{"id":8017,"date":"2024-08-31T17:52:27","date_gmt":"2024-08-31T15:52:27","guid":{"rendered":"https:\/\/gastropedia.pub\/es\/?p=8017"},"modified":"2025-05-10T00:33:02","modified_gmt":"2025-05-09T22:33:02","slug":"sindrome-de-gilbert-que-necesitamos-saber","status":"publish","type":"post","link":"https:\/\/gastropedia.pub\/es\/gastroenterologia\/sindrome-de-gilbert-que-necesitamos-saber\/","title":{"rendered":"S\u00edndrome de Gilbert: \u00bfqu\u00e9 necesitamos saber?"},"content":{"rendered":"\r\n<p>El S\u00edndrome de Gilbert (SG) es un trastorno hep\u00e1tico del metabolismo de la bilirrubina con reducci\u00f3n en la glucuronidaci\u00f3n de la bilirrubina y consecuente hiperbilirrubinemia indirecta (no conjugada).<\/p>\r\n\r\n\r\n\r\n<p>Es una condici\u00f3n com\u00fan (3-10% de la poblaci\u00f3n), con reducci\u00f3n en la actividad de la UGT1A1 en 25-40%. Las mutaciones ocurren en la secuencia de la regi\u00f3n promotora (TATA box) del gen UGT1A1, que tiene la funci\u00f3n de controlar los niveles de la prote\u00edna normal producida. De esta manera, en el SG, la prote\u00edna producida es estructuralmente normal, pero en menor cantidad.<\/p>\r\n\r\n\r\n\r\n<figure class=\"wp-block-table is-style-regular has-normal-font-size\">\r\n<div class=\"pcrstb-wrap\"><table class=\"has-background\" style=\"background-color: #c9cee1;\">\r\n<tbody>\r\n<tr>\r\n<td><strong>Gen UGT1A1<\/strong><br \/>Promueve la producci\u00f3n de la enzima bilirrubina-UGT, responsable de la conjugaci\u00f3n de bilirrubina. Por lo tanto, las mutaciones en la UGT1A1 generan la producci\u00f3n de una prote\u00edna anormal, con p\u00e9rdida completa o niveles menores de actividad de la bilirrubina-UGT.<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table><\/div>\r\n<\/figure>\r\n\r\n\r\n\r\n<h2 id=\"h-apresentacao-clinico-laboratorial\" class=\"wp-block-heading\"><strong>Presentaci\u00f3n cl\u00ednico-laboratorial<\/strong><\/h2>\r\n\r\n\r\n\r\n<p>Cl\u00ednicamente, los pacientes suelen ser asintom\u00e1ticos e identificar elevaciones en los niveles de bilirrubinas totales con predominio de bilirrubina indirecta (&lt;4-5mg\/dL), de forma incidental, o pueden presentar cuadros intermitentes de ictericia, en especial, desencadenados por gatillos como ejercicio f\u00edsico intenso, baja ingesta cal\u00f3rica\/ayuno, per\u00edodo menstrual, deshidrataci\u00f3n e infecciones.<\/p>\r\n\r\n\r\n\r\n<p>Laboratorialmente, no hay elevaci\u00f3n de enzimas hep\u00e1ticas o alteraciones en los dem\u00e1s ex\u00e1menes de funci\u00f3n hep\u00e1tica (tiempo de protrombina y alb\u00famina), adem\u00e1s de no haber indicios de hem\u00f3lisis o enfermedad estructural del h\u00edgado.<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<h2 id=\"h-diagnostico-diferencial\" class=\"wp-block-heading\"><strong>Diagn\u00f3stico diferencial<\/strong><\/h2>\r\n<p>\r\n\r\n<\/p>\r\n<p>Los trastornos en la captaci\u00f3n hep\u00e1tica, almacenamiento, conjugaci\u00f3n y excreci\u00f3n pueden causar hiperbilirrubinemia. Entre las causas hereditarias de hiperbilirrubinemia indirecta, con ex\u00e1menes normales de funci\u00f3n hep\u00e1tica y sin alteraci\u00f3n de la histolog\u00eda hep\u00e1tica, adem\u00e1s del SG, se realiza el diagn\u00f3stico diferencial con:<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<ul class=\"wp-block-list\">\r\n<li><strong>S\u00edndrome de Crigler-Najar tipo I<\/strong>: condici\u00f3n muy rara con herencia autos\u00f3mica recesiva que se manifiesta poco despu\u00e9s del nacimiento. Debido a la ausencia de actividad hep\u00e1tica UGT1A1, se produce ictericia grave (20-45mg\/dL o m\u00e1s) y riesgo de da\u00f1o neurol\u00f3gico y muerte por <em>kernicterus<\/em> (encefalopat\u00eda bilirrub\u00ednica) en los primeros d\u00edas despu\u00e9s del nacimiento. El tratamiento temprano para la reducci\u00f3n de los niveles de bilirrubina indirecta en la sangre es la fototerapia, debi\u00e9ndose considerar la realizaci\u00f3n de trasplante hep\u00e1tico como \u00fanica terapia curativa.<\/li>\r\n\r\n\r\n\r\n<li><strong>S\u00edndrome de Crigler-Najar tipo II<\/strong>: condici\u00f3n rara con herencia autos\u00f3mica recesiva. Hay actividad hep\u00e1tica UGT1A1 de 10% o menos, con ictericia cr\u00f3nica (6-20mg\/dL) y evoluci\u00f3n potencialmente benigna. El tratamiento con fenobarbital propicia la reducci\u00f3n de alrededor del 25-30% de los niveles de bilirrubina indirecta por la inducci\u00f3n de la actividad de la UGT1A1 residual.<\/li>\r\n<\/ul>\r\n<p>\r\n\r\n<\/p>\r\n<h2 id=\"h-investigacao-diagnostica\" class=\"wp-block-heading\"><strong>Investigaci\u00f3n diagn\u00f3stica<\/strong><\/h2>\r\n<p>\r\n\r\n<\/p>\r\n<p>Identificada la hiperbilirrubinemia indirecta, se recomienda anamnesis y examen f\u00edsico detallados, dosificaci\u00f3n s\u00e9rica de enzimas hep\u00e1ticas (TGO, TGP, fosfatasa alcalina y GGT) y funci\u00f3n hep\u00e1tica (tiempo de protrombina y alb\u00famina).<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<p>Si hay alteraciones en esta primera etapa de evaluaci\u00f3n, se dirige la investigaci\u00f3n a la evaluaci\u00f3n de hepatopat\u00edas, siendo prudente complementar con examen de imagen\/ecograf\u00eda de abdomen superior y dem\u00e1s ex\u00e1menes laboratoriales espec\u00edficos.<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<p>Si no se identifican alteraciones en la primera etapa de evaluaci\u00f3n, es obligatorio descartar hem\u00f3lisis con la dosificaci\u00f3n de DHL, haptoglobina y reticulocitos.<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<p>En adolescentes o adultos, en ausencia de hem\u00f3lisis y niveles de bilirrubina indirecta &lt;5mg\/dL, se presume el diagn\u00f3stico de s\u00edndrome de Gilbert. La confirmaci\u00f3n se hace por la prueba gen\u00e9tica para detectar mutaciones en el gen UGT1A1\/TATA box.<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<div class=\"wp-block-image\">\r\n<figure class=\"aligncenter size-full\"><img fetchpriority=\"high\" decoding=\"async\" class=\"alignnone size-full wp-image-9045\" src=\"https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1.png\" alt=\"\" width=\"2828\" height=\"1593\" srcset=\"https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1.png 2828w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-300x169.png 300w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-1024x577.png 1024w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-768x433.png 768w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-1536x865.png 1536w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-2048x1154.png 2048w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-1920x1082.png 1920w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-1170x659.png 1170w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert1-1-585x330.png 585w\" sizes=\"(max-width: 2828px) 100vw, 2828px\" \/><br \/>\r\n<figcaption class=\"wp-element-caption\">Figura 1. Diagrama de flujo de investigaci\u00f3n de hiperbilirrubinemia indirecta.<\/figcaption>\r\n<\/figure>\r\n<\/div>\r\n<p>\r\n\r\n<\/p>\r\n<h2 id=\"h-diagnostico-genetico\" class=\"wp-block-heading\"><strong>Diagn\u00f3stico Gen\u00e9tico<\/strong><\/h2>\r\n<p>\r\n\r\n<\/p>\r\n<p>Ante la posibilidad de reacciones adversas a algunos medicamentos metabolizados por la UGT1A1, como el irinotecano y el atazanavir, se recomienda considerar la confirmaci\u00f3n del SG mediante la investigaci\u00f3n de la mutaci\u00f3n UGT1A1 por el m\u00e9todo de PCR en tiempo real (Imagen 1).<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<p>Cuando en homocigosis, no hay necesidad de rastreo adicional, sin embargo, si el paciente posee solo un alelo de la mutaci\u00f3n UGT1A1 o ambos alelos son normales, se debe investigar las mutaciones G71R y Y486D, que tambi\u00e9n se asocian con el SG.<a href=\"https:\/\/gastropedia.com.br\/wp-content\/uploads\/2023\/08\/WhatsApp-Image-2023-08-15-at-13.08.43.png\" data-rel=\"penci-gallery-image-content\" ><img decoding=\"async\" class=\"alignnone size-full wp-image-9046\" src=\"https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert2.png\" alt=\"\" width=\"914\" height=\"525\" srcset=\"https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert2.png 914w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert2-300x172.png 300w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert2-768x441.png 768w, https:\/\/gastropedia.pub\/es\/wp-content\/uploads\/2023\/08\/gilbert2-585x336.png 585w\" sizes=\"(max-width: 914px) 100vw, 914px\" \/><\/a>Imagen 1. Resultado de la prueba gen\u00e9tica para el S\u00edndrome de Gilbert con homocigosis del alelo 28 en el gen UGT1A1 (en portugu\u00e9s).<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<h2 id=\"h-tratamiento\" class=\"wp-block-heading\"><strong>Tratamiento<\/strong><\/h2>\r\n<p>\r\n\r\n<\/p>\r\n<p>Por ser una condici\u00f3n benigna, el tratamiento es conservador solo con observaci\u00f3n. El pron\u00f3stico de los pacientes con SG es excelente y no requiere tratamiento espec\u00edfico.<\/p>\r\n<p>\r\n\r\n<\/p>\r\n<h2 id=\"h-referencias\" class=\"wp-block-heading\"><strong>Referencias<\/strong><\/h2>\r\n<p>\r\n\r\n<\/p>\r\n<ol class=\"wp-block-list\">\r\n<li>Thoguluva Chandrasekar V, Faust TW, John S. S\u00edndrome de Gilbert. 2023 Feb 6. En: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan\u2013. PMID: 29262099.<\/li>\r\n\r\n\r\n\r\n<li>Singh A, Koritala T, Jialal I. Hiperbilirrubinemia no conjugada. 2023 Feb 20. En: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan\u2013. PMID: 31747203.<\/li>\r\n\r\n\r\n\r\n<li>King D, Armstrong MJ. Resumen del s\u00edndrome de Gilbert. Drug Ther Bull. 2019 Feb;57(2):27-31. doi: 10.1136\/dtb.2018.000028. PMID: 30709860.<\/li>\r\n\r\n\r\n\r\n<li>Wagner KH, Shiels RG, Lang CA, Seyed Khoei N, Bulmer AC. Criterios diagn\u00f3sticos y contribuyentes al s\u00edndrome de Gilbert. Crit Rev Clin Lab Sci. 2018 Mar;55(2):129-139. doi: 10.1080\/10408363.2018.1428526. Epub 2018 Feb 1. PMID: 29390925.<\/li>\r\n\r\n\r\n\r\n<li>Rodrigues C, Vieira E, Santos R, de Carvalho J, Santos-Silva A, Costa E, Bronze-da-Rocha E. Impacto de las variantes del gen UGT1A1 en los niveles totales de bilirrubina en pacientes con s\u00edndrome de Gilbert y en sujetos sanos. Blood Cells Mol Dis. 2012 Mar 15;48(3):166-72. doi: 10.1016\/j.bcmd.2012.01.004. Epub 2012 Feb 9. PMID: 22325916.<\/li>\r\n<\/ol>\r\n<p>\r\n\r\n<\/p>\r\n<h2 id=\"h-como-citar-este-artigo\" class=\"wp-block-heading\">C\u00f3mo citar este art\u00edculo<\/h2>\r\n<p>\r\n\r\n<\/p>\r\n<p>Oti KST; Gamarra ACQ. S\u00edndrome de Gilbert: \u00bfqu\u00e9 necesitamos saber? Gastropedia 2024, vol. 2. Disponible en: https:\/\/gastropedia.pub\/es\/gastroenterologia\/sindrome-de-gilbert-que-necesitamos-saber<\/p>\r\n<p><\/p>","protected":false},"excerpt":{"rendered":"<p>El S\u00edndrome de Gilbert (SG) es un trastorno hep\u00e1tico del metabolismo de la bilirrubina con reducci\u00f3n en la glucuronidaci\u00f3n de la bilirrubina y consecuente hiperbilirrubinemia indirecta (no conjugada). Es una&hellip;<\/p>\n","protected":false},"author":5590,"featured_media":8010,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_lmt_disableupdate":"no","_lmt_disable":"","footnotes":""},"categories":[18,21],"tags":[],"ano":[395],"tipo":[121],"volumen":[44],"class_list":["post-8017","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-gastroenterologia","category-higado","ano-395","tipo-temas-generales","volumen-volume-ii"],"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v27.2 (Yoast SEO v27.3) - https:\/\/yoast.com\/product\/yoast-seo-premium-wordpress\/ -->\n<title>S\u00edndrome de Gilbert: \u00bfqu\u00e9 necesitamos saber? - Gastropedia<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/gastropedia.pub\/es\/gastroenterologia\/sindrome-de-gilbert-que-necesitamos-saber\/\" \/>\n<meta property=\"og:locale\" content=\"es_ES\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"S\u00edndrome de Gilbert: \u00bfqu\u00e9 necesitamos saber?\" \/>\n<meta property=\"og:description\" content=\"El S\u00edndrome de Gilbert (SG) es un trastorno hep\u00e1tico del metabolismo de la bilirrubina con reducci\u00f3n en la glucuronidaci\u00f3n de la bilirrubina y consecuente hiperbilirrubinemia indirecta (no conjugada). 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