dc.date.coverdateNoviembre 2018en_US
dc.identifier.ulpgcNoen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr1,369
dc.description.jcr4,232
dc.description.sjrqQ1
dc.description.jcrqQ2
dc.description.scieSCIE
item.grantfulltextopen-
item.fulltextCon texto completo-
crisitem.project.principalinvestigatorCastro López-Tarruella, Enrique-
crisitem.author.deptGIR IUIBS: Patología y Tecnología médica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.deptGIR IUIBS: Patología y Tecnología médica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Médicas y Quirúrgicas-
crisitem.author.orcid0000-0002-6812-2739-
crisitem.author.orcid0000-0002-4344-8644-
crisitem.author.orcid0000-0002-3047-8908-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameRodríguez De Castro, Felipe Carlos B.-
crisitem.author.fullNameRodríguez Gallego, José Carlos-
crisitem.author.fullNameCarrillo Díaz, Teresa-
Colección:Artículos
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