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          "es" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Modificaci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en pacientes VHC con presencia y ausencia de placa de ateroma&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Introducci&#243;n</span><p id="par0005" class="elsevierStylePara elsevierViewall">La infecci&#243;n cr&#243;nica por el virus de la hepatitis C &#40;VHC&#41; es un problema de salud global&#46; La prevalencia mundial es de aproximadamente 71 millones de personas infectadas&#44; lo que representa 399&#46;000 muertes cada a&#241;o&#46; En Espa&#241;a&#44; el VHC afecta a casi 500&#46;000 personas&#44; aunque esta prevalencia se ha modificado en los &#250;ltimos a&#241;os desde el uso de las nuevas terapias libres de interfer&#243;n<a class="elsevierStyleCrossRefs" href="#bib0155"><span class="elsevierStyleSup">1&#44;2</span></a>&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">La infecci&#243;n por VHC es una de las principales causas de enfermedad hep&#225;tica cr&#243;nica y de carcinoma hepatocelular&#44; pero tambi&#233;n se asocia a manifestaciones extrahep&#225;ticas e importantes alteraciones metab&#243;licas<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">3&#44;4</span></a>&#46; Recientemente se ha informado del aumento de ateromatosis subcl&#237;nica y de una mayor incidencia de eventos cardiovasculares en pacientes con VHC<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">5&#44;6</span></a>&#46; Algunos estudios muestran que la infecci&#243;n cr&#243;nica por VHC es un factor de riesgo independiente para la ateromatosis carot&#237;dea&#44; enfermedad coronaria y accidente cerebrovascular&#59; sin embargo&#44; los resultados de los diferentes trabajos son poco concluyentes<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">7-11</span></a>&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">La infecci&#243;n por VHC aumenta la secreci&#243;n de citoquinas proinflamatorias y modifica la actividad del sistema inmunol&#243;gico&#46; Este estado inflamatorio sostenido puede promover la aterog&#233;nesis en pacientes infectados<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">12</span></a>&#46; Adem&#225;s&#44; es conocido que el VHC y la enfermedad hep&#225;tica provocan una modificaci&#243;n de los l&#237;pidos y de las lipoprote&#237;nas&#44; sobre todo de la apolipoprote&#237;na B&#44; utiliz&#225;ndolos como hu&#233;sped para su replicaci&#243;n y difusi&#243;n&#46; El VHC circula unido a las lipoprote&#237;nas de baja densidad &#40;LDL&#41; y a las lipoprote&#237;nas de muy baja densidad &#40;VLDL&#41;&#44; e interacciona con los receptores celulares de las LDL atravesando la pared de las arterias<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">13</span></a>&#46; Estudios in vivo demuestran ARN del VHC colonizando y reproduci&#233;ndose en las placas de ateroma ricas en colesterol<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">14&#44;15</span></a>&#46; Este riesgo cardiovascular puede verse incrementado por otros trastornos asociados al VHC&#44; como son la hiperhomocisteinemia&#44; la hipoadiponectinemia y sobre todo la resistencia a la insulina&#46; A pesar de la falta de consenso en ciertos aspectos sobre la relaci&#243;n entre la infecci&#243;n por el VHC y la formaci&#243;n de placas de ateroma&#44; la enfermedad cardiovascular es un problema emergente en los pacientes infectados por este virus<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">16-20</span></a>&#46; Por lo tanto&#44; aunque actualmente existen tratamientos antivirales efectivos para curar la infecci&#243;n viral&#44; es necesario comprender mejor c&#243;mo la infecci&#243;n por VHC influye en el riesgo cardiovascular&#46; En este estudio&#44; se ha investigado si el VHC es un factor de riesgo independiente de ateromatosis subcl&#237;nica&#44; si existen diferencias en el perfil lip&#237;dico de los pacientes infectados con o sin placas de ateroma&#44; as&#237; como su asociaci&#243;n con la carga viral y la progresi&#243;n de la enfermedad hep&#225;tica medida por el grado de fibrosis&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Pacientes y m&#233;todos</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Dise&#241;o del estudio y pacientes</span><p id="par0020" class="elsevierStylePara elsevierViewall">En este estudio observacional y transversal se incluyeron pacientes ambulatorios con infecci&#243;n cr&#243;nica por VHC &#40;VHC-positivos&#41; y pacientes sin infecci&#243;n &#8212;grupo control&#8212; &#40;VHC-negativos&#41; seguidos en 2 hospitales universitarios entre marzo de 2015 y junio de 2016&#46; El grupo con VHC-positivo estaba formado por pacientes con infecci&#243;n cr&#243;nica por VHC serol&#243;gicamente confirmada &#40;es decir&#44; positivo para anticuerpos anti-VHC y carga viral detectable&#41; de cualquier genotipo y grado de fibrosis hep&#225;tica&#46; Estos pacientes fueron reclutados en las Unidades de Hepatolog&#237;a de los hospitales universitarios Arnau de Vilanova y Santa Mar&#237;a de Lleida&#59; y entraron en el estudio antes de iniciar tratamiento con antivirales de acci&#243;n directa &#40;AAD&#41;&#46; El grupo control incluy&#243; pacientes con VHC negativos y riesgo cardiovascular moderado-bajo &#40;&#237;ndice SCORE<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>5&#37;&#44; tablas SCORE European Low Risk Chart&#41;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">21</span></a>&#44; procedentes de una unidad de riesgo cardiovascular donde se realiza ecograf&#237;a arterial para el diagn&#243;stico de ateromatosis subcl&#237;nica &#40;Unidad de Detecci&#243;n y Tratamiento de Enfermedades Aterotromb&#243;ticas &#91;UDETMA&#93; del Hospital Universitario Arnau de Vilanova de Lleida&#41;&#46; Los criterios de exclusi&#243;n para ambos grupos incluyeron&#58; <span class="elsevierStyleItalic">1&#41;</span> edad &#60;<span class="elsevierStyleHsp" style=""></span>30 o &#62;<span class="elsevierStyleHsp" style=""></span>75 a&#241;os&#59; <span class="elsevierStyleItalic">2&#41;</span> cirrosis descompensada&#59; <span class="elsevierStyleItalic">3&#41;</span> presencia de carcinoma hepatocelular u otros tumores&#59; <span class="elsevierStyleItalic">4&#41;</span> enfermedad hep&#225;tica cr&#243;nica no VHC &#40;por alcohol&#44; virus hepatitis B&#44; patolog&#237;a autoinmune o por dep&#243;sito de hierro&#41;&#59; <span class="elsevierStyleItalic">5&#41;</span> infecci&#243;n por VIH&#59; <span class="elsevierStyleItalic">6&#41;</span> enfermedad inflamatoria o infecciosa aguda o cr&#243;nica&#59; <span class="elsevierStyleItalic">7&#41;</span> antecedentes de eventos cardiovasculares previos seg&#250;n la Clasificaci&#243;n Internacional de Enfermedades&#44; 10&#46;<span class="elsevierStyleSup">a</span> revisi&#243;n &#40;ICD10-CM&#41; &#91;a&#41; enfermedad cerebrovascular&#58; ataque isqu&#233;mico transitorio y&#47;o accidente cerebrovascular estable&#59; b&#41; enfermedad card&#237;aca isqu&#233;mica&#58; infarto agudo de miocardio&#44; angina de pecho inestable&#44; arritmias y&#47;o insuficiencia card&#237;aca congestiva&#59; c&#41; enfermedad arterial perif&#233;rica de las extremidades inferiores o aneurisma a&#243;rtico&#93;&#59; <span class="elsevierStyleItalic">8&#41;</span> insuficiencia renal cr&#243;nica &#40;ecuaci&#243;n CKD-EPI<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>60<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#47;1&#44;73 m<span class="elsevierStyleSup">2</span>&#41;&#59; <span class="elsevierStyleItalic">9&#41;</span> diagn&#243;stico de diabetes mellitus&#59; <span class="elsevierStyleItalic">10&#41;</span> pacientes con dislipidemia tratados con hipolipemiantes&#59; <span class="elsevierStyleItalic">11&#41;</span> antecedentes de hipertensi&#243;n arterial &#40;HTA&#41; en tratamiento&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Todos los pacientes firmaron un consentimiento informado antes de entrar en el estudio&#44; que fue aprobado por el comit&#233; de &#233;tica de los 2 hospitales involucrados&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Datos cl&#237;nicos y anal&#237;ticos</span><p id="par0030" class="elsevierStylePara elsevierViewall">Los datos cl&#237;nicos fueron recogidos en una entrevista estandarizada en la visita de seguimiento de consultas&#46; Se utilizaron muestras de sangre en ayunas para medir los siguientes par&#225;metros s&#233;ricos&#58; glucosa&#44; colesterol total &#40;CT&#41;&#44; colesterol LDL y HDL&#44; triglic&#233;ridos &#40;TG&#41;&#44; creatinina y prote&#237;na C reactiva &#40;PCR&#41;&#46; Se calcularon los coeficientes lip&#237;dicos&#58; colesterol no HDL &#40;colesterol total<span class="elsevierStyleHsp" style=""></span>&#8722;<span class="elsevierStyleHsp" style=""></span>colesterol HDL&#41;&#44; TG&#47;HDL colesterol &#40;indicador de resistencia a la insulina&#41; y CT&#47;HDL colesterol &#40;&#237;ndice aterog&#233;nico&#41;&#44; realizando todas las determinaciones en el mismo laboratorio&#46; Las mediciones antropom&#233;tricas &#40;peso y altura&#41; para el c&#225;lculo del &#237;ndice de masa corporal &#40;IMC&#41; y la presi&#243;n arterial se registraron en la UDETMA antes de realizar la ecograf&#237;a arterial&#46; La presi&#243;n arterial sist&#243;lica y diast&#243;lica se midi&#243; en 3 ocasiones en posici&#243;n sedestaci&#243;n&#44; y tras 10<span class="elsevierStyleHsp" style=""></span>min de reposo&#44; utilizando un oscil&#243;metro autom&#225;tico &#40;OMRON HEM-705 CP<span class="elsevierStyleSup">&#174;</span>&#41;&#46; Se registr&#243; la media de las 2 &#250;ltimas mediciones&#46; Los pacientes tambi&#233;n fueron clasificados de acuerdo con su historial de tabaquismo como fumadores&#44; exfumadores o no fumadores&#46; El riesgo cardiovascular se calcul&#243; utilizando las tablas de riesgo SCORE<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">21</span></a>&#46; En el grupo de pacientes con hepatitis cr&#243;nica&#44; la carga viral de ARN del VHC se analiz&#243; mediante transcripci&#243;n inversa-reacci&#243;n en cadena de la polimerasa &#40;RT-PCR&#41;&#44; con un l&#237;mite de detecci&#243;n de 12<span class="elsevierStyleHsp" style=""></span>UI&#47;ml&#46; Se realiz&#243; elastograf&#237;a de transici&#243;n hep&#225;tica &#40;Fibroscan<span class="elsevierStyleSup">&#174;</span> &#91;FS&#93;&#44; Echosens&#44; Par&#237;s&#44; Francia&#41; para valorar el grado de fibrosis hep&#225;tica clasific&#225;ndolo as&#237;&#58; menor de 7&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; no fibrosis &#40;F0-1&#41;&#59; de 7&#44;6-9&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; fibrosis moderada &#40;F2&#41;&#59; de 9&#44;6-12&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; fibrosis significativa &#40;F3&#41;&#59; y mayor de 12&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; cirrosis hep&#225;tica &#40;F4&#41;&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Evaluaci&#243;n de la ateromatosis arterial subcl&#237;nica</span><p id="par0035" class="elsevierStylePara elsevierViewall">La presencia de placas de ateroma en territorios carot&#237;deo y femoral se determin&#243; usando un ec&#243;grafo General Electric &#40;modelo Vivid-I<span class="elsevierStyleSup">&#174;</span>&#41; con una sonda vascular 12L-RS siguiendo un m&#233;todo estandarizado descrito previamente<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a>&#46; Todas las im&#225;genes fueron capturadas y le&#237;das por un &#250;nico equipo&#44; formado por profesionales previamente acreditados&#46; El coeficiente de kappa para la confiabilidad intraobservador se estableci&#243; en 1&#46; La placa de ateroma se defini&#243; como una estructura focal que sobresale en la luz vascular&#44; o un grosor &#237;ntima-media &#40;GIMc&#41; &#62;<span class="elsevierStyleHsp" style=""></span>1&#44;5<span class="elsevierStyleHsp" style=""></span>mm&#44; de acuerdo con el consenso de Mannheim<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">23</span></a>&#46; Se analizaron 12 territorios vasculares para diagnosticar presencia de placa de ateroma&#58; se exploraron arterias car&#243;tidas &#40;com&#250;n&#44; bifurcaci&#243;n&#44; interna y externa&#41; y arterias femorales &#40;comunes y superficiales&#41; de forma bilateral&#44; utilizando un plano axial y longitudinal&#44; con ultrasonograf&#237;a eco-Doppler en modo B y eco-color&#46; Se defini&#243; ateromatosis subcl&#237;nica como la presencia de una o m&#225;s placas en cualquiera de los territorios estudiados&#46; Se midi&#243; el GIM carot&#237;deo&#44; en el segmento distal de la arteria siendo el valor final la media del territorio carot&#237;deo&#44; en los pacientes sin placas de ateroma&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">An&#225;lisis estad&#237;stico</span><p id="par0040" class="elsevierStylePara elsevierViewall">Las variables categ&#243;ricas se describieron como frecuencia y porcentaje y se compararon usando la prueba de Chi-cuadrado de Pearson&#46; Las variables cuantitativas se describieron como la mediana y el intervalo intercuartil &#40;IQR&#41;&#44; o la media y desviaci&#243;n est&#225;ndar &#40;DE&#41; seg&#250;n su distribuci&#243;n&#46; Las variables distribuidas normalmente se compararon mediante la prueba t de Student&#44; mientras que la prueba no param&#233;trica de Mann-Whitney se utiliz&#243; para comparar variables no normalmente distribuidas&#46; Las variables que muestran diferencias significativas entre los pacientes con y sin placas de ateroma se incluyeron en una regresi&#243;n log&#237;stica m&#250;ltiple condicional por pasos hacia atr&#225;s para predecir la presencia de placas de ateroma&#46; Se utiliz&#243; un an&#225;lisis de las caracter&#237;sticas del operador receptor &#40;ROC&#41; para establecer un l&#237;mite para edad&#44; y se calcul&#243; la presencia de placa seg&#250;n la edad de la poblaci&#243;n a estudio&#44; transformando la variable cuantitativa en variable dicot&#243;mica de acuerdo con los valores de corte obtenidos&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Se estudi&#243; la asociaci&#243;n de las modificaciones del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica por ANOVA y la existencia de correlaci&#243;n entre la carga viral y los l&#237;pidos por R de Spearman&#46; La significaci&#243;n estad&#237;stica se estableci&#243; en un valor &#945; bilateral &#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#44; y todos los an&#225;lisis se realizaron utilizando el software SPSS &#40;IBM Statistics for Windows&#44; versi&#243;n 20&#46;0&#44; Armonk&#44; NY&#58; IBM Corp&#46;&#41;&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Resultados</span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Caracter&#237;sticas de la poblaci&#243;n estudiada</span><p id="par0050" class="elsevierStylePara elsevierViewall">La muestra del estudio incluy&#243; 204 pacientes&#58; 102 en el grupo con VHC positivo y 102 en el grupo control&#46; La <a class="elsevierStyleCrossRef" href="#tbl0005">tabla 1</a> describe los datos cl&#237;nicos y de laboratorio relativos a ambas poblaciones&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">Los grupos estudiados no presentaron diferencias estad&#237;sticamente significativas en cuanto a sexo&#44; edad ni historia de tabaquismo&#46; El grupo control present&#243; valores significativamente m&#225;s altos en la mayor&#237;a de los factores de riesgo cardiovasculares tradicionales&#44; incluyendo el IMC&#44; la presi&#243;n arterial sist&#243;lica y diast&#243;lica&#44; y el perfil de l&#237;pidos s&#233;ricos&#46; No se observaron diferencias significativas en cuanto a las cifras de glucosa&#44; triglic&#233;ridos&#44; ni en el coeficiente TG&#47;HDL o indicador de resistencia a la insulina&#44; aunque los niveles fueron en todos los casos superiores en los pacientes control &#40;96&#44;5 vs&#46; 94&#44;2<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;888&#59; 121&#44;5 vs&#46; 102&#44;9<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;070&#59; y 2&#44;3 vs&#46; 2&#44;1&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;449&#41;&#46; Adem&#225;s&#44; los pacientes control presentaron niveles significativamente superiores de creatinina s&#233;rica&#44; de PCR y de &#237;ndice de riesgo cardiovascular &#40;SCORE&#41;&#44; aunque el riesgo era bajo-moderado en ambos grupos&#46; En los pacientes con infecci&#243;n cr&#243;nica por VHC&#44; casi un 55&#37; presentaba enfermedad hep&#225;tica avanzada &#40;de ellos&#44; el 29&#44;4&#37; cirrosis o fibrosis grado 4 por elastograf&#237;a hep&#225;tica&#41;&#46; Un 67&#44;2&#37; eran genotipo 1&#44; un 6&#44;7&#37; genotipo 2&#44; un 9&#44;7&#37; genotipo 3 y el 16&#44;4&#37; genotipo 4&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">El porcentaje de pacientes con ateromatosis fue significativamente mayor en el grupo con VHC positivo que en el grupo control &#40;58&#44;8 vs&#46; 28&#44;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; sin observarse diferencias significativas en el GIM carot&#237;deo medido en los pacientes sin ateromatosis &#40;0&#44;76 vs&#46; 0&#44;89<span class="elsevierStyleHsp" style=""></span>mm&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;18&#41; aunque fue superior en los pacientes infectados&#46; En el grupo control las placas se distribuyeron un 35&#37; en territorio carot&#237;deo&#44; un 23&#44;9&#37; en territorio femoral y un 41&#44;1&#37; en ambos territorios&#44; mientras que en los pacientes infectados con VHC un 45&#44;3&#37; de placas de ateroma se detectaron en car&#243;tidas&#44; un 19&#44;8&#37; en femorales y un 34&#44;9&#37; en ambas &#225;reas vasculares&#46; El n&#250;mero medio de placas de ateroma fue de 2&#44;95 &#40;1-10&#41; en pacientes infectados frente a 2&#44;44 &#40;1-8&#41; en los pacientes no infectados&#46; No se observaron diferencias significativas entre las poblaciones ni por territorio vascular afecto &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;710&#41; ni por el n&#250;mero de placas medio detectado &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;420&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">En la <a class="elsevierStyleCrossRef" href="#tbl0010">tabla 2</a> se analizan los factores asociados a la presencia de placa de ateroma en cada una de las poblaciones estudiadas&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0070" class="elsevierStylePara elsevierViewall">La presencia de placa de ateroma en ambos grupos &#40;con y sin infecci&#243;n por VHC&#41; se asoci&#243; de forma estad&#237;sticamente significativa al sexo masculino&#44; a cifras superiores de presi&#243;n arterial&#44; a niveles elevados de triglic&#233;ridos&#44; y a un mayor riesgo cardiovascular seg&#250;n las tablas &#40;SCORE&#41;&#46; Respecto a la edad&#44; no se observ&#243; asociaci&#243;n con la presencia de placa de ateroma en los pacientes infectados&#44; mientras que s&#237; que se identific&#243; en el grupo control&#44; de manera que la presencia de placa se asoci&#243; a mayor edad &#40;51&#44;8 a&#241;os en pacientes control sin ateromatosis vs&#46; 67&#44;3 a&#241;os en pacientes control con ateromatosis&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; Respecto al h&#225;bito tab&#225;quico&#44; se detect&#243; asociaci&#243;n en los pacientes con VHC &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;003&#41; siendo m&#225;s frecuente la placa en los pacientes fumadores y&#47;o exfumadores &#40;81&#44;6&#37;&#41;&#59; pero no en los controles &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;499&#41;&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">En cuanto al perfil lip&#237;dico&#44; los pacientes VHC con placa presentaban menores cifras de colesterol HDL &#40;57&#44;6 vs&#46; 50&#44;9<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;023&#41; y mayores niveles de triglic&#233;ridos &#40;89&#44;3 vs&#46; 112&#44;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;029&#41;&#44; coeficiente TG&#47;HDL &#40;1&#44;7 vs&#46; 2&#44;3&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;026&#41; y coeficiente CT&#47;HDL &#40;3 vs&#46; 3&#44;4&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;035&#41; que los pacientes infectados sin placa&#46; No se ha observado significaci&#243;n de estos factores lip&#237;dicos entre los pacientes controles sin o con presencia de placa de ateroma&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">Respecto a los factores virales en los pacientes infectados por VHC&#44; no se detect&#243; asociaci&#243;n entre la presencia de placa y la carga viral cuantificada por ARN &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;936&#41;&#44; pero s&#237; se encontraron diferencias significativas con el grado de fibrosis hep&#225;tica&#44; siendo m&#225;s frecuente la presencia de placa en los pacientes con fibrosis avanzada &#40;F4 sin ateroma 23&#44;8&#37; vs&#46; F4 con ateromatosis 33&#44;3&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;016&#41;&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">Se analiz&#243; la edad&#44; seg&#250;n el an&#225;lisis de la ROC&#44; y la edad superior a 54 a&#241;os fue el mejor valor de corte para predecir la presencia de placas de ateroma &#40;AUC<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;682&#44; error est&#225;ndar<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;039 &#91;IC 95&#37;&#58; 0&#44;6-0&#44;7&#93;&#44; 67&#37; de sensibilidad y 60&#37; de especificidad&#41;&#46; Por debajo de este punto de corte &#40;&#60;<span class="elsevierStyleHsp" style=""></span>54 a&#241;os&#41;&#44; el porcentaje de pacientes con placas de ateroma fue del 57&#37; en el grupo VHC positivo y del 4&#37; en el grupo control &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; En los pacientes con edad mayor o igual a 54 a&#241;os&#44; la ateromatosis aument&#243; hasta un 61&#37; en el grupo con VHC positivo y hasta el 50&#37; en el grupo control&#44; sin observarse diferencias significativas en este tramo de edad entre poblaciones &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;252&#41;&#46; En el grupo con edad menor de 54 a&#241;os&#44; los pacientes con VHC positivo ten&#237;an mucha m&#225;s probabilidad de ateromatosis que el grupo control &#40;OR &#61; 30&#59; IC95&#37;&#58; 6&#44;58-136&#44;67&#59; p &#60; 0&#44;001&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0010">fig&#46; 2</a>&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Factores asociados con ateromatosis subcl&#237;nica</span><p id="par0090" class="elsevierStylePara elsevierViewall">La <a class="elsevierStyleCrossRef" href="#tbl0015">tabla 3</a> muestra las caracter&#237;sticas cl&#237;nicas de los pacientes con y sin ateromatosis subcl&#237;nica&#46; La infecci&#243;n cr&#243;nica por VHC se asoci&#243; significativamente a la presencia de ateromatosis subcl&#237;nica&#44; al igual que los factores de riesgo cardiovascular tradicionales como el sexo masculino&#44; la edad avanzada&#44; la presi&#243;n arterial sist&#243;lica&#44; puntuaciones elevadas en el SCORE&#44; los niveles s&#233;ricos bajos de colesterol HDL y m&#225;s elevados de triglic&#233;ridos&#46; Tambi&#233;n se asoci&#243; con valores incrementados del cociente TG&#47;HDL&#46; La presencia de placas de ateroma no se asoci&#243; con el IMC&#44; los niveles de glucosa ni los valores de PCR&#46; Tampoco se observ&#243; asociaci&#243;n con el perfil lip&#237;dico formado por colesterol total&#44; LDL y colesterol no HDL&#44; ni con el &#237;ndice aterog&#233;nico &#40;CT&#47;HDL&#41;&#46;</p><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><p id="par0095" class="elsevierStylePara elsevierViewall">El an&#225;lisis multivariado revel&#243; una probabilidad muy superior de ateromatosis en pacientes con VHC positivo en comparaci&#243;n con el grupo control &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37 &#91;5&#44;5-37&#44;5&#93;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41; &#40;<a class="elsevierStyleCrossRef" href="#tbl0015">tabla 3</a>&#41;&#46; Otros factores de riesgo independientes de ateromatosis subcl&#237;nica incluyeron el sexo masculino&#44; la edad avanzada y el mayor coeficiente TG&#47;HDL o indicador indirecto de resistencia a la insulina&#46; Ni la presi&#243;n arterial sist&#243;lica&#44; ni el perfil lip&#237;dico contribuyeron al modelo predictivo para la presencia de placas de ateroma&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Descripci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en los pacientes con VHC en relaci&#243;n con la presencia de placa de ateroma</span><p id="par0100" class="elsevierStylePara elsevierViewall">Analizamos el perfil lip&#237;dico en los pacientes VHC con y sin enfermedad ateromatosa&#44; teniendo en cuenta el grado de fibrosis hep&#225;tica medida mediante elastograf&#237;a&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">En los pacientes VHC sin enfermedad ateromatosa&#44; no observamos diferencias significativas en ninguno de los valores del perfil lip&#237;dico tradicional&#44; ni en los coeficientes indicativos de resistencia a la insulina &#40;TG&#47;HDL&#41; ni en el factor aterog&#233;nico &#40;CT&#47;HDL&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>a y b&#41;&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0110" class="elsevierStylePara elsevierViewall">En los pacientes VHC con enfermedad ateromatosa &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>c y d&#41;&#44; se observaron diferencias significativas en las cifras de colesterol total &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;018&#41;&#44; en los niveles de colesterol no HDL &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;002&#41; y de colesterol LDL &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;002&#41;&#44; as&#237; como en el &#237;ndice aterog&#233;nico &#40;CT&#47;HDL&#41; &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; con tendencia a aumentar a medida que progresa la fibrosis hep&#225;tica&#44; y disminuyendo significativamente en presencia de cirrosis&#46; No se observaron cambios en los niveles de colesterol HDL&#44; triglic&#233;ridos ni en el coeficiente TG&#47;HDL y los grados de fibrosis en presencia de placa de ateroma&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Al analizar la correlaci&#243;n entre la carga viral y el perfil lip&#237;dico&#44; tan solo se detect&#243; una leve asociaci&#243;n entre el ARN del VHC y los niveles de colesterol no HDL &#40;r<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;219&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;04&#41;&#44; sin detectarse asociaci&#243;n con ning&#250;n otro par&#225;metro anal&#237;tico&#46;</p></span></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Discusi&#243;n</span><p id="par0120" class="elsevierStylePara elsevierViewall">Este estudio observacional analiza la presencia de enfermedad ateromatosa en sujetos con y sin infecci&#243;n cr&#243;nica por VHC&#44; encontrando que los pacientes infectados tienen mayor presencia de ateromatosis subcl&#237;nica y en edades m&#225;s precoces que los controles&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Nuestros resultados concuerdan con lo publicado recientemente en 2 metaan&#225;lisis que describen una mayor presencia de ateromatosis en poblaciones infectadas por VHC &#40;entre un 38 y un 65&#37;&#41;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">5&#44;6</span></a>&#46; En estos estudios&#44; las placas de ateroma se identificaron por ecograf&#237;a Doppler vascular&#44; y el diagn&#243;stico se estableci&#243; con un valor de GIMc<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1&#44;3<span class="elsevierStyleHsp" style=""></span>mm<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">20</span></a>&#46; En nuestro trabajo se siguieron los criterios de Manheim para el diagn&#243;stico de ateromatosis&#44; definiendo la placa como un GIMc<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1&#44;5<span class="elsevierStyleHsp" style=""></span>mm&#46; Una de las posibles razones de nuestra tasa m&#225;s elevada es la ampliaci&#243;n del estudio femoral&#44; que aumenta la probabilidad de detectar ateromatosis&#46; Se ha publicado la existencia de enfermedad ateromatosa en territorio femoral en ausencia de placas carot&#237;deas en poblaci&#243;n general<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">24</span></a>&#46; Adem&#225;s&#44; nosotros tambi&#233;n analizamos diferentes genotipos virales&#44; que no han sido evaluados en estudios previamente publicados<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">20</span></a>&#44; aunque es conocido que el genotipo 3 produce m&#225;s alteraciones metab&#243;licas que el resto<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">25&#44;26</span></a>&#46; Aunque la presencia de placa fue mayor en los pacientes infectados&#44; estos presentaban un bajo &#237;ndice de riesgo cardiovascular seg&#250;n las tablas SCORE European Risk Chart&#46; Varios estudios poblacionales han demostrado asociaci&#243;n entre la presencia de placas en arterias perif&#233;ricas e incidencia de eventos cardiovasculares&#44; incluso en sujetos sin eventos previos &#40;1&#44;8 veces el aumento del riesgo de eventos coronarios y 4&#44;1 veces el aumento del riesgo de eventos cardiovasculares&#41;<a class="elsevierStyleCrossRefs" href="#bib0315"><span class="elsevierStyleSup">27&#44;28</span></a>&#46; En l&#237;nea con estas publicaciones&#44; la presencia de placas de ateroma en nuestra poblaci&#243;n no se asoci&#243; con factores de riesgo cardiovascular tradicionales como el IMC&#44; la glucemia o la dislipidemia&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">Nuestro estudio involucra la primera cohorte espa&#241;ola de pacientes monoinfectados con VHC cr&#243;nica&#44; aunque cuenta con las limitaciones intr&#237;nsecas de un dise&#241;o transversal y del sesgo de selecci&#243;n en los pacientes controles&#44; ya que pertenecen a un grupo de pacientes de una consulta de riesgo cardiovascular&#46; Para minimizar este sesgo&#44; limitamos los criterios de selecci&#243;n a sujetos con riesgo bajo a moderado &#40;probabilidad &#60;<span class="elsevierStyleHsp" style=""></span>5&#37; de experimentar eventos cardiovasculares a los 10 a&#241;os&#41; sin presencia de enfermedad cardiovascular previa ni toma de f&#225;rmacos para hipertensi&#243;n ni dislipidemia&#46; Excluimos los pacientes con diabetes y enfermedad renal cr&#243;nica para evitar factores de confusi&#243;n&#46; Algunas publicaciones identifican que el virus VHC promueve el desarrollo de diabetes e insuficiencia renal cr&#243;nica&#44; lo que predispone a la presencia de lesiones ateromatosas<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">16</span></a>&#46; Tambi&#233;n podr&#237;a crear confusi&#243;n el hecho de observar una mayor presencia de exfumadores o fumadores activos entre aquellos con placa VHC&#43;&#44; as&#237; como las diferencias entre el grado de fibrosis hep&#225;tica en los sujetos con y sin placa&#59; pero tal como demuestra el an&#225;lisis multivariante&#44; ni el tabaquismo ni la fibrosis influ&#237;an en el desarrollo de las placas de ateroma&#44; mientras que s&#237; se observ&#243; una asociaci&#243;n elevada &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37&#41; del VHC <span class="elsevierStyleItalic">per se</span>&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">Ante estos resultados&#44; identificamos como factor independiente de ateromatosis la infecci&#243;n cr&#243;nica por VHC sin influencia de otros factores cardiovasculares tradicionalmente conocidos&#44; lo que sugiere un papel directo del VHC en el desarrollo de las lesiones ateromatosas&#46; Estudios recientes han demostrado la presencia de ARN del VHC en la placa carot&#237;dea<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">14&#44;15</span></a> y por el entorno proinflamatorio que induce el virus<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">4-12</span></a>&#46; En nuestro estudio&#44; los niveles de PCR marcador de riesgo cardiovascular e inflamaci&#243;n sist&#233;mica&#44; ampliamente aceptado para la poblaci&#243;n<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a>&#44; no mostraron diferencias significativas entre ambos grupos&#44; si bien las prote&#237;nas de s&#237;ntesis hep&#225;ticas como PCR pueden estar alteradas en pacientes con enfermedad hep&#225;tica cr&#243;nica&#46; Adem&#225;s&#44; detectamos que la presencia de ateromatosis en la poblaci&#243;n VHC se desarrolla en edades mucho m&#225;s tempranas que en el grupo sin infecci&#243;n&#46; Tal y como se observa en la <a class="elsevierStyleCrossRef" href="#fig0010">figura 2</a>&#44; hemos encontrado que por debajo de 54 a&#241;os existen diferencias significativas de presencia de placa en los pacientes infectados frente a los controles&#46; Este hallazgo sugiere que los pacientes con infecci&#243;n por VHC presentan ateromatosis acelerada o envejecimiento vascular prematuro&#44; de forma similar a lo observado en otras enfermedades cr&#243;nicas inflamatorias y autoinmunes<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">29</span></a>&#46; Adem&#225;s de la edad y la infecci&#243;n por VHC&#44; el sexo masculino y el coeficiente TG&#47;HDL &#40;marcador indirecto de insulinorresistencia&#41; fueron los &#250;nicos factores significativamente asociados con la presencia de ateromatosis&#46; Este coeficiente es un &#237;ndice predictivo pron&#243;stico de enfermedad cardiovascular&#44; utilizado como marcador de aterog&#233;nesis en poblaci&#243;n general&#44; y aunque hay pocos datos&#44; su valor predictivo en cardiopat&#237;a es alto<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">30</span></a>&#46; Adem&#225;s&#44; es un buen marcador de aterog&#233;nesis en la poblaci&#243;n infectada&#44; ya que no se modifica significativamente con la progresi&#243;n de la enfermedad hep&#225;tica ni con la carga viral&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">En este trabajo&#44; analizamos la modificaci&#243;n del perfil lip&#237;dico en diferentes estadios de progresi&#243;n de enfermedad hep&#225;tica medida por elastograf&#237;a &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>&#41;&#44; detectando que en los pacientes infectados sin placa de ateroma no existen diferencias en cuanto a los niveles de l&#237;pidos s&#233;ricos y la fibrosis hep&#225;tica&#46; Pero en los pacientes VHC con ateromatosis&#44; las part&#237;culas m&#225;s aterog&#233;nicas &#40;formadas por LDL y VLDL&#41;&#44; que son el transportador principal del VHC en plasma&#44; aumentan conforme progresa la fibrosis&#44; y descienden significativamente al establecerse la cirrosis hep&#225;tica&#46; Estas part&#237;culas m&#225;s aterog&#233;nicas se correlacionan d&#233;bilmente con la carga viral&#44; sin observar asociaci&#243;n con el desarrollo de placa de ateroma&#44; lo que podr&#237;a deberse a la fluctuaci&#243;n en el tiempo de la viremia o a que estos valores dependen de la progresi&#243;n de la fibrosis hep&#225;tica&#44; descendiendo en estadios de cirrosis&#46;</p><p id="par0145" class="elsevierStylePara elsevierViewall">En resumen&#44; nuestros resultados muestran que los pacientes con infecci&#243;n cr&#243;nica por VHC tienen una mayor prevalencia de ateromatosis subcl&#237;nica que la poblaci&#243;n no infectada&#44; con inicio en edades precoces &#40;ateromatosis acelerada&#41;&#46; El perfil metab&#243;lico y la valoraci&#243;n del riesgo cardiovascular mediante el uso de las tablas tradicionales no son buenos predictores&#44; ya que la mayor&#237;a de estos pacientes presentan SCORES de bajo riesgo y un perfil lip&#237;dico tambi&#233;n de &#171;bajo riesgo&#187; &#40;menores cifras de colesterol no HDL y de colesterol LDL&#41;&#46; Esto apoya la necesidad de pruebas cardiovasculares no invasivas adicionales de uso rutinario&#44; como la ecograf&#237;a arterial&#44; que podr&#237;a mejorar la estratificaci&#243;n del riesgo en esta poblaci&#243;n&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Conflicto de intereses</span><p id="par0150" class="elsevierStylePara elsevierViewall">Los autores declaran no tener ning&#250;n conflicto de intereses&#46;</p></span></span>"
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            1 => array:2 [
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          "titulo" => "Abstract"
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            0 => array:2 [
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              "titulo" => "Background"
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            1 => array:2 [
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            3 => array:2 [
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              "titulo" => "Dise&#241;o del estudio y pacientes"
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              "titulo" => "Datos cl&#237;nicos y anal&#237;ticos"
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              "titulo" => "Evaluaci&#243;n de la ateromatosis arterial subcl&#237;nica"
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              "titulo" => "An&#225;lisis estad&#237;stico"
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              "titulo" => "Caracter&#237;sticas de la poblaci&#243;n estudiada"
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              "titulo" => "Factores asociados con ateromatosis subcl&#237;nica"
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              "identificador" => "sec0050"
              "titulo" => "Descripci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en los pacientes con VHC en relaci&#243;n con la presencia de placa de ateroma"
            ]
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          "titulo" => "Agradecimientos"
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    "fechaRecibido" => "2018-07-06"
    "fechaAceptado" => "2018-12-04"
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          "titulo" => "Palabras clave"
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            0 => "Virus de la hepatitis C &#40;VHC&#41;"
            1 => "Placa de ateroma"
            2 => "Arteriosclerosis subcl&#237;nica"
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          "clase" => "keyword"
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            0 => "Hepatitis C virus &#40;HCV&#41;"
            1 => "Atheromatous plaque"
            2 => "Subclinical atherosclerosis"
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        "titulo" => "Resumen"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Introducci&#243;n</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Se desconoce la asociaci&#243;n entre ateromatosis subcl&#237;nica e infecci&#243;n cr&#243;nica por el virus de la hepatitis C &#40;VHC&#41;&#44; relevante ahora que los antivirales mejoran la supervivencia en los pacientes infectados&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Objetivos</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Conocer si el VHC es factor de riesgo independiente de ateromatosis subcl&#237;nica y analizar las modificaciones del perfil lip&#237;dico seg&#250;n niveles de ARN viral y fibrosis hep&#225;tica&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Pacientes y m&#233;todos</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Estudio observacional y transversal&#59; incluye 102 pacientes VHC positivos y 102 sujetos VHC negativos con paridad de sexo y edad&#44; sin antecedentes de enfermedad cardiovascular&#44; renal ni diabetes&#46; La ateromatosis &#40;presencia de placas de ateroma&#41; y el grosor &#237;ntima-media carot&#237;deo &#40;GIMc&#41; se evalu&#243; mediante ecograf&#237;a de arterias car&#243;tidas y femorales&#46;</p></span> <span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Resultados</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La presencia de ateromatosis en cualquier territorio vascular fue mayor en pacientes VHC que en sujetos no infectados &#40;58&#44;8&#37; frente a 28&#44;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; En el an&#225;lisis multivariante&#44; los factores significativamente asociados con ateromatosis incluyeron infecci&#243;n por VHC &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37 &#91;5&#44;5-37&#44;3&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; edad &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>1&#44;12 &#91;1&#44;1-1&#44;2&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; sexo masculino &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>4&#44;32 &#91;1&#44;9-9&#44;5&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41; y el coeficiente triglic&#233;ridos&#47;colesterol HDL &#40;TG&#47;HDL-indicador indirecto de insulinorresistencia&#41; &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>1&#44;34 &#91;1&#44;1-1&#44;6&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;007&#41;&#46; Los pacientes VHC con placas de ateroma presentaban mayor coeficiente TG&#47;HDL&#44; sin diferencias significativas en cuanto a la carga viral ni grado de fibrosis hep&#225;tica con un perfil lip&#237;dico de &#171;bajo riesgo&#187;&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Conclusiones</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">La infecci&#243;n VHC es factor de riesgo independiente de ateromatosis subcl&#237;nica&#46; La ecograf&#237;a arterial sist&#233;mica en esta poblaci&#243;n mejora la evaluaci&#243;n del riesgo cardiovascular m&#225;s all&#225; de las alteraciones del perfil lip&#237;dico y del c&#225;lculo de riesgo por tablas SCORE&#46;</p></span>"
        "secciones" => array:5 [
          0 => array:2 [
            "identificador" => "abst0005"
            "titulo" => "Introducci&#243;n"
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          1 => array:2 [
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            "titulo" => "Objetivos"
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          2 => array:2 [
            "identificador" => "abst0015"
            "titulo" => "Pacientes y m&#233;todos"
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          3 => array:2 [
            "identificador" => "abst0020"
            "titulo" => "Resultados"
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          4 => array:2 [
            "identificador" => "abst0025"
            "titulo" => "Conclusiones"
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      "en" => array:3 [
        "titulo" => "Abstract"
        "resumen" => "<span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Background</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">The association between subclinical atheromatosis and chronic hepatitis C virus &#40;HCV&#41; infection is unknown but is relevant now that antivirals are improving the survival of patients with the infection&#46;</p></span> <span id="abst0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Objectives</span><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis&#46;</p></span> <span id="abst0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Patients and methods</span><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">We conducted an observational&#44; cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age&#44; with no history of cardiovascular or kidney disease or diabetes&#46; Atheromatosis &#40;the presence of atheromatous plaques&#41; and the carotid intima-media thickness &#40;CIMT&#41; were assessed using ultrasonography of the carotid and femoral arteries&#46;</p></span> <span id="abst0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Results</span><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection &#40;58&#46;8&#37; vs&#46; 28&#46;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;0001&#41;&#46; In the multivariate analysis&#44; the factors significantly associated with atheromatosis included HCV infection &#40;OR&#44; 14&#46;37 &#91;5&#46;5-37&#46;3&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41;&#44; age &#40;OR&#44; 1&#46;12 &#91;1&#46;1-1&#46;2&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41;&#44; male sex &#40;OR&#44; 4&#46;32 &#91;1&#46;9-9&#46;5&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41; and the triglyceride&#47;HDL cholesterol coefficient &#40;TG&#47;HDL-indirect indicator of insulin resistance&#41; &#40;OR&#44; 1&#46;34 &#91;1&#46;1-1&#46;6&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>&#46;007&#41;&#46; The HCV-positive patients with atheromatous plaques had a higher TG&#47;HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a &#8216;low risk&#8217; lipid profile&#46;</p></span> <span id="abst0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Conclusions</span><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">HCV infection is an independent risk factor for subclinical atheromatosis&#46; Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables&#46;</p></span>"
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            "titulo" => "Objectives"
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            "titulo" => "Patients and methods"
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            "titulo" => "Results"
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            "titulo" => "Conclusions"
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          "es" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Modificaci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en pacientes VHC con presencia y ausencia de placa de ateroma&#46;</p>"
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                  \t\t\t\t"><span class="elsevierStyleItalic">HDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">1 &#40;1&#44;6&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">60 &#40;58&#44;8&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">PAS &#40;mmHg&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">PAD &#40;mmHg&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Glucemia &#40;g&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Creatinina &#40;g&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Colesterol total &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">No HDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">LDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">HDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Triglic&#233;ridos &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t">159 &#40;134&#44;2&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">0&#44;047&nbsp;\t\t\t\t\t\t\n
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                  """
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Original
Infección crónica por el virus de la hepatitis C: un factor de riesgo independiente para la ateromatosis subclínica
Chronic hepatitis C infection: An independent risk factor for subclinical atheromatosis
T. Revuelto Artigasa,b,c,d,
Autor para correspondencia
tamararevuelto@gmail.com

Autor para correspondencia.
, N. Zaragoza Velascob,c,d, X. Gómez Arbonesd,e, T. Vidal Ballesterc, C. Piñol Felisd,e, J.M. Reñe Espinetb,d,e, A. Betriu Barsc,d
a Servicio de Aparato Digestivo, Hospital Universitario Santa María, Lleida, España
b Servicio de Aparato Digestivo, Hospital Universitario Arnau de Vilanova, Lleida, España
c Unidad de Detección y Tratamiento de Enfermedades Aterotrombóticas (UDETMA), Hospital Universitario Arnau de Vilanova (Grupo de Investigación Translacional Vascular y Renal, IRBLleida), Lleida, España
d Instituto de Investigación Biomédica, Lleida, España
e Universidad de Lleida (UdL), Lleida, España
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pero tambi&#233;n se asocia a manifestaciones extrahep&#225;ticas e importantes alteraciones metab&#243;licas<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">3&#44;4</span></a>&#46; Recientemente se ha informado del aumento de ateromatosis subcl&#237;nica y de una mayor incidencia de eventos cardiovasculares en pacientes con VHC<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">5&#44;6</span></a>&#46; Algunos estudios muestran que la infecci&#243;n cr&#243;nica por VHC es un factor de riesgo independiente para la ateromatosis carot&#237;dea&#44; enfermedad coronaria y accidente cerebrovascular&#59; sin embargo&#44; los resultados de los diferentes trabajos son poco concluyentes<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">7-11</span></a>&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">La infecci&#243;n por VHC aumenta la secreci&#243;n de citoquinas proinflamatorias y modifica la actividad del sistema inmunol&#243;gico&#46; Este estado inflamatorio sostenido puede promover la aterog&#233;nesis en pacientes infectados<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">12</span></a>&#46; Adem&#225;s&#44; es conocido que el VHC y la enfermedad hep&#225;tica provocan una modificaci&#243;n de los l&#237;pidos y de las lipoprote&#237;nas&#44; sobre todo de la apolipoprote&#237;na B&#44; utiliz&#225;ndolos como hu&#233;sped para su replicaci&#243;n y difusi&#243;n&#46; El VHC circula unido a las lipoprote&#237;nas de baja densidad &#40;LDL&#41; y a las lipoprote&#237;nas de muy baja densidad &#40;VLDL&#41;&#44; e interacciona con los receptores celulares de las LDL atravesando la pared de las arterias<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">13</span></a>&#46; Estudios in vivo demuestran ARN del VHC colonizando y reproduci&#233;ndose en las placas de ateroma ricas en colesterol<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">14&#44;15</span></a>&#46; Este riesgo cardiovascular puede verse incrementado por otros trastornos asociados al VHC&#44; como son la hiperhomocisteinemia&#44; la hipoadiponectinemia y sobre todo la resistencia a la insulina&#46; A pesar de la falta de consenso en ciertos aspectos sobre la relaci&#243;n entre la infecci&#243;n por el VHC y la formaci&#243;n de placas de ateroma&#44; la enfermedad cardiovascular es un problema emergente en los pacientes infectados por este virus<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">16-20</span></a>&#46; Por lo tanto&#44; aunque actualmente existen tratamientos antivirales efectivos para curar la infecci&#243;n viral&#44; es necesario comprender mejor c&#243;mo la infecci&#243;n por VHC influye en el riesgo cardiovascular&#46; En este estudio&#44; se ha investigado si el VHC es un factor de riesgo independiente de ateromatosis subcl&#237;nica&#44; si existen diferencias en el perfil lip&#237;dico de los pacientes infectados con o sin placas de ateroma&#44; as&#237; como su asociaci&#243;n con la carga viral y la progresi&#243;n de la enfermedad hep&#225;tica medida por el grado de fibrosis&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Pacientes y m&#233;todos</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Dise&#241;o del estudio y pacientes</span><p id="par0020" class="elsevierStylePara elsevierViewall">En este estudio observacional y transversal se incluyeron pacientes ambulatorios con infecci&#243;n cr&#243;nica por VHC &#40;VHC-positivos&#41; y pacientes sin infecci&#243;n &#8212;grupo control&#8212; &#40;VHC-negativos&#41; seguidos en 2 hospitales universitarios entre marzo de 2015 y junio de 2016&#46; El grupo con VHC-positivo estaba formado por pacientes con infecci&#243;n cr&#243;nica por VHC serol&#243;gicamente confirmada &#40;es decir&#44; positivo para anticuerpos anti-VHC y carga viral detectable&#41; de cualquier genotipo y grado de fibrosis hep&#225;tica&#46; Estos pacientes fueron reclutados en las Unidades de Hepatolog&#237;a de los hospitales universitarios Arnau de Vilanova y Santa Mar&#237;a de Lleida&#59; y entraron en el estudio antes de iniciar tratamiento con antivirales de acci&#243;n directa &#40;AAD&#41;&#46; El grupo control incluy&#243; pacientes con VHC negativos y riesgo cardiovascular moderado-bajo &#40;&#237;ndice SCORE<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>5&#37;&#44; tablas SCORE European Low Risk Chart&#41;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">21</span></a>&#44; procedentes de una unidad de riesgo cardiovascular donde se realiza ecograf&#237;a arterial para el diagn&#243;stico de ateromatosis subcl&#237;nica &#40;Unidad de Detecci&#243;n y Tratamiento de Enfermedades Aterotromb&#243;ticas &#91;UDETMA&#93; del Hospital Universitario Arnau de Vilanova de Lleida&#41;&#46; Los criterios de exclusi&#243;n para ambos grupos incluyeron&#58; <span class="elsevierStyleItalic">1&#41;</span> edad &#60;<span class="elsevierStyleHsp" style=""></span>30 o &#62;<span class="elsevierStyleHsp" style=""></span>75 a&#241;os&#59; <span class="elsevierStyleItalic">2&#41;</span> cirrosis descompensada&#59; <span class="elsevierStyleItalic">3&#41;</span> presencia de carcinoma hepatocelular u otros tumores&#59; <span class="elsevierStyleItalic">4&#41;</span> enfermedad hep&#225;tica cr&#243;nica no VHC &#40;por alcohol&#44; virus hepatitis B&#44; patolog&#237;a autoinmune o por dep&#243;sito de hierro&#41;&#59; <span class="elsevierStyleItalic">5&#41;</span> infecci&#243;n por VIH&#59; <span class="elsevierStyleItalic">6&#41;</span> enfermedad inflamatoria o infecciosa aguda o cr&#243;nica&#59; <span class="elsevierStyleItalic">7&#41;</span> antecedentes de eventos cardiovasculares previos seg&#250;n la Clasificaci&#243;n Internacional de Enfermedades&#44; 10&#46;<span class="elsevierStyleSup">a</span> revisi&#243;n &#40;ICD10-CM&#41; &#91;a&#41; enfermedad cerebrovascular&#58; ataque isqu&#233;mico transitorio y&#47;o accidente cerebrovascular estable&#59; b&#41; enfermedad card&#237;aca isqu&#233;mica&#58; infarto agudo de miocardio&#44; angina de pecho inestable&#44; arritmias y&#47;o insuficiencia card&#237;aca congestiva&#59; c&#41; enfermedad arterial perif&#233;rica de las extremidades inferiores o aneurisma a&#243;rtico&#93;&#59; <span class="elsevierStyleItalic">8&#41;</span> insuficiencia renal cr&#243;nica &#40;ecuaci&#243;n CKD-EPI<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>60<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#47;1&#44;73 m<span class="elsevierStyleSup">2</span>&#41;&#59; <span class="elsevierStyleItalic">9&#41;</span> diagn&#243;stico de diabetes mellitus&#59; <span class="elsevierStyleItalic">10&#41;</span> pacientes con dislipidemia tratados con hipolipemiantes&#59; <span class="elsevierStyleItalic">11&#41;</span> antecedentes de hipertensi&#243;n arterial &#40;HTA&#41; en tratamiento&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Todos los pacientes firmaron un consentimiento informado antes de entrar en el estudio&#44; que fue aprobado por el comit&#233; de &#233;tica de los 2 hospitales involucrados&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Datos cl&#237;nicos y anal&#237;ticos</span><p id="par0030" class="elsevierStylePara elsevierViewall">Los datos cl&#237;nicos fueron recogidos en una entrevista estandarizada en la visita de seguimiento de consultas&#46; Se utilizaron muestras de sangre en ayunas para medir los siguientes par&#225;metros s&#233;ricos&#58; glucosa&#44; colesterol total &#40;CT&#41;&#44; colesterol LDL y HDL&#44; triglic&#233;ridos &#40;TG&#41;&#44; creatinina y prote&#237;na C reactiva &#40;PCR&#41;&#46; Se calcularon los coeficientes lip&#237;dicos&#58; colesterol no HDL &#40;colesterol total<span class="elsevierStyleHsp" style=""></span>&#8722;<span class="elsevierStyleHsp" style=""></span>colesterol HDL&#41;&#44; TG&#47;HDL colesterol &#40;indicador de resistencia a la insulina&#41; y CT&#47;HDL colesterol &#40;&#237;ndice aterog&#233;nico&#41;&#44; realizando todas las determinaciones en el mismo laboratorio&#46; Las mediciones antropom&#233;tricas &#40;peso y altura&#41; para el c&#225;lculo del &#237;ndice de masa corporal &#40;IMC&#41; y la presi&#243;n arterial se registraron en la UDETMA antes de realizar la ecograf&#237;a arterial&#46; La presi&#243;n arterial sist&#243;lica y diast&#243;lica se midi&#243; en 3 ocasiones en posici&#243;n sedestaci&#243;n&#44; y tras 10<span class="elsevierStyleHsp" style=""></span>min de reposo&#44; utilizando un oscil&#243;metro autom&#225;tico &#40;OMRON HEM-705 CP<span class="elsevierStyleSup">&#174;</span>&#41;&#46; Se registr&#243; la media de las 2 &#250;ltimas mediciones&#46; Los pacientes tambi&#233;n fueron clasificados de acuerdo con su historial de tabaquismo como fumadores&#44; exfumadores o no fumadores&#46; El riesgo cardiovascular se calcul&#243; utilizando las tablas de riesgo SCORE<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">21</span></a>&#46; En el grupo de pacientes con hepatitis cr&#243;nica&#44; la carga viral de ARN del VHC se analiz&#243; mediante transcripci&#243;n inversa-reacci&#243;n en cadena de la polimerasa &#40;RT-PCR&#41;&#44; con un l&#237;mite de detecci&#243;n de 12<span class="elsevierStyleHsp" style=""></span>UI&#47;ml&#46; Se realiz&#243; elastograf&#237;a de transici&#243;n hep&#225;tica &#40;Fibroscan<span class="elsevierStyleSup">&#174;</span> &#91;FS&#93;&#44; Echosens&#44; Par&#237;s&#44; Francia&#41; para valorar el grado de fibrosis hep&#225;tica clasific&#225;ndolo as&#237;&#58; menor de 7&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; no fibrosis &#40;F0-1&#41;&#59; de 7&#44;6-9&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; fibrosis moderada &#40;F2&#41;&#59; de 9&#44;6-12&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; fibrosis significativa &#40;F3&#41;&#59; y mayor de 12&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; cirrosis hep&#225;tica &#40;F4&#41;&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Evaluaci&#243;n de la ateromatosis arterial subcl&#237;nica</span><p id="par0035" class="elsevierStylePara elsevierViewall">La presencia de placas de ateroma en territorios carot&#237;deo y femoral se determin&#243; usando un ec&#243;grafo General Electric &#40;modelo Vivid-I<span class="elsevierStyleSup">&#174;</span>&#41; con una sonda vascular 12L-RS siguiendo un m&#233;todo estandarizado descrito previamente<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a>&#46; Todas las im&#225;genes fueron capturadas y le&#237;das por un &#250;nico equipo&#44; formado por profesionales previamente acreditados&#46; El coeficiente de kappa para la confiabilidad intraobservador se estableci&#243; en 1&#46; La placa de ateroma se defini&#243; como una estructura focal que sobresale en la luz vascular&#44; o un grosor &#237;ntima-media &#40;GIMc&#41; &#62;<span class="elsevierStyleHsp" style=""></span>1&#44;5<span class="elsevierStyleHsp" style=""></span>mm&#44; de acuerdo con el consenso de Mannheim<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">23</span></a>&#46; Se analizaron 12 territorios vasculares para diagnosticar presencia de placa de ateroma&#58; se exploraron arterias car&#243;tidas &#40;com&#250;n&#44; bifurcaci&#243;n&#44; interna y externa&#41; y arterias femorales &#40;comunes y superficiales&#41; de forma bilateral&#44; utilizando un plano axial y longitudinal&#44; con ultrasonograf&#237;a eco-Doppler en modo B y eco-color&#46; Se defini&#243; ateromatosis subcl&#237;nica como la presencia de una o m&#225;s placas en cualquiera de los territorios estudiados&#46; Se midi&#243; el GIM carot&#237;deo&#44; en el segmento distal de la arteria siendo el valor final la media del territorio carot&#237;deo&#44; en los pacientes sin placas de ateroma&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">An&#225;lisis estad&#237;stico</span><p id="par0040" class="elsevierStylePara elsevierViewall">Las variables categ&#243;ricas se describieron como frecuencia y porcentaje y se compararon usando la prueba de Chi-cuadrado de Pearson&#46; Las variables cuantitativas se describieron como la mediana y el intervalo intercuartil &#40;IQR&#41;&#44; o la media y desviaci&#243;n est&#225;ndar &#40;DE&#41; seg&#250;n su distribuci&#243;n&#46; Las variables distribuidas normalmente se compararon mediante la prueba t de Student&#44; mientras que la prueba no param&#233;trica de Mann-Whitney se utiliz&#243; para comparar variables no normalmente distribuidas&#46; Las variables que muestran diferencias significativas entre los pacientes con y sin placas de ateroma se incluyeron en una regresi&#243;n log&#237;stica m&#250;ltiple condicional por pasos hacia atr&#225;s para predecir la presencia de placas de ateroma&#46; Se utiliz&#243; un an&#225;lisis de las caracter&#237;sticas del operador receptor &#40;ROC&#41; para establecer un l&#237;mite para edad&#44; y se calcul&#243; la presencia de placa seg&#250;n la edad de la poblaci&#243;n a estudio&#44; transformando la variable cuantitativa en variable dicot&#243;mica de acuerdo con los valores de corte obtenidos&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Se estudi&#243; la asociaci&#243;n de las modificaciones del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica por ANOVA y la existencia de correlaci&#243;n entre la carga viral y los l&#237;pidos por R de Spearman&#46; La significaci&#243;n estad&#237;stica se estableci&#243; en un valor &#945; bilateral &#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#44; y todos los an&#225;lisis se realizaron utilizando el software SPSS &#40;IBM Statistics for Windows&#44; versi&#243;n 20&#46;0&#44; Armonk&#44; NY&#58; IBM Corp&#46;&#41;&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Resultados</span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Caracter&#237;sticas de la poblaci&#243;n estudiada</span><p id="par0050" class="elsevierStylePara elsevierViewall">La muestra del estudio incluy&#243; 204 pacientes&#58; 102 en el grupo con VHC positivo y 102 en el grupo control&#46; La <a class="elsevierStyleCrossRef" href="#tbl0005">tabla 1</a> describe los datos cl&#237;nicos y de laboratorio relativos a ambas poblaciones&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">Los grupos estudiados no presentaron diferencias estad&#237;sticamente significativas en cuanto a sexo&#44; edad ni historia de tabaquismo&#46; El grupo control present&#243; valores significativamente m&#225;s altos en la mayor&#237;a de los factores de riesgo cardiovasculares tradicionales&#44; incluyendo el IMC&#44; la presi&#243;n arterial sist&#243;lica y diast&#243;lica&#44; y el perfil de l&#237;pidos s&#233;ricos&#46; No se observaron diferencias significativas en cuanto a las cifras de glucosa&#44; triglic&#233;ridos&#44; ni en el coeficiente TG&#47;HDL o indicador de resistencia a la insulina&#44; aunque los niveles fueron en todos los casos superiores en los pacientes control &#40;96&#44;5 vs&#46; 94&#44;2<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;888&#59; 121&#44;5 vs&#46; 102&#44;9<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;070&#59; y 2&#44;3 vs&#46; 2&#44;1&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;449&#41;&#46; Adem&#225;s&#44; los pacientes control presentaron niveles significativamente superiores de creatinina s&#233;rica&#44; de PCR y de &#237;ndice de riesgo cardiovascular &#40;SCORE&#41;&#44; aunque el riesgo era bajo-moderado en ambos grupos&#46; En los pacientes con infecci&#243;n cr&#243;nica por VHC&#44; casi un 55&#37; presentaba enfermedad hep&#225;tica avanzada &#40;de ellos&#44; el 29&#44;4&#37; cirrosis o fibrosis grado 4 por elastograf&#237;a hep&#225;tica&#41;&#46; Un 67&#44;2&#37; eran genotipo 1&#44; un 6&#44;7&#37; genotipo 2&#44; un 9&#44;7&#37; genotipo 3 y el 16&#44;4&#37; genotipo 4&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">El porcentaje de pacientes con ateromatosis fue significativamente mayor en el grupo con VHC positivo que en el grupo control &#40;58&#44;8 vs&#46; 28&#44;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; sin observarse diferencias significativas en el GIM carot&#237;deo medido en los pacientes sin ateromatosis &#40;0&#44;76 vs&#46; 0&#44;89<span class="elsevierStyleHsp" style=""></span>mm&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;18&#41; aunque fue superior en los pacientes infectados&#46; En el grupo control las placas se distribuyeron un 35&#37; en territorio carot&#237;deo&#44; un 23&#44;9&#37; en territorio femoral y un 41&#44;1&#37; en ambos territorios&#44; mientras que en los pacientes infectados con VHC un 45&#44;3&#37; de placas de ateroma se detectaron en car&#243;tidas&#44; un 19&#44;8&#37; en femorales y un 34&#44;9&#37; en ambas &#225;reas vasculares&#46; El n&#250;mero medio de placas de ateroma fue de 2&#44;95 &#40;1-10&#41; en pacientes infectados frente a 2&#44;44 &#40;1-8&#41; en los pacientes no infectados&#46; No se observaron diferencias significativas entre las poblaciones ni por territorio vascular afecto &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;710&#41; ni por el n&#250;mero de placas medio detectado &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;420&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">En la <a class="elsevierStyleCrossRef" href="#tbl0010">tabla 2</a> se analizan los factores asociados a la presencia de placa de ateroma en cada una de las poblaciones estudiadas&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0070" class="elsevierStylePara elsevierViewall">La presencia de placa de ateroma en ambos grupos &#40;con y sin infecci&#243;n por VHC&#41; se asoci&#243; de forma estad&#237;sticamente significativa al sexo masculino&#44; a cifras superiores de presi&#243;n arterial&#44; a niveles elevados de triglic&#233;ridos&#44; y a un mayor riesgo cardiovascular seg&#250;n las tablas &#40;SCORE&#41;&#46; Respecto a la edad&#44; no se observ&#243; asociaci&#243;n con la presencia de placa de ateroma en los pacientes infectados&#44; mientras que s&#237; que se identific&#243; en el grupo control&#44; de manera que la presencia de placa se asoci&#243; a mayor edad &#40;51&#44;8 a&#241;os en pacientes control sin ateromatosis vs&#46; 67&#44;3 a&#241;os en pacientes control con ateromatosis&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; Respecto al h&#225;bito tab&#225;quico&#44; se detect&#243; asociaci&#243;n en los pacientes con VHC &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;003&#41; siendo m&#225;s frecuente la placa en los pacientes fumadores y&#47;o exfumadores &#40;81&#44;6&#37;&#41;&#59; pero no en los controles &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;499&#41;&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">En cuanto al perfil lip&#237;dico&#44; los pacientes VHC con placa presentaban menores cifras de colesterol HDL &#40;57&#44;6 vs&#46; 50&#44;9<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;023&#41; y mayores niveles de triglic&#233;ridos &#40;89&#44;3 vs&#46; 112&#44;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;029&#41;&#44; coeficiente TG&#47;HDL &#40;1&#44;7 vs&#46; 2&#44;3&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;026&#41; y coeficiente CT&#47;HDL &#40;3 vs&#46; 3&#44;4&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;035&#41; que los pacientes infectados sin placa&#46; No se ha observado significaci&#243;n de estos factores lip&#237;dicos entre los pacientes controles sin o con presencia de placa de ateroma&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">Respecto a los factores virales en los pacientes infectados por VHC&#44; no se detect&#243; asociaci&#243;n entre la presencia de placa y la carga viral cuantificada por ARN &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;936&#41;&#44; pero s&#237; se encontraron diferencias significativas con el grado de fibrosis hep&#225;tica&#44; siendo m&#225;s frecuente la presencia de placa en los pacientes con fibrosis avanzada &#40;F4 sin ateroma 23&#44;8&#37; vs&#46; F4 con ateromatosis 33&#44;3&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;016&#41;&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">Se analiz&#243; la edad&#44; seg&#250;n el an&#225;lisis de la ROC&#44; y la edad superior a 54 a&#241;os fue el mejor valor de corte para predecir la presencia de placas de ateroma &#40;AUC<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;682&#44; error est&#225;ndar<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;039 &#91;IC 95&#37;&#58; 0&#44;6-0&#44;7&#93;&#44; 67&#37; de sensibilidad y 60&#37; de especificidad&#41;&#46; Por debajo de este punto de corte &#40;&#60;<span class="elsevierStyleHsp" style=""></span>54 a&#241;os&#41;&#44; el porcentaje de pacientes con placas de ateroma fue del 57&#37; en el grupo VHC positivo y del 4&#37; en el grupo control &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; En los pacientes con edad mayor o igual a 54 a&#241;os&#44; la ateromatosis aument&#243; hasta un 61&#37; en el grupo con VHC positivo y hasta el 50&#37; en el grupo control&#44; sin observarse diferencias significativas en este tramo de edad entre poblaciones &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;252&#41;&#46; En el grupo con edad menor de 54 a&#241;os&#44; los pacientes con VHC positivo ten&#237;an mucha m&#225;s probabilidad de ateromatosis que el grupo control &#40;OR &#61; 30&#59; IC95&#37;&#58; 6&#44;58-136&#44;67&#59; p &#60; 0&#44;001&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0010">fig&#46; 2</a>&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Factores asociados con ateromatosis subcl&#237;nica</span><p id="par0090" class="elsevierStylePara elsevierViewall">La <a class="elsevierStyleCrossRef" href="#tbl0015">tabla 3</a> muestra las caracter&#237;sticas cl&#237;nicas de los pacientes con y sin ateromatosis subcl&#237;nica&#46; La infecci&#243;n cr&#243;nica por VHC se asoci&#243; significativamente a la presencia de ateromatosis subcl&#237;nica&#44; al igual que los factores de riesgo cardiovascular tradicionales como el sexo masculino&#44; la edad avanzada&#44; la presi&#243;n arterial sist&#243;lica&#44; puntuaciones elevadas en el SCORE&#44; los niveles s&#233;ricos bajos de colesterol HDL y m&#225;s elevados de triglic&#233;ridos&#46; Tambi&#233;n se asoci&#243; con valores incrementados del cociente TG&#47;HDL&#46; La presencia de placas de ateroma no se asoci&#243; con el IMC&#44; los niveles de glucosa ni los valores de PCR&#46; Tampoco se observ&#243; asociaci&#243;n con el perfil lip&#237;dico formado por colesterol total&#44; LDL y colesterol no HDL&#44; ni con el &#237;ndice aterog&#233;nico &#40;CT&#47;HDL&#41;&#46;</p><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><p id="par0095" class="elsevierStylePara elsevierViewall">El an&#225;lisis multivariado revel&#243; una probabilidad muy superior de ateromatosis en pacientes con VHC positivo en comparaci&#243;n con el grupo control &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37 &#91;5&#44;5-37&#44;5&#93;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41; &#40;<a class="elsevierStyleCrossRef" href="#tbl0015">tabla 3</a>&#41;&#46; Otros factores de riesgo independientes de ateromatosis subcl&#237;nica incluyeron el sexo masculino&#44; la edad avanzada y el mayor coeficiente TG&#47;HDL o indicador indirecto de resistencia a la insulina&#46; Ni la presi&#243;n arterial sist&#243;lica&#44; ni el perfil lip&#237;dico contribuyeron al modelo predictivo para la presencia de placas de ateroma&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Descripci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en los pacientes con VHC en relaci&#243;n con la presencia de placa de ateroma</span><p id="par0100" class="elsevierStylePara elsevierViewall">Analizamos el perfil lip&#237;dico en los pacientes VHC con y sin enfermedad ateromatosa&#44; teniendo en cuenta el grado de fibrosis hep&#225;tica medida mediante elastograf&#237;a&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">En los pacientes VHC sin enfermedad ateromatosa&#44; no observamos diferencias significativas en ninguno de los valores del perfil lip&#237;dico tradicional&#44; ni en los coeficientes indicativos de resistencia a la insulina &#40;TG&#47;HDL&#41; ni en el factor aterog&#233;nico &#40;CT&#47;HDL&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>a y b&#41;&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0110" class="elsevierStylePara elsevierViewall">En los pacientes VHC con enfermedad ateromatosa &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>c y d&#41;&#44; se observaron diferencias significativas en las cifras de colesterol total &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;018&#41;&#44; en los niveles de colesterol no HDL &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;002&#41; y de colesterol LDL &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;002&#41;&#44; as&#237; como en el &#237;ndice aterog&#233;nico &#40;CT&#47;HDL&#41; &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; con tendencia a aumentar a medida que progresa la fibrosis hep&#225;tica&#44; y disminuyendo significativamente en presencia de cirrosis&#46; No se observaron cambios en los niveles de colesterol HDL&#44; triglic&#233;ridos ni en el coeficiente TG&#47;HDL y los grados de fibrosis en presencia de placa de ateroma&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Al analizar la correlaci&#243;n entre la carga viral y el perfil lip&#237;dico&#44; tan solo se detect&#243; una leve asociaci&#243;n entre el ARN del VHC y los niveles de colesterol no HDL &#40;r<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;219&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;04&#41;&#44; sin detectarse asociaci&#243;n con ning&#250;n otro par&#225;metro anal&#237;tico&#46;</p></span></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Discusi&#243;n</span><p id="par0120" class="elsevierStylePara elsevierViewall">Este estudio observacional analiza la presencia de enfermedad ateromatosa en sujetos con y sin infecci&#243;n cr&#243;nica por VHC&#44; encontrando que los pacientes infectados tienen mayor presencia de ateromatosis subcl&#237;nica y en edades m&#225;s precoces que los controles&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Nuestros resultados concuerdan con lo publicado recientemente en 2 metaan&#225;lisis que describen una mayor presencia de ateromatosis en poblaciones infectadas por VHC &#40;entre un 38 y un 65&#37;&#41;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">5&#44;6</span></a>&#46; En estos estudios&#44; las placas de ateroma se identificaron por ecograf&#237;a Doppler vascular&#44; y el diagn&#243;stico se estableci&#243; con un valor de GIMc<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1&#44;3<span class="elsevierStyleHsp" style=""></span>mm<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">20</span></a>&#46; En nuestro trabajo se siguieron los criterios de Manheim para el diagn&#243;stico de ateromatosis&#44; definiendo la placa como un GIMc<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1&#44;5<span class="elsevierStyleHsp" style=""></span>mm&#46; Una de las posibles razones de nuestra tasa m&#225;s elevada es la ampliaci&#243;n del estudio femoral&#44; que aumenta la probabilidad de detectar ateromatosis&#46; Se ha publicado la existencia de enfermedad ateromatosa en territorio femoral en ausencia de placas carot&#237;deas en poblaci&#243;n general<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">24</span></a>&#46; Adem&#225;s&#44; nosotros tambi&#233;n analizamos diferentes genotipos virales&#44; que no han sido evaluados en estudios previamente publicados<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">20</span></a>&#44; aunque es conocido que el genotipo 3 produce m&#225;s alteraciones metab&#243;licas que el resto<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">25&#44;26</span></a>&#46; Aunque la presencia de placa fue mayor en los pacientes infectados&#44; estos presentaban un bajo &#237;ndice de riesgo cardiovascular seg&#250;n las tablas SCORE European Risk Chart&#46; Varios estudios poblacionales han demostrado asociaci&#243;n entre la presencia de placas en arterias perif&#233;ricas e incidencia de eventos cardiovasculares&#44; incluso en sujetos sin eventos previos &#40;1&#44;8 veces el aumento del riesgo de eventos coronarios y 4&#44;1 veces el aumento del riesgo de eventos cardiovasculares&#41;<a class="elsevierStyleCrossRefs" href="#bib0315"><span class="elsevierStyleSup">27&#44;28</span></a>&#46; En l&#237;nea con estas publicaciones&#44; la presencia de placas de ateroma en nuestra poblaci&#243;n no se asoci&#243; con factores de riesgo cardiovascular tradicionales como el IMC&#44; la glucemia o la dislipidemia&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">Nuestro estudio involucra la primera cohorte espa&#241;ola de pacientes monoinfectados con VHC cr&#243;nica&#44; aunque cuenta con las limitaciones intr&#237;nsecas de un dise&#241;o transversal y del sesgo de selecci&#243;n en los pacientes controles&#44; ya que pertenecen a un grupo de pacientes de una consulta de riesgo cardiovascular&#46; Para minimizar este sesgo&#44; limitamos los criterios de selecci&#243;n a sujetos con riesgo bajo a moderado &#40;probabilidad &#60;<span class="elsevierStyleHsp" style=""></span>5&#37; de experimentar eventos cardiovasculares a los 10 a&#241;os&#41; sin presencia de enfermedad cardiovascular previa ni toma de f&#225;rmacos para hipertensi&#243;n ni dislipidemia&#46; Excluimos los pacientes con diabetes y enfermedad renal cr&#243;nica para evitar factores de confusi&#243;n&#46; Algunas publicaciones identifican que el virus VHC promueve el desarrollo de diabetes e insuficiencia renal cr&#243;nica&#44; lo que predispone a la presencia de lesiones ateromatosas<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">16</span></a>&#46; Tambi&#233;n podr&#237;a crear confusi&#243;n el hecho de observar una mayor presencia de exfumadores o fumadores activos entre aquellos con placa VHC&#43;&#44; as&#237; como las diferencias entre el grado de fibrosis hep&#225;tica en los sujetos con y sin placa&#59; pero tal como demuestra el an&#225;lisis multivariante&#44; ni el tabaquismo ni la fibrosis influ&#237;an en el desarrollo de las placas de ateroma&#44; mientras que s&#237; se observ&#243; una asociaci&#243;n elevada &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37&#41; del VHC <span class="elsevierStyleItalic">per se</span>&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">Ante estos resultados&#44; identificamos como factor independiente de ateromatosis la infecci&#243;n cr&#243;nica por VHC sin influencia de otros factores cardiovasculares tradicionalmente conocidos&#44; lo que sugiere un papel directo del VHC en el desarrollo de las lesiones ateromatosas&#46; Estudios recientes han demostrado la presencia de ARN del VHC en la placa carot&#237;dea<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">14&#44;15</span></a> y por el entorno proinflamatorio que induce el virus<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">4-12</span></a>&#46; En nuestro estudio&#44; los niveles de PCR marcador de riesgo cardiovascular e inflamaci&#243;n sist&#233;mica&#44; ampliamente aceptado para la poblaci&#243;n<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a>&#44; no mostraron diferencias significativas entre ambos grupos&#44; si bien las prote&#237;nas de s&#237;ntesis hep&#225;ticas como PCR pueden estar alteradas en pacientes con enfermedad hep&#225;tica cr&#243;nica&#46; Adem&#225;s&#44; detectamos que la presencia de ateromatosis en la poblaci&#243;n VHC se desarrolla en edades mucho m&#225;s tempranas que en el grupo sin infecci&#243;n&#46; Tal y como se observa en la <a class="elsevierStyleCrossRef" href="#fig0010">figura 2</a>&#44; hemos encontrado que por debajo de 54 a&#241;os existen diferencias significativas de presencia de placa en los pacientes infectados frente a los controles&#46; Este hallazgo sugiere que los pacientes con infecci&#243;n por VHC presentan ateromatosis acelerada o envejecimiento vascular prematuro&#44; de forma similar a lo observado en otras enfermedades cr&#243;nicas inflamatorias y autoinmunes<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">29</span></a>&#46; Adem&#225;s de la edad y la infecci&#243;n por VHC&#44; el sexo masculino y el coeficiente TG&#47;HDL &#40;marcador indirecto de insulinorresistencia&#41; fueron los &#250;nicos factores significativamente asociados con la presencia de ateromatosis&#46; Este coeficiente es un &#237;ndice predictivo pron&#243;stico de enfermedad cardiovascular&#44; utilizado como marcador de aterog&#233;nesis en poblaci&#243;n general&#44; y aunque hay pocos datos&#44; su valor predictivo en cardiopat&#237;a es alto<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">30</span></a>&#46; Adem&#225;s&#44; es un buen marcador de aterog&#233;nesis en la poblaci&#243;n infectada&#44; ya que no se modifica significativamente con la progresi&#243;n de la enfermedad hep&#225;tica ni con la carga viral&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">En este trabajo&#44; analizamos la modificaci&#243;n del perfil lip&#237;dico en diferentes estadios de progresi&#243;n de enfermedad hep&#225;tica medida por elastograf&#237;a &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>&#41;&#44; detectando que en los pacientes infectados sin placa de ateroma no existen diferencias en cuanto a los niveles de l&#237;pidos s&#233;ricos y la fibrosis hep&#225;tica&#46; Pero en los pacientes VHC con ateromatosis&#44; las part&#237;culas m&#225;s aterog&#233;nicas &#40;formadas por LDL y VLDL&#41;&#44; que son el transportador principal del VHC en plasma&#44; aumentan conforme progresa la fibrosis&#44; y descienden significativamente al establecerse la cirrosis hep&#225;tica&#46; Estas part&#237;culas m&#225;s aterog&#233;nicas se correlacionan d&#233;bilmente con la carga viral&#44; sin observar asociaci&#243;n con el desarrollo de placa de ateroma&#44; lo que podr&#237;a deberse a la fluctuaci&#243;n en el tiempo de la viremia o a que estos valores dependen de la progresi&#243;n de la fibrosis hep&#225;tica&#44; descendiendo en estadios de cirrosis&#46;</p><p id="par0145" class="elsevierStylePara elsevierViewall">En resumen&#44; nuestros resultados muestran que los pacientes con infecci&#243;n cr&#243;nica por VHC tienen una mayor prevalencia de ateromatosis subcl&#237;nica que la poblaci&#243;n no infectada&#44; con inicio en edades precoces &#40;ateromatosis acelerada&#41;&#46; El perfil metab&#243;lico y la valoraci&#243;n del riesgo cardiovascular mediante el uso de las tablas tradicionales no son buenos predictores&#44; ya que la mayor&#237;a de estos pacientes presentan SCORES de bajo riesgo y un perfil lip&#237;dico tambi&#233;n de &#171;bajo riesgo&#187; &#40;menores cifras de colesterol no HDL y de colesterol LDL&#41;&#46; Esto apoya la necesidad de pruebas cardiovasculares no invasivas adicionales de uso rutinario&#44; como la ecograf&#237;a arterial&#44; que podr&#237;a mejorar la estratificaci&#243;n del riesgo en esta poblaci&#243;n&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Conflicto de intereses</span><p id="par0150" class="elsevierStylePara elsevierViewall">Los autores declaran no tener ning&#250;n conflicto de intereses&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Introducci&#243;n</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Se desconoce la asociaci&#243;n entre ateromatosis subcl&#237;nica e infecci&#243;n cr&#243;nica por el virus de la hepatitis C &#40;VHC&#41;&#44; relevante ahora que los antivirales mejoran la supervivencia en los pacientes infectados&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Objetivos</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Conocer si el VHC es factor de riesgo independiente de ateromatosis subcl&#237;nica y analizar las modificaciones del perfil lip&#237;dico seg&#250;n niveles de ARN viral y fibrosis hep&#225;tica&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Pacientes y m&#233;todos</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Estudio observacional y transversal&#59; incluye 102 pacientes VHC positivos y 102 sujetos VHC negativos con paridad de sexo y edad&#44; sin antecedentes de enfermedad cardiovascular&#44; renal ni diabetes&#46; La ateromatosis &#40;presencia de placas de ateroma&#41; y el grosor &#237;ntima-media carot&#237;deo &#40;GIMc&#41; se evalu&#243; mediante ecograf&#237;a de arterias car&#243;tidas y femorales&#46;</p></span> <span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Resultados</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La presencia de ateromatosis en cualquier territorio vascular fue mayor en pacientes VHC que en sujetos no infectados &#40;58&#44;8&#37; frente a 28&#44;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; En el an&#225;lisis multivariante&#44; los factores significativamente asociados con ateromatosis incluyeron infecci&#243;n por VHC &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37 &#91;5&#44;5-37&#44;3&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; edad &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>1&#44;12 &#91;1&#44;1-1&#44;2&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; sexo masculino &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>4&#44;32 &#91;1&#44;9-9&#44;5&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41; y el coeficiente triglic&#233;ridos&#47;colesterol HDL &#40;TG&#47;HDL-indicador indirecto de insulinorresistencia&#41; &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>1&#44;34 &#91;1&#44;1-1&#44;6&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;007&#41;&#46; Los pacientes VHC con placas de ateroma presentaban mayor coeficiente TG&#47;HDL&#44; sin diferencias significativas en cuanto a la carga viral ni grado de fibrosis hep&#225;tica con un perfil lip&#237;dico de &#171;bajo riesgo&#187;&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Conclusiones</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">La infecci&#243;n VHC es factor de riesgo independiente de ateromatosis subcl&#237;nica&#46; La ecograf&#237;a arterial sist&#233;mica en esta poblaci&#243;n mejora la evaluaci&#243;n del riesgo cardiovascular m&#225;s all&#225; de las alteraciones del perfil lip&#237;dico y del c&#225;lculo de riesgo por tablas SCORE&#46;</p></span>"
        "secciones" => array:5 [
          0 => array:2 [
            "identificador" => "abst0005"
            "titulo" => "Introducci&#243;n"
          ]
          1 => array:2 [
            "identificador" => "abst0010"
            "titulo" => "Objetivos"
          ]
          2 => array:2 [
            "identificador" => "abst0015"
            "titulo" => "Pacientes y m&#233;todos"
          ]
          3 => array:2 [
            "identificador" => "abst0020"
            "titulo" => "Resultados"
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          4 => array:2 [
            "identificador" => "abst0025"
            "titulo" => "Conclusiones"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Background</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">The association between subclinical atheromatosis and chronic hepatitis C virus &#40;HCV&#41; infection is unknown but is relevant now that antivirals are improving the survival of patients with the infection&#46;</p></span> <span id="abst0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Objectives</span><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis&#46;</p></span> <span id="abst0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Patients and methods</span><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">We conducted an observational&#44; cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age&#44; with no history of cardiovascular or kidney disease or diabetes&#46; Atheromatosis &#40;the presence of atheromatous plaques&#41; and the carotid intima-media thickness &#40;CIMT&#41; were assessed using ultrasonography of the carotid and femoral arteries&#46;</p></span> <span id="abst0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Results</span><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection &#40;58&#46;8&#37; vs&#46; 28&#46;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;0001&#41;&#46; In the multivariate analysis&#44; the factors significantly associated with atheromatosis included HCV infection &#40;OR&#44; 14&#46;37 &#91;5&#46;5-37&#46;3&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41;&#44; age &#40;OR&#44; 1&#46;12 &#91;1&#46;1-1&#46;2&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41;&#44; male sex &#40;OR&#44; 4&#46;32 &#91;1&#46;9-9&#46;5&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41; and the triglyceride&#47;HDL cholesterol coefficient &#40;TG&#47;HDL-indirect indicator of insulin resistance&#41; &#40;OR&#44; 1&#46;34 &#91;1&#46;1-1&#46;6&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>&#46;007&#41;&#46; The HCV-positive patients with atheromatous plaques had a higher TG&#47;HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a &#8216;low risk&#8217; lipid profile&#46;</p></span> <span id="abst0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Conclusions</span><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">HCV infection is an independent risk factor for subclinical atheromatosis&#46; Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables&#46;</p></span>"
        "secciones" => array:5 [
          0 => array:2 [
            "identificador" => "abst0030"
            "titulo" => "Background"
          ]
          1 => array:2 [
            "identificador" => "abst0035"
            "titulo" => "Objectives"
          ]
          2 => array:2 [
            "identificador" => "abst0040"
            "titulo" => "Patients and methods"
          ]
          3 => array:2 [
            "identificador" => "abst0045"
            "titulo" => "Results"
          ]
          4 => array:2 [
            "identificador" => "abst0050"
            "titulo" => "Conclusions"
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        ]
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          "es" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Distribuci&#243;n de las placas de ateroma seg&#250;n el territorio afectado y la carga vascular &#40;n&#250;mero de placas de ateroma&#41; por cada poblaci&#243;n&#46;</p>"
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          "es" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Presencia de placa de ateroma seg&#250;n el grupo de edad &#40;menor o mayor de 54 a&#241;os&#41; y la poblaci&#243;n a estudio&#46;</p>"
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        "etiqueta" => "Figura 3"
        "tipo" => "MULTIMEDIAFIGURA"
        "mostrarFloat" => true
        "mostrarDisplay" => false
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          "es" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Modificaci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en pacientes VHC con presencia y ausencia de placa de ateroma&#46;</p>"
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          "leyenda" => "<p id="spar0075" class="elsevierStyleSimplePara elsevierViewall">CT&#58; colesterol total&#59; GIMc&#58; &#237;ndice de masa corporal&#59; HDL&#58; lipoprote&#237;na de alta densidad&#59; IMT&#58; grosor &#237;ntima-media&#59; LDL&#58; lipoprote&#237;na de baja densidad&#59; NS&#58; no significativo&#59; PAD&#58; presi&#243;n arterial diast&#243;lica&#59; PAS&#58; presi&#243;n arterial sist&#243;lica&#59; PCR&#58; prote&#237;na C reactiva&#59; TG&#58; triglic&#233;ridos&#59; VHC&#58; virus de la hepatitis C&#46;</p><p id="spar0080" class="elsevierStyleSimplePara elsevierViewall">Variable cuantitativa&#58; media &#40;DE&#44; rango&#41;&#46;</p><p id="spar0085" class="elsevierStyleSimplePara elsevierViewall">Variable cualitativa&#58; n &#40;&#37;&#41;&#46;</p><p id="spar0090" class="elsevierStyleSimplePara elsevierViewall">Umbral significativo&#58; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#46;</p>"
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                  \t\t\t\t" scope="col" style="border-bottom: 2px solid black">&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t" scope="col" style="border-bottom: 2px solid black">VHC positivo &#40;N<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>102&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">50 &#40;49&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">53 &#40;52&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">NS&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>No fumador&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">30 &#40;29&#44;4&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">37 &#40;36&#44;3&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Fumador&#47;exfumador&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">72 &#40;70&#44;6&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
                  \t\t\t\t\ttop\n
                  \t\t\t\t"><span class="elsevierStyleItalic">IMC &#40;kg&#47;m</span><span class="elsevierStyleSup"><span class="elsevierStyleItalic">2</span></span><span class="elsevierStyleItalic">&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t">26&#44;4 &#40;4&#44;1&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">27&#44;8 &#40;5&#44;1&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">0&#44;024&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">PAS &#40;mmHg&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">124 &#40;16&#44;2&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">135 &#40;20&#44;8&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="\n
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                  \t\t\t\t\ttop\n
                  \t\t\t\t">147&#44;2 &#40;16&#44;6&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">No HDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t" scope="col" style="border-bottom: 2px solid black">An&#225;lisis multivariante</th></tr><tr title="table-row"><th class="td" title="\n
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                  \t\t\t\t  " align="" valign="\n
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                  \t\t\t\t" scope="col" style="border-bottom: 2px solid black">&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t" scope="col" style="border-bottom: 2px solid black">OR &#40;IC 95&#37;&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t" scope="col" style="border-bottom: 2px solid black">p&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Sexo masculino</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">43 &#40;37&#44;4&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">60 &#40;67&#44;4&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">4&#44;32 &#40;1&#44;9-9&#44;5&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Edad &#40;a&#241;os&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">1&#44;12 &#40;1&#44;1-1&#44;2&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Infecci&#243;n cr&#243;nica por VHC</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">42 &#40;36&#44;5&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">60 &#40;67&#44;4&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">14&#44;37 &#40;5&#44;5-37&#44;3&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">H&#225;bito tab&#225;quico</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">NS&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>No fumador&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t  " align="left" valign="\n
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                  \t\t\t\t">23 &#40;25&#44;8&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleHsp" style=""></span>Fumador&#47;exfumador&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">71 &#40;61&#44;7&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">66 &#40;74&#44;2&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">IMC &#40;kg&#47;my&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">27 &#40;4&#44;1&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">PAS &#40;mmHg&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">PAD &#40;mmHg&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Glucemia &#40;g&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Creatinina &#40;g&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">NS&nbsp;\t\t\t\t\t\t\n
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                  "referenciaCompleta" => "World Health Organization&#46; Hepatitis C n&#46;d&#46; &#91;consultado 2018&#93;&#46; Disponible en&#58; <a target="_blank" href="http://www.euro.who.int/en/what-we-do/health-topics/communicable-diseases/hepatitis">http&#58;&#47;&#47;www&#46;euro&#46;who&#46;int&#47;en&#47;what-we-do&#47;health-topics&#47;communicable-diseases&#47;hepatitis</a>"
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                    0 => array:2 [
                      "titulo" => "Hepatitis C en Espa&#241;a"
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                            0 => "M&#46; Bruguera"
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                      "Revista" => array:6 [
                        "tituloSerie" => "Med Clin &#40;Barc&#41;&#46;"
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                        "volumen" => "127"
                        "paginaInicial" => "113"
                        "paginaFinal" => "117"
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                            "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16828003"
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                    0 => array:2 [
                      "titulo" => "Associations between hepatitis C viremia and low serum triglyceride and cholesterol levels&#58; a community-based study"
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                          "etal" => true
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                            0 => "C&#46;Y&#46; Dai"
                            1 => "W&#46;L&#46; Chuang"
                            2 => "C&#46;K&#46; Ho"
                            3 => "M&#46;Y&#46; Hsieh"
                            4 => "J&#46;F&#46; Huang"
                            5 => "L&#46;P&#46; Lee"
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                      "Revista" => array:5 [
                        "tituloSerie" => "J Hepatol&#46;"
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                      "titulo" => "Chronic HCV infection and inflammation&#58; Clinical impact on hepatic and extra-hepatic manifestations"
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                          "etal" => true
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                            2 => "L&#46; Restivo"
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                            4 => "A&#46; Sellitto"
                            5 => "L&#46; Rinaldi"
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                      "doi" => "10.4254/wjh.v5.i10.528"
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ISSN: 00142565
Idioma original: Español
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