<?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>1699-714X</journal-id>
<journal-title><![CDATA[Revista de la OFIL ]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. OFIL·ILAPHAR]]></abbrev-journal-title>
<issn>1699-714X</issn>
<publisher>
<publisher-name><![CDATA[Organización de Farmacéuticos Ibero-Latinoamericanos]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1699-714X2020000300233</article-id>
<article-id pub-id-type="doi">10.4321/s1699-714x2020000300014</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Daños citogenéticos generados por el uso de metrotrexate para tratamiento de artritis reumatoidea]]></article-title>
<article-title xml:lang="en"><![CDATA[Cytogenetic damage generated by the use of methotrexate for the treatment of rheumatoid arthritis]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Jiménez Madrid]]></surname>
<given-names><![CDATA[JH]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Lucumí Moreno]]></surname>
<given-names><![CDATA[A]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Libre Facultad de Ciencias de la Salud Laboratorio de Genética y Biología Molecular]]></institution>
<addr-line><![CDATA[Seccional Cali ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2020</year>
</pub-date>
<volume>30</volume>
<numero>3</numero>
<fpage>233</fpage>
<lpage>238</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_arttext&amp;pid=S1699-714X2020000300233&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_abstract&amp;pid=S1699-714X2020000300233&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_pdf&amp;pid=S1699-714X2020000300233&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN  Objetivo:  Determinar los daños citogenéticos generados por el uso de metrotrexate para tratamiento de artritis reumatoidea.  Metodología:  Nuestra experiencia en el uso del metotrexate para sincronización celular como retardante del ciclo celular en fase &#8220;S&#8221; y su posterior inhibición por competencia con la bromodeoxiuridina en la obtención de cromosomas con bandas &#8220;R&#8221; de replicación, nos indujo a realizar este estudio citogenético utilizando linfocitos de sangre periférica cultivados en medio PB-Max durante 72 horas, provenientes de una paciente de 46 años de edad, con diagnóstico médico de artritis reumatoidea, tratada con metotrexate durante un mes.  Resultados:  Clínicamente la paciente presentó inflamación de las articulaciones de los dedos de las manos y hombro izquierdo, con impedimento para flexionar el dedo anular de la mano derecha, además de dolor que impide el movimiento de las mismas articulaciones, en ocasiones y debido al dolor no se puede levantar sin ayuda de su lecho. El resultado del análisis citogenético convencional, indicó que de 50 células analizadas, 23 (46%) presentaron cariotipo normal; 17 (34%) muestran aneuploidías de los diferentes grupos cromosómicos del cariotipo humano incluido el (X) y 10 (20%) de polimorfonucleares anormales. Se discute la etiología génica del control molecular del ciclo celular, pensando en que los hallazgos mencionados, estarían más direccionados a los ciclos aberrantes de duplicación del centrosoma y del huso mitótico en general, así como a la alteración parcial de la síntesis del ADN y el ARN, causados probablemente por la acción del metotrexate, lo cual se ve reflejado en que los hallazgos aneuploídicos en el cariotipo son al azar, sin comprometer en particular cromosomas de un grupo determinado.  Conclusiones:  Se sugiere a los médicos tratantes tener en cuenta alguna directriz en el protocolo terapéutico, relacionada con la cronicidad y el monitoreo citogenético durante el tratamiento con este medicamento.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[SUMMARY  Objective:  To determine the cytogenetic damages generated by the use of methotrexate for the treatment of rheumatoid arthritis.  Methods:  Our experience in the use of methotrexate for cell synchronization as a retarder of the &#8220;S&#8221; phase cell cycle and its subsequent inhibition by competition with bromodeoxyuridine in obtaining chromosomes with &#8220;R&#8221; bands of replication, induced us to perform this cytogenetic study using peripheral blood lymphocytes cultured in PB-Max medium for 72 hours, from a 46-year-old patient, with a medical diagnosis of rheumatoid arthritis, treated with methotrexate for one month.  Results:  Clinically the patient presented inflammation articulations of left hand fingers and left shoulder, with impediment flex of the annular finger right hand, besides she has pain that prevent the movement of the same articulations, in occasions and because of this problem she cannot get up without help. The conventionally cytogenetic analysis, shows that of the 50 analyzed cells, 23 (46%) presents normal karyotype; 17 (34%) presents aneuploidies of the chromosomic different groups including de (X) chromosome, and 10 (20%) of abnormal polymorphonuclear. We discuss the genetic etiology of the biology cellular control, keep in mind that mentioned findings are preferentially directed due to aberrant cycles of centrosome duplication and mitotic spindle in general, as well as the partial disturbance of the ADN and ARN synthesis, probably caused by methotrexate action, this fact that is reflected in the aneuploidy findings in the karyotype are to random, without compromise of any particular chromosome of the determined group.  Conclusions:  It is suggested to the treating doctor should really take implement some rule in the therapeutic protocol of corresponding management, relationed with the chronicity and cytogenetic monitoring during the treatment with this medicine.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Artritis reumatoidea]]></kwd>
<kwd lng="es"><![CDATA[metotrexate]]></kwd>
<kwd lng="es"><![CDATA[aneuploidías]]></kwd>
<kwd lng="es"><![CDATA[polimorfonucleares]]></kwd>
<kwd lng="es"><![CDATA[centrosomas]]></kwd>
<kwd lng="es"><![CDATA[proteosomas]]></kwd>
<kwd lng="es"><![CDATA[microtúbulos]]></kwd>
<kwd lng="es"><![CDATA[grupos cromosómicos]]></kwd>
<kwd lng="en"><![CDATA[Rheumatoid arthritis]]></kwd>
<kwd lng="en"><![CDATA[methotrexate]]></kwd>
<kwd lng="en"><![CDATA[aneuploidies]]></kwd>
<kwd lng="en"><![CDATA[polymorphonuclear]]></kwd>
<kwd lng="en"><![CDATA[centrosome]]></kwd>
<kwd lng="en"><![CDATA[proteasome]]></kwd>
<kwd lng="en"><![CDATA[microtubules]]></kwd>
<kwd lng="en"><![CDATA[chromosomic group]]></kwd>
</kwd-group>
</article-meta>
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