Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/76963
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dc.contributor.authorCulebras, C.en_US
dc.contributor.authorIrurita, Maria M.en_US
dc.contributor.authorIrurita, J.en_US
dc.contributor.authorFuentes, J.en_US
dc.contributor.authorLópez, L.en_US
dc.contributor.authorDeniz, C.en_US
dc.contributor.authorMartínez Saavedra, M.en_US
dc.contributor.authorChirino Godoy, Ricardoen_US
dc.contributor.authorNieto, V.en_US
dc.date.accessioned2020-12-23T13:15:49Z-
dc.date.available2020-12-23T13:15:49Z-
dc.date.issued2004en_US
dc.identifier.issn1567-5688en_US
dc.identifier.otherWoS-
dc.identifier.urihttp://hdl.handle.net/10553/76963-
dc.description.abstractPatients with prematme coronary syndromes impose an enormous challenge to the long-term management of atherosclerosis. Though the inflammatory markers available are sensible, but lack specificity and are not permanent. We analysed the polymorphisms of two pleiotropic inflammatory media- tors, interleukin IL-8 (-251 A/T), and IL-6 (-174 G/C) promoters. PCR-SSP techniques rendered hyper, medium and hypoproductive phenotypes. We studied 393 patients (P), after a premature coronary syndrome were com- pared with 276 aged, healthy controls (C); both had similar AA-AT/TT and GG-GC/CC distributions. Results: Patients were 44 years old and controls 69; (p<0.000). With the exception of smoking (P81% vs. c52%; p<0.000), dyslipidemia (P63% vs. c37%; p<0.05), and family history of premature CHD (P37%vs. c14%; p<0.000) major risk factors were more prevalent among conU'ols. Patient study showed males were 4 years younger (F47 vs. M43; p<0.048). Gen- der diffelences included higher prevalence of diabetics (M74%vs. F25%; p<0.028), and smokers (M86%vs. F14%; p<0.000) among males. Multi- vessel disease related to dyslipidemia (86%; p<0.007), metabolic syndrome (35%; p<0.041) and hyperproductive IL-8 phenotype (75%; p<0.033) in males. Reculxence related to smoking (p<0.045), diabetes (p<0.05) and PCI (p<0.041). Hyperproductive IL-6 col~elated with metabolic syndrome (p<0.001) and IL-8 with multivessel disease (p<0.011). Hyperproductive IL-8 phenotype (p<0.010) explained 73.4% of recua~ence in a logistic regression model built with risk factors, gender, clinical features and both phenotypes. Conclusions: Despite an unusual model with a considerable age gap between patients and controls, patients had a higher prevalence of some major risk factors. Hyperproductive interleukin-8 phenotype is a suitable and permanent marker of rectuxence that may conU'ibute to characterise individual variability.en_US
dc.languageengen_US
dc.relation.ispartofAtherosclerosis Supplementsen_US
dc.sourceAtherosclerosis Supplements [ISSN 1567-5688], v. 5 (1) sup. S, p. 4, 2004en_US
dc.subject32 Ciencias médicasen_US
dc.subject.otherAtherosclerosisen_US
dc.subject.otherCoronary arteriosclerosisen_US
dc.subject.otherPhenotypeen_US
dc.titleW01.15. Interleukin inflammatory phenotypes in premature coronary atherosclerosisen_US
dc.typeinfo:eu-repo/semantics/conferenceObjecten_US
dc.typeConferenceObjecten_US
dc.relation.conference74th Congress of the European-Atherosclerosis-Societyen_US
dc.identifier.doi10.1016/S1567-5688(04)90015-9en_US
dc.identifier.isi000221639000016-
dc.description.lastpage4en_US
dc.identifier.issue1-
dc.description.firstpage4en_US
dc.relation.volume5en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Actas de congresosen_US
dc.contributor.daisngid1456553-
dc.contributor.daisngid1534651-
dc.contributor.daisngid1533088-
dc.contributor.daisngid1942381-
dc.contributor.daisngid28238373-
dc.contributor.daisngid10570973-
dc.contributor.daisngid6278241-
dc.contributor.daisngid880609-
dc.contributor.daisngid25611320-
dc.description.numberofpages1en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Culebras, C-
dc.contributor.wosstandardWOS:Irurita, M-
dc.contributor.wosstandardWOS:Irurita, J-
dc.contributor.wosstandardWOS:Fuentes, J-
dc.contributor.wosstandardWOS:Lopez, L-
dc.contributor.wosstandardWOS:Deniz, C-
dc.contributor.wosstandardWOS:Saavedra, MM-
dc.contributor.wosstandardWOS:Chirino, R-
dc.contributor.wosstandardWOS:Nieto, V-
dc.date.coverdateAbril 2004en_US
dc.identifier.supplementS-
dc.identifier.conferenceidevents120406-
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.jcr4,14
dc.description.jcrqQ1
dc.description.scieSCIE
item.grantfulltextopen-
item.fulltextCon texto completo-
crisitem.author.deptGIR IUIBS: Diabetes y endocrinología aplicada-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología-
crisitem.author.orcid0000-0002-5681-8931-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameChirino Godoy, Ricardo-
crisitem.event.eventsstartdate17-04-2004-
crisitem.event.eventsenddate17-04-2004-
Colección:Actas de congresos
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