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dc.contributor.authorResino, Salvador 
dc.contributor.authorFernandez-Rodriguez, Amanda 
dc.contributor.authorPineda-Tenor, Daniel 
dc.contributor.authorGómez-Moreno, Ana Zaida
dc.contributor.authorSánchez-Ruano, Juan José
dc.contributor.authorArtaza-Varasa, Tomas
dc.contributor.authorMuñoz-Gómez, María José 
dc.contributor.authorVirseda-Berdices, Ana 
dc.contributor.authorMartin-Vicente, Maria 
dc.contributor.authorMartinez, Isidoro 
dc.contributor.authorJimenez-Sousa, Maria Angeles 
dc.date.accessioned2021-03-09T09:38:47Z
dc.date.available2021-03-09T09:38:47Z
dc.date.issued2021-01-28
dc.identifier.citationJ Clin Med. 2021 Jan 28;10(3):483.es_ES
dc.identifier.issn2077-0383es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12156
dc.description.abstractTRPM5 (transient receptor potential cation channel subfamily M member 5) rs886277 polymorphism has been related to liver cirrhosis from different etiologies. The present study investigates the association of TRPM5 rs886277 polymorphism with liver fibrosis progression and cirrhosis development in chronic hepatitis C (CHC) patients. We conducted a retrospective study of 208 non-cirrhotic patients with CHC, who had at least two liver stiffness measurements (LSM) with a separation of 12 months (baseline LSM (LSM1) and the last LSM (LSM2)). Two outcome variables were considered: (1) LSM2/LSM1 ratio; (2) cirrhosis progression (F4; LSM ≥ 12.5 kPa). DNA genotyping was done at the CeGen using a MassARRAY platform. The follow-up time was similar irrespective of the rs886277 genotype (46.4 months in TT genotype, 46.4 months in CT genotype, and 49.2 months in CC genotype; p = 0.649). The highest LSM increases were found in patients with CC genotype compared with TT and CT genotypes (p = 0.044 and p = 0.038, respectively). The cirrhosis progression was higher in patients with CC genotype than TT genotype (p = 0.033). Thus, the rs886277 C allele was associated with higher cirrhosis progression (adjusted odds ratio (aOR) = 2.64; p = 0.014). Moreover, rs886277 CC genotype was also related to higher values of LSM2/LSM1 ratio (adjusted arithmetic mean ratio a(AMR) = 1.31; p = 0.001) and cirrhosis progression (aOR = 4.33; p = 0.027). TRPM5 rs886277 polymorphism was associated with liver fibrosis progression and cirrhosis development among hepatitis C virus (HCV)-infected patients. Specifically, the rs886277 C allele and CC genotype were risk factors for advancing liver fibrosis and cirrhosis compared to the rs886277 T allele and CT/TT genotype, respectively.es_ES
dc.description.sponsorshipThis study is supported by grants from Instituto de Salud Carlos III (ISCIII) (grant # PI20CIII/00004 to S.R.). M.A.J.-S. and A.F.-R. are supported by “Instituto de Salud Carlos III” (grant # CP17CIII/00007 and CP14CIII/00010, respectively).es_ES
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectChronic hepatitis Ces_ES
dc.subjectHepatic fibrosises_ES
dc.subjectCirrhosises_ES
dc.subjectLiver stiffnesses_ES
dc.subjectTRPM5es_ES
dc.subjectSNPses_ES
dc.titleTRPM5 rs886277 Polymorphism Predicts Hepatic Fibrosis Progression in Non-Cirrhotic HCV-Infected Patientses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33525598es_ES
dc.format.volume10es_ES
dc.format.number3es_ES
dc.identifier.doi10.3390/jcm10030483es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/jcm10030483es_ES
dc.identifier.journalJournal of clinical medicinees_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI20CIII/00004es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CP17CIII/00007es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CP14CIII/00010es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Atribución 4.0 Internacional