<?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>0121-5256</journal-id>
<journal-title><![CDATA[Revista Med]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. Med]]></abbrev-journal-title>
<issn>0121-5256</issn>
<publisher>
<publisher-name><![CDATA[Universidad Militar Nueva Granada. Facultad de Medicina]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0121-52562018000100026</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[DIAGNÓSTICO CLÍNICO Y BIOQUÍMICO DEL SÍNDROME DE LEIGH EN CINCO PACIENTES COLOMBIANOS]]></article-title>
<article-title xml:lang="en"><![CDATA[CLINICAL AND BIOCHEMICAL DIAGNOSIS OF LEIGH SYNDROME IN FIVE COLOMBIAN PATIENTS]]></article-title>
<article-title xml:lang="pt"><![CDATA[DIAGNÓSTICO CLÍNICO E BIOQUÍMICO DA SÍNDROME DE LEIGH EM CINCO PACIENTES COLOMBIANOS]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[HERRERA]]></surname>
<given-names><![CDATA[MILTON DAVID]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[ESPINOSA GARCÍA]]></surname>
<given-names><![CDATA[EUGENIA]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[GUEVARA MORALES]]></surname>
<given-names><![CDATA[JOHANA MARÍA]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[ECHEVERRI PEÑA]]></surname>
<given-names><![CDATA[OLGA YANETH]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Militar Nueva Granada  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Militar Nueva Granada  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Pontificia Universidad Javeriana  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Pontificia Universidad Javeriana  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>06</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>06</month>
<year>2018</year>
</pub-date>
<volume>26</volume>
<numero>1</numero>
<fpage>26</fpage>
<lpage>33</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0121-52562018000100026&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0121-52562018000100026&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0121-52562018000100026&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen El síndrome de Leigh (SL) es una enfermedad neurodegenerativa, descrita como una encefalomielopatía necrotizante subaguda, y es una de las enfermedades de origen mitocondrial más frecuentes. El SL es causado por el déficit en la producción de energía, originada en defectos en los genes que codifican alguno de los complejos mitocondriales; el gen afectado puede ser de codificación tanto nuclear como mitocondrial, lo que explica que se encuentren diferentes mecanismos de herencia, incluyendo autosómica recesiva y herencia materna, lo que, a su vez, hace más difícil su diagnóstico molecular. Clínicamente se presenta con regresión del desarrollo cognitivo y pérdida de habilidades motoras con trastorno de movimiento, de rápida progresión. El diagnóstico se basa en la demostración bioquímica de la elevación del ácido láctico y de la relación lactato/piruvato, así como hallazgos en las neuroimágenes por resonancia magnética que muestran lesiones focales, bilaterales y simétricas en ganglios basales o tallo cerebral asociadas a leucoencefalopatía y atrofia cerebral. Se reportan cinco casos con diagnóstico clínico y bioquímico del SL que ejemplifican la variabilidad clínica y gravedad encontrada en este grupo de pacientes.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Summary Leigh syndrome (LS) is a neurodegenerative disease, described as a subacute necrotizing encephalomyelopathy and is one of the most frequent diseases of mitochondrial origin. LS is caused by a deficit in the energy production due to defects in the genes that encode some of the mitochondrial complexes. The affected gene can be due to either nuclear and/or mitochondrial coding, which explains why there are different ways of inheriting the disease, including autosomal recessive and maternal inheritance, which makes its molecular diagnosis even more difficult. Clinically, LS is characterized by regression in cognitive development and motor abilities, as well as movement disorders of rapid progression. Its diagnosis is based on the biochemical demonstration of an increase in lactic acid and lactate / pyruvate ratio, as well as magnetic resonance neuroimaging findings showing focal, bilateral and symmetric lesions in basal ganglia or brainstem associated with leukoencephalopathy and cerebral atrophy. Five cases are reported with clinical and biochemical diagnosis of LS that exemplify the clinical variability and severity found in this group of patients.]]></p></abstract>
<abstract abstract-type="short" xml:lang="pt"><p><![CDATA[Resumo A síndrome de Leigh (SL) é uma doença neurodegenerativa, descrita como uma encefalomielopatia necrotizante subaguda e é uma das doenças de origem mitocondrial mais frequente. A SL é causada pelo déficit na produção de energia originada em defeitos nos genes que codificam algum dos complexos mitocondriais; o gene afetado pode ser de codificação tanto nuclear como mitocondrial, o que explica que se encontrem diferentes mecanismos de herança, incluindo autossômica recessiva e herança materna, o que torna mais difícil seu diagnóstico molecular. Clinicamente se apresenta com regressão do desenvolvimento do desenvolvimento cognitivo e perda de habilidades motoras com transtorno de movimento, de rápida progressão. O diagnóstico se baseia na demonstração bioquímica da elevação do ácido láctico e da relação lactato/piruvato, assim como descobertas nas neuro imagens por ressonância magnética que mostram lesões focais, bilaterais e simétricas em gânglios basais ou talo cerebral associadas a leucoencefalopatia e atrofia cerebral. Reportam-se cinco casos com diagnóstico clínico e bioquímico da SL que exemplificam a variabilidade clínica e gravidade encontrada neste grupo de pacientes.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[enfermedad neurodegenerativa]]></kwd>
<kwd lng="es"><![CDATA[enfermedad mitocondrial]]></kwd>
<kwd lng="es"><![CDATA[acidosis láctica]]></kwd>
<kwd lng="es"><![CDATA[síndrome de Leigh]]></kwd>
<kwd lng="en"><![CDATA[neurogenerative disease]]></kwd>
<kwd lng="en"><![CDATA[mitochondrial disease]]></kwd>
<kwd lng="en"><![CDATA[lactic acidosis]]></kwd>
<kwd lng="en"><![CDATA[Leigh syndrome]]></kwd>
<kwd lng="pt"><![CDATA[doença neurodegenerativa]]></kwd>
<kwd lng="pt"><![CDATA[doença mitocondrial]]></kwd>
<kwd lng="pt"><![CDATA[acidose láctica]]></kwd>
<kwd lng="pt"><![CDATA[síndrome de Leigh]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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