Please use this identifier to cite or link to this item:
http://hdl.handle.net/10553/76963
DC Field | Value | Language |
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dc.contributor.author | Culebras, C. | en_US |
dc.contributor.author | Irurita, Maria M. | en_US |
dc.contributor.author | Irurita, J. | en_US |
dc.contributor.author | Fuentes, J. | en_US |
dc.contributor.author | López, L. | en_US |
dc.contributor.author | Deniz, C. | en_US |
dc.contributor.author | Martínez Saavedra, M. | en_US |
dc.contributor.author | Chirino Godoy, Ricardo | en_US |
dc.contributor.author | Nieto, V. | en_US |
dc.date.accessioned | 2020-12-23T13:15:49Z | - |
dc.date.available | 2020-12-23T13:15:49Z | - |
dc.date.issued | 2004 | en_US |
dc.identifier.issn | 1567-5688 | en_US |
dc.identifier.other | WoS | - |
dc.identifier.uri | http://hdl.handle.net/10553/76963 | - |
dc.description.abstract | Patients 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.language | eng | en_US |
dc.relation.ispartof | Atherosclerosis Supplements | en_US |
dc.source | Atherosclerosis Supplements [ISSN 1567-5688], v. 5 (1) sup. S, p. 4, 2004 | en_US |
dc.subject | 32 Ciencias médicas | en_US |
dc.subject.other | Atherosclerosis | en_US |
dc.subject.other | Coronary arteriosclerosis | en_US |
dc.subject.other | Phenotype | en_US |
dc.title | W01.15. Interleukin inflammatory phenotypes in premature coronary atherosclerosis | en_US |
dc.type | info:eu-repo/semantics/conferenceObject | en_US |
dc.type | ConferenceObject | en_US |
dc.relation.conference | 74th Congress of the European-Atherosclerosis-Society | en_US |
dc.identifier.doi | 10.1016/S1567-5688(04)90015-9 | en_US |
dc.identifier.isi | 000221639000016 | - |
dc.description.lastpage | 4 | en_US |
dc.identifier.issue | 1 | - |
dc.description.firstpage | 4 | en_US |
dc.relation.volume | 5 | en_US |
dc.investigacion | Ciencias de la Salud | en_US |
dc.type2 | Actas de congresos | en_US |
dc.contributor.daisngid | 1456553 | - |
dc.contributor.daisngid | 1534651 | - |
dc.contributor.daisngid | 1533088 | - |
dc.contributor.daisngid | 1942381 | - |
dc.contributor.daisngid | 28238373 | - |
dc.contributor.daisngid | 10570973 | - |
dc.contributor.daisngid | 6278241 | - |
dc.contributor.daisngid | 880609 | - |
dc.contributor.daisngid | 25611320 | - |
dc.description.numberofpages | 1 | en_US |
dc.utils.revision | Sí | en_US |
dc.contributor.wosstandard | WOS:Culebras, C | - |
dc.contributor.wosstandard | WOS:Irurita, M | - |
dc.contributor.wosstandard | WOS:Irurita, J | - |
dc.contributor.wosstandard | WOS:Fuentes, J | - |
dc.contributor.wosstandard | WOS:Lopez, L | - |
dc.contributor.wosstandard | WOS:Deniz, C | - |
dc.contributor.wosstandard | WOS:Saavedra, MM | - |
dc.contributor.wosstandard | WOS:Chirino, R | - |
dc.contributor.wosstandard | WOS:Nieto, V | - |
dc.date.coverdate | Abril 2004 | en_US |
dc.identifier.supplement | S | - |
dc.identifier.conferenceid | events120406 | - |
dc.identifier.ulpgc | Sí | en_US |
dc.contributor.buulpgc | BU-MED | en_US |
dc.description.jcr | 4,14 | |
dc.description.jcrq | Q1 | |
dc.description.scie | SCIE | |
item.grantfulltext | open | - |
item.fulltext | Con texto completo | - |
crisitem.author.dept | GIR IUIBS: Diabetes y endocrinología aplicada | - |
crisitem.author.dept | IU de Investigaciones Biomédicas y Sanitarias | - |
crisitem.author.dept | Departamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología | - |
crisitem.author.orcid | 0000-0002-5681-8931 | - |
crisitem.author.parentorg | IU de Investigaciones Biomédicas y Sanitarias | - |
crisitem.author.fullName | Chirino Godoy, Ricardo | - |
crisitem.event.eventsstartdate | 17-04-2004 | - |
crisitem.event.eventsenddate | 17-04-2004 | - |
Appears in Collections: | Actas de congresos |
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