<?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>0121-0793</journal-id>
<journal-title><![CDATA[Iatreia]]></journal-title>
<abbrev-journal-title><![CDATA[Iatreia]]></abbrev-journal-title>
<issn>0121-0793</issn>
<publisher>
<publisher-name><![CDATA[Universidad de Antioquia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0121-07932021000100042</article-id>
<article-id pub-id-type="doi">10.17533/udea.iatreia.76</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Leucemia promielocítica aguda. Estado del arte]]></article-title>
<article-title xml:lang="en"><![CDATA[Acute promyelocytic leukemia. State of the art]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Mejía-Buriticá]]></surname>
<given-names><![CDATA[Leonardo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Torres-Hernández]]></surname>
<given-names><![CDATA[José Domingo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Vásquez]]></surname>
<given-names><![CDATA[Gonzalo de Jesús]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad de Antioquia  ]]></institution>
<addr-line><![CDATA[Medellín ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad de Antioquia  ]]></institution>
<addr-line><![CDATA[Medellín ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad de Antioquia Laboratorio Integrado de Medicina Especializada (LIME) ]]></institution>
<addr-line><![CDATA[Medellín ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2021</year>
</pub-date>
<volume>34</volume>
<numero>1</numero>
<fpage>42</fpage>
<lpage>53</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0121-07932021000100042&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0121-07932021000100042&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0121-07932021000100042&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN La leucemia promielocítica aguda (LPA) es un subtipo de leucemia mieloide aguda (LMA) que se origina por una traslocación balanceada entre los cromosomas 15 y 17, involucra al gen que codifica para el receptor alfa del ácido retinoico (RARA) en el cromosoma 17 y el de la leucemia promielocítica (PML) en el cromosoma 15, lo que da origen a la traslocación t(15;17) PML/RARA. Dicho reordenamiento origina la proteína de fusión PML/RAR alfa, que bloquea la diferenciación de las células madre mieloides en el estadio de promielocito. La LPA afecta con mayor frecuencia a adultos jóvenes y conlleva un alto riesgo de mortalidad temprana, en especial por el desarrollo de una coagulopatía grave, que sin tratamiento es definitivamente fatal. El diagnóstico temprano, el tratamiento de soporte y la introducción de fármacos que promueven la diferenciación terminal de los promielocitos patológicos como la tretinoina, también conocida como ácido todo transretinoico (ATRA) o trióxido de arsénico (ATO), ha hecho que en la actua-lidad esta sea una enfermedad curable con altas tasas de remisión completa.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[SUMMARY Acute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia (AML) that results from a balanced translocation between chromosomes 15 and 17, which involves the gene encoding the retinoic acid receptor alpha (RARA) on chromosome 17 and the gene for promyelocytic leukemia (PML) on chromosome 15, causing the translocation t (15; 17) PML / RARA. This rearrangement originates the PML / RAR alpha fusion protein, which blocks the differentiation of myeloid stem cells at the promyelocyte stage. APL affects young adults more frequently and carries a high risk of early mortality, especially due to development of severe coagulopathy that, without treatment, is invariably fatal. Early diagnosis, supportive treatment, and the introduction of drugs that promote the terminal differentiation of pathological promyelocytes such as alltrans retinoic acid (ATRA) and arsenic trioxide (ATO), have currently made this a curable disease with high rates of complete remission.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Leucemia Promielocítica Aguda]]></kwd>
<kwd lng="es"><![CDATA[Tretinoina]]></kwd>
<kwd lng="es"><![CDATA[Trióxido de Arsénico]]></kwd>
<kwd lng="en"><![CDATA[Arsenic Trioxide]]></kwd>
<kwd lng="en"><![CDATA[Leukemia, Promyelocytic, Acute]]></kwd>
<kwd lng="en"><![CDATA[Tretinoin]]></kwd>
</kwd-group>
</article-meta>
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