<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0121-0319</journal-id>
<journal-title><![CDATA[Medicas UIS]]></journal-title>
<abbrev-journal-title><![CDATA[Medicas UIS]]></abbrev-journal-title>
<issn>0121-0319</issn>
<publisher>
<publisher-name><![CDATA[Universidad Industrial de Santander]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0121-03192024000300071</article-id>
<article-id pub-id-type="doi">10.18273/revmed.v37n3-2024007</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Familial hypercholesterolemia due to an heterozygous LDLR promoter mutation: a case report]]></article-title>
<article-title xml:lang="es"><![CDATA[Hipercolesterolemia familiar secundaria a mutación heterocigota en el promotor del gen LDLR: reporte de caso]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Figueroa-Buitrago]]></surname>
<given-names><![CDATA[Lorena]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Diaz-Giraldo]]></surname>
<given-names><![CDATA[Jorge A]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Saldarriaga-Gil]]></surname>
<given-names><![CDATA[Wilmar]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Libre  ]]></institution>
<addr-line><![CDATA[Cali ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Fundación Universitaria San Martín  ]]></institution>
<addr-line><![CDATA[Cali ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad del Valle  ]]></institution>
<addr-line><![CDATA[Cali ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2024</year>
</pub-date>
<volume>37</volume>
<numero>3</numero>
<fpage>71</fpage>
<lpage>79</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0121-03192024000300071&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0121-03192024000300071&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0121-03192024000300071&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Familial hypercholesterolemia is a disease caused by mutations in genes related to lipid metabolism, characterized by elevated low-density cholesterol, personal and family history of premature atherosclerotic cardiovascular disease. We present two cases with heterozygous mutation in the promoter of the low-density lipoprotein receptor gene C-135OG. The index case had low-density lipoprotein levels above 300 mg/dL at 10 years old, suffered a major cardiovascular event at the age of 40, and a stroke at 48. At the age of 52, a clinical geneticist built a genogram that suggested an autosomal dominant inheritance pattern of familial hypercholesterolemia and performed a molecular panel for the patient and her daughter at 26 years old. Both cases presented therapeutic failure with lovastatin monotherapy. A significant reduction in cholesterol levels was achieved with dual therapy, in the case 1 with alirocumab+rosuvastatin and case 2 with atorvastatin+ezetimibe.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La hipercolesterolemia familiar es una enfermedad causada por mutaciones en genes relacionados con el metabolismo de los lípidos, caracterizada por colesterol de baja densidad elevado y antecedentes personales y familiares de enfermedad cardiovascular aterosclerótica prematura. Presentamos dos casos con mutación heterocigota en el promotor del gen del receptor de lipoproteínas de baja densidad c.-135C&gt;G. El caso índice tuvo colesterol de baja densidad &gt;300mg/dL a los 10 años, sufrió un evento cardiovascular mayor a los 40 años y un evento cerebrovascular a los 48. A los 52 años, un genetista clínico elaboró un genograma que sugería patrón de herencia autosómico dominante de la hipercolesterolemia familiar y realizó panel molecular al caso y su hija de 26 años. Ambos casos presentaron fracaso terapéutico con lovastatina. Se consiguió una reducción significativa de los niveles de colesterol con terapia dual, en el caso 1 con alirocumab+rosuvastatina y en el caso 2 con atorvastatina+ezetimiba.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Familial Hypercholesterolemia]]></kwd>
<kwd lng="en"><![CDATA[Hyperlipoproteinemia Type II]]></kwd>
<kwd lng="en"><![CDATA[Receptors LDL]]></kwd>
<kwd lng="en"><![CDATA[Cholesterol]]></kwd>
<kwd lng="en"><![CDATA[LDL]]></kwd>
<kwd lng="es"><![CDATA[Hipercolesterolemia Familiar]]></kwd>
<kwd lng="es"><![CDATA[Hiperlipoproteinemia Tipo II]]></kwd>
<kwd lng="es"><![CDATA[Receptores de LDL]]></kwd>
<kwd lng="es"><![CDATA[LDL-Colesterol]]></kwd>
</kwd-group>
</article-meta>
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