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<front>
<journal-meta>
<journal-id pub-id-type="pid">S1017-854620020001</journal-id>
<journal-title>Revista Médica del Hospital Nacional de Niños Dr. Carlos Sáenz Herrera</journal-title>
<abbrev-journal-title>Rev. méd. Hosp. Nac. Niños (Costa Rica)</abbrev-journal-title>
<issn>1017-8546</issn>
<publisher>
<publisher-name>Editorial Nacional de Salud y Seguridad Social</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1017-85462002000100001</article-id>
<title-group>
<article-title xml:lang="es">Autoanticuerpos en pacientes con enfermedad autoinmune en el Hospital Nacional de Niños</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Campos</surname>
<given-names>Marlen</given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Barzuna</surname>
<given-names>Laura</given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Carrillo</surname>
<given-names>Pedro</given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Vives</surname>
<given-names>Carlos</given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
</contrib-group>
<aff id="A01">
<institution>,CCSS Hospital Nacional de Niños </institution>
<addr-line>San José </addr-line>
<country>Costa Rica</country>
</aff>
<pub-date pub-type="pub">
<year>2002</year>
</pub-date>
<pub-date pub-type="epub">
<year>2002</year>
</pub-date>
<volume>37</volume>
<fpage>3</fpage>
<lpage>8</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http:/www.scielo.sa.cr/scielo.php?script=sci_arttext&amp;pid=S1017-85462002000100001&amp;lng=en&amp;nrm=iso&amp;tlng=en"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_abstract&amp;pid=S1017-85462002000100001&amp;lng=en&amp;nrm=iso&amp;tlng=en"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_pdf&amp;pid=S1017-85462002000100001&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p>Los análisis de autoanticuerpos se han empleado para el diagnóstico, monitore y pronóstico de las enfermedades autoinmunes. Se realizó un estudio retrospectivo con el objetivo de conocer la frecuencia de anticuerpos antinucleares (ANA), anti-ADN doble banda, anti-Sm, anti-SSA (Ro), anti SSB (La), anti ribonúcleoproteína (RNP) y anticardiolipina en el suero de pacientes pedrátricos con problemas autoinmunes, los cuales se clasificaron en dos grupos, 46 pacientes diagnosticados con enfermedades reumáticas autoinmunes y 12 con otras enfermedades. Para los autoanticuerpos analizados los porcentajes de positividad fueron los sieguientes: 69% ANA, 21% anti-ADNdb, 16% anti-SS A, 5% anti-SS B, 15% anti-SM, 21% anti-RNP, 35% anti-cardiolipina IgG y 12% anti-cardiolipina IgM. Ninguno de 12 con otras enfermedades autoinmunes presentaron ANA, anti-ADNdb, anti-SS A, anti-SS B ni anti-SM positivos, 2 presentaron anticuerpos anti-RNP, 4 anti-cardiolipina IgG y 2 anti-cardiolipina IgM. Mientras que de los 46 pacientes con enfermedades reumáticas autoinmunes 35 presentaron ANA positivos y 12 anti-ADN db positivo. Se recomienda una valoración clínica apropiada para el paciente, antes de solicitar este perfil de autoanticuerpos, dado que no tiene utilidad para las enfermedades autoinmunes no reumáticas.</p></abstract>
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<front>
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<journal-title>Revista Médica del Hospital Nacional de Niños Dr. Carlos Sáenz Herrera</journal-title>
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<pub-date pub-type="pub">
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<pub-date pub-type="epub">
<year>2002</year>
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<volume>37</volume>
<fpage>9</fpage>
<lpage>14</lpage>
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<self-uri xlink:href="http:/www.scielo.sa.cr/scielo.php?script=sci_arttext&amp;pid=S1017-85462002000100009&amp;lng=en&amp;nrm=iso&amp;tlng=en"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_abstract&amp;pid=S1017-85462002000100009&amp;lng=en&amp;nrm=iso&amp;tlng=en"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_pdf&amp;pid=S1017-85462002000100009&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p>La enfermedad de Chagas es causada por un protozoario flagelado denominado Trypanosoma cruzi y éste es transmitido al ser humano por un triatómino hematófago, que se le conoce como chinche. Se calcula que unos veinticinco miIlones de personas en todo Latinoamérica sufren sus consecuencias y que más de 100 millones están en riesgo de contagio. El mal de Chagas se caracteriza por ser una infección que invade una gran variedad de células del huésped vertebrado. El mecanismo de invasión depende del parásito y también de los receptores moleculares en la superficie de las células blanco. La respuesta humoral a este parásito está dada contra una mezcla compleja de antígenos que varían de un ciclo parasitario a otro, con estímulos constantes del sistema inmune que determinan la respuesta del huésped durante la fase crónica de la enfermedad. En la infección aguda la respuesta inmune por células TH 1 (Células T cooperadoras tipo 1) es estimulada por Interleukina 2 (lL-2) e Interferón gama, lo cual se relaciona con el daño tisular generado en el huésped. Por otro lado la inducción de una respuesta I por parte de las células T cooperadoras de tipo 2 (TH2) por aumento de Interleukina 4 (lL-4) e InterIeukina 10 (lL-10), hace al huésped más susceptible a la infección por Trypanosoma cruzi. Al igual que en cualquier infección por agentes patógenos, el grado de susceptibilidad del huésped y el daño tisular generado, depende de la inmunoregulación de la respuesta inmune TH 1 - TH2 y del predominio en la acción de las diferentes citokinas.</p></abstract>
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<self-uri xlink:href="http:/www.scielo.sa.cr/scielo.php?script=sci_arttext&amp;pid=S1017-85462002000100010&amp;lng=en&amp;nrm=iso&amp;tlng=en"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_abstract&amp;pid=S1017-85462002000100010&amp;lng=en&amp;nrm=iso&amp;tlng=en"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_pdf&amp;pid=S1017-85462002000100010&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p>El Virus de Inmunadeficiencia Humana, &quot;HIV&quot;, por sus siglas en inglés para &quot;Human Immunodeficiency Virus&quot; y el Virus de la Leucemia de Células T de Humanos, &quot;HTLV&quot;, para las siglas de inglés &quot;Human T-Cell Leukemia Virus&quot; son dos retrovirus que infectan células del sistema inmune y por lo tanto interfieren con la función de defensa contra microorganismos como bacterias, virus, hongos y parásitos, este organizado sistema es parte del organismo de seres superiores como los mamíferos y cumple además con la función de vigilancia, que tiene que ver con eliminar células propias alteradas. Debido a que estos virus infectan linfocitos T cooperadores principalmente, a la permanencia y agresividad de la infección, se presentan entidades clínicas que a la postre acaban can la vida del individuo. El propósito de este trabajo es dar a conocer de manera general como es que se presenta y cómo se lleva a cabo la infección en estas dos virosis.</p></abstract>
<abstract abstract-type="short" xml:lang="en"><p>Human Immunodeficiency Virus ( HIV) and Human T-Cell Leukemia Virus are retroviruses they infect cells of immune sistem and so alter the natural function of the immune sistem that is defense against microrganisms, such as bacteria, viruses, fungi and parasites and survillance against altered self cells. The immune sistem is part of higher animal's body, such as mammals and due these viruses infect T cell and the long and permanent infection the clinical course sickness appears and take to individual to death. This paper describe on general way how does infection occur and go on.</p></abstract>
<kwd-group>
<kwd>retrovirus</kwd>
<kwd>HIV</kwd>
<kwd>HTLV</kwd>
<kwd>infección del sistema inmune</kwd>
<kwd>linfocitos T</kwd>
<kwd>retroviruses</kwd>
<kwd>HIV</kwd>
<kwd>HTLV</kwd>
<kwd>immune system infection</kwd>
<kwd>T cell</kwd>
<kwd>Iymphocytes</kwd>
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