<?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>0871-3413</journal-id>
<journal-title><![CDATA[Arquivos de Medicina]]></journal-title>
<abbrev-journal-title><![CDATA[Arq Med]]></abbrev-journal-title>
<issn>0871-3413</issn>
<publisher>
<publisher-name><![CDATA[ArquiMed - Edições Científicas AEFMUP ]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0871-34132008000300001</article-id>
<title-group>
<article-title xml:lang="pt"><![CDATA[Determinação de Anticorpos Anti-Mielina na Esclerose Múltipla]]></article-title>
<article-title xml:lang="en"><![CDATA[Anti-Myelin Autoantibodies in Multiple Sclerosis]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Lima]]></surname>
<given-names><![CDATA[Eduardo]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Guimarães]]></surname>
<given-names><![CDATA[Joana]]></given-names>
</name>
<xref ref-type="aff" rid="A02"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pereira]]></surname>
<given-names><![CDATA[Ana]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bodas]]></surname>
<given-names><![CDATA[Abília]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Delgado]]></surname>
<given-names><![CDATA[Luís]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
<xref ref-type="aff" rid="A03"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sá]]></surname>
<given-names><![CDATA[Maria José]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
</contrib-group>
<aff id="A01">
<institution><![CDATA[,Hospital de São João Laboratório de Imunologia ]]></institution>
<addr-line><![CDATA[Porto ]]></addr-line>
</aff>
<aff id="A02">
<institution><![CDATA[,Hospital de São João Serviço de Neurologia ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<aff id="A03">
<institution><![CDATA[,Universidade do Porto Faculdade de Medicina Serviço de Imunologia]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2008</year>
</pub-date>
<volume>22</volume>
<numero>4-5</numero>
<fpage>107</fpage>
<lpage>111</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_arttext&amp;pid=S0871-34132008000300001&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_abstract&amp;pid=S0871-34132008000300001&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_pdf&amp;pid=S0871-34132008000300001&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="pt"><p><![CDATA[Introdução: A Esclerose Múltipla é uma doença desmielinizante primária de carácter autoimune, envolvendo diferentes mecanismos imunopatológicos. Pensa-se que anticorpos dirigidos contra antigénios da mielina podem estar associados aos danos na mielina ou surgirem devido a estes, pelo que, o seu doseamento poderá constituir um marcador de evolução da doença. No entanto, a positividade desta pesquisa pode levantar dúvidas em termos de valorização clínica dada a descrição destes auto-anticorpos também em indivíduos sem doença. O objectivo deste trabalho foi a avaliação da presença de auto-anticorpos para a mielina em pacientes com o diagnóstico de Esclerose Múltipla, comparativamente a amostras de controlo, avaliando a sua associação com sintomas clínicos em pacientes com diferentes formas clínicas da Esclerose Múltipla. Métodos: A pesquisa de anticorpos para a mielina foi realizada por uma técnica de imuno&#64258;uorescência indirecta usando como substrato, nervo periférico de primata (EUROIMMUN®). Foram estudados 34 doentes (14M/11H), observados no serviço de Neurologia do Hospital de São João: 8 com forma monosintomática em surto, 11 com forma Surto/Remissão (SR) em remissão, 11 com forma SR em surto e 4 com forma Primária Progressiva (PP) em remissão. A população de controlo foi constituída por 25 amostras de indivíduos saudáveis (26M/8H). Resultados: Encontraram-se diferenças signi&#64257;cativas nas duas populações em relação à presença de anticorpos para a mielina (p<0,001). A análise dos diferentes tipos clínicos demonstrou uma prevalência de 87,5% nos casos com SCI, 77,3% na forma SR e 75,0% na forma PP. Em relação à situação clínica, 94,7% dos doentes em surto possuíam anticorpos anti-mielina enquanto que nos doentes em remissão 60,0% foram positivos. No grupo sem patologia, 32,0% apresentou positividade para os anticorpos anti-mielina. Conclusões: Apesar deste teste não ser especí&#64257;co na Esclerose Múltipla, na população de doentes estudada veri&#64257;cou-se uma maior prevalência dos anticorpos anti-mielina por imuno&#64258;uorescência indirecta nos pacientes em surto. Até que novos e melhores marcadores serológicos estejam disponíveis, este teste poderá ser útil para monitorizar pacientes com diagnóstico de&#64257;nitivo ou possível de Esclerose Múltipla, na qual a presença destes auto anticorpos poderá indicar um possível surto.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Introduction: Multiple Sclerosis (MS) is a primary demyelinating disease of autoimmune ethiology with different immunopathologic mechanisms. Anti-myelin autoantibodies may be associated with myelin damage and a possible marker of the disease evolution. However, the clinical usefulness of these autoantibodies is questionable as they may be present in healthy individuals. The aim of this work was the evaluation of autoantibodies against myelin in patients with MS comparatively with control samples, and their association with differents clinical types. Methology: For the search of anti-myelin antibodies we used indirect immunofluorescence in primate peripheral nerves (EUROIMMUN®). Thirty four patients (14 female/11 male) followed in the Neurology department were studied: 8 with the Clinically Isolated Syndrome (CIS) with relapse, 11 with Relapsing/Remitting (RR) in remission, 11 with RR with relapse and 4 with Primary Progressive (PP); 25 samples of healthy individuals (26 female/8 male) were studied as controls. Results: The presence of autoantibodies to myelin was signifiantly different in the two studied populations (p<0.001). Within the different clinical types we found a prevalence of 87.5% in CIS, 77.3% in RR and 75.0% in the patients with PP. Most patients (94.7%) in relapse had antibodies against myelin versus 60.0% of those in remision. In the control group, 32.0% presented anti-myelin antibodies. Conclusions: Although this test was not specific for MS, in the patient population studied the presence of anti-myelin antibodies by indirect immunofluorescence was higher in those in relapse. Until new and better serologic markers are available, this test may be useful to monitor patients with possible or definitive diagnosis of MS, in witch the presence of anti-myelin antibodies may support a possible relapse.]]></p></abstract>
<kwd-group>
<kwd lng="pt"><![CDATA[esclerose múltipla]]></kwd>
<kwd lng="pt"><![CDATA[auto-anticorpos]]></kwd>
<kwd lng="pt"><![CDATA[mielina]]></kwd>
<kwd lng="pt"><![CDATA[imunouorescência indirecta]]></kwd>
<kwd lng="en"><![CDATA[multiple sclerosis]]></kwd>
<kwd lng="en"><![CDATA[auto-antibody]]></kwd>
<kwd lng="en"><![CDATA[myelin]]></kwd>
<kwd lng="en"><![CDATA[indirect immunofluorescence]]></kwd>
</kwd-group>
</article-meta>
</front><body><![CDATA[ <p   align="justify" ><B>Determina&ccedil;&atilde;o de Anticorpos Anti-Mielina na Esclerose M&uacute;ltipla    </b></p >     <p   align="justify" >&nbsp;</p >     <P   align="justify" >Eduardo Lima*, Joana Guimar&atilde;es&#8224;&dagger;, Ana Pereira*, Ab&iacute;lia    Bodas*, Lu&iacute;s Delgado*&#8225;, Maria Jos&eacute; S&aacute;* </P >     <P   ><I>*Laborat&oacute;rio de Imunologia, Hospital de S&atilde;o Jo&atilde;o, Porto;    &#8224; &dagger;Servi&ccedil;o de Neurologia, Hospital de S&atilde;o Jo&atilde;o,    Porto; </I>&#8225;<I> Servi&ccedil;o de Imunologia, Faculdade de Medicina, Universidade    do Porto </I></P >     <P   align="justify" >&nbsp;</P >     <P   align="justify" >Introdu&ccedil;&atilde;o: A Esclerose M&uacute;ltipla &eacute; uma doen&ccedil;a    desmielinizante prim&aacute;ria de car&aacute;cter autoimune, envolvendo diferentes    mecanismos imunopatol&oacute;gicos. Pensa-se que anticorpos dirigidos contra    antig&eacute;nios da mielina podem estar associa</B>dos aos danos na mielina    ou surgirem devido a estes, pelo que, o seu doseamento poder&aacute; constituir    um marcador de evolu&ccedil;&atilde;o da doen&ccedil;a. No entanto, a positividade    desta pesquisa pode levantar d&uacute;vidas em termos de valoriza&ccedil;&atilde;o    cl&iacute;nica dada a descri&ccedil;&atilde;o destes auto-anticorpos tamb&eacute;m    em indiv&iacute;duos sem doen&ccedil;a. O objectivo deste trabalho foi a avalia&ccedil;&atilde;o    da presen&ccedil;a de auto-anticorpos para a mielina em pacientes com o diagn&oacute;stico    de Esclerose M&uacute;ltipla, comparativamente a amostras de controlo, avaliando    a sua associa&ccedil;&atilde;o com sintomas cl&iacute;nicos em pacientes com    diferentes formas cl&iacute;nicas da Esclerose M&uacute;ltipla. M&eacute;todos:    A pesquisa de anticorpos para a mielina foi realizada por uma t&eacute;cnica    de imuno&#64258;uoresc&ecirc;ncia indirecta usando como substrato, nervo perif&eacute;rico    de primata (EUROIMMUN&reg;). Foram estudados 34 doentes (14M/11H), observados    no servi&ccedil;o de Neurologia do Hospital de S&atilde;o Jo&atilde;o: 8 com    forma monosintom&aacute;tica em surto, 11 com forma Surto/Remiss&atilde;o (SR)    em remiss&atilde;o, 11 com forma SR em surto e 4 com forma Prim&aacute;ria Progressiva    (PP) em remiss&atilde;o. A popula&ccedil;&atilde;o de controlo foi constitu&iacute;da    por 25 amostras de indiv&iacute;duos saud&aacute;veis (26M/8H). Resultados:    Encontraram-se diferen&ccedil;as signi&#64257;cativas nas duas popula&ccedil;&otilde;es    em rela&ccedil;&atilde;o &agrave; presen&ccedil;a de anticorpos para a mielina    (p<0,001). A an&aacute;lise dos diferentes tipos cl&iacute;nicos demonstrou    uma preval&ecirc;ncia de 87,5% nos casos com SCI, 77,3% na forma SR e 75,0%    na forma PP. Em rela&ccedil;&atilde;o &agrave; situa&ccedil;&atilde;o cl&iacute;nica,    94,7% dos doentes em surto possu&iacute;am anticorpos anti-mielina enquanto    que nos doentes em remiss&atilde;o 60,0% foram positivos. No grupo sem patologia,    32,0% apresentou positividade para os anticorpos anti-mielina. Conclus&otilde;es:    Apesar deste teste n&atilde;o ser espec&iacute;&#64257;co na Esclerose M&uacute;ltipla,    na popula&ccedil;&atilde;o de doentes estudada veri&#64257;cou-se uma maior    preval&ecirc;ncia dos anticorpos anti-mielina por imuno&#64258;uoresc&ecirc;ncia    indirecta nos pacientes em surto. At&eacute; que novos e melhores marcadores    serol&oacute;gicos estejam dispon&iacute;veis, este teste poder&aacute; ser    &uacute;til para monitorizar pacientes com diagn&oacute;stico de&#64257;nitivo    ou poss&iacute;vel de Esclerose M&uacute;ltipla, na qual a presen&ccedil;a destes    auto anticorpos poder&aacute; indicar um poss&iacute;vel surto.</P >     <P   align="justify" ><B>Palavras-chave:</B> esclerose m&uacute;ltipla; auto-anticorpos; mielina; imuno&#64258;uoresc&ecirc;ncia    indirecta. </P >     <P   align="justify" >&nbsp;</P >     <P   align="justify" ><b>Anti-Myelin Autoantibodies in Multiple Sclerosis</b></P >     <P   align="justify" >Introduction: Multiple Sclerosis (MS) is a primary demyelinating disease of autoimmune    ethiology with different immunopathologic mechanisms. Anti-myelin autoantibodies    may be associated with myelin damage and a possible marker of the disease evolution.    However, the clinical usefulness of these autoantibodies is questionable as    they may be present in healthy individuals. The aim of this work was the evaluation    of autoantibodies against myelin in patients with MS comparatively with control    samples, and their association with differents clinical types. Methology: For    the search of anti-myelin antibodies we used indirect immunofluorescence in    primate peripheral nerves (EUROIMMUN&reg;). Thirty four patients (14 female/11    male) followed in the Neurology department were studied: 8 with the Clinically    Isolated Syndrome (CIS) with relapse, 11 with Relapsing/Remitting (RR) in remission,    11 with RR with relapse and 4 with Primary Progressive (PP); 25 samples of healthy    individuals (26 female/8 male) were studied as controls. Results: The presence    of autoantibodies to myelin was signifiantly different in the two studied populations    (p&lt;0.001). Within the different clinical types we found a prevalence of 87.5%    in CIS, 77.3% in RR and 75.0% in the patients with PP. Most patients (94.7%)    in relapse had antibodies against myelin versus 60.0% of those in remision.    In the control group, 32.0% presented anti-myelin antibodies. Conclusions: Although    this test was not specific for MS, in the patient population studied the presence    of anti-myelin antibodies by indirect immunofluorescence was higher in those    in relapse. Until new and better serologic markers are available, this test    may be useful to monitor patients with possible or definitive diagnosis of MS,    in witch the presence of anti-myelin antibodies may support a possible relapse.  </P >     ]]></body>
<body><![CDATA[<P   align="justify" ><b>Key-words:</b> multiple sclerosis; auto-antibody; myelin; indirect immunofluorescence.</P >     <P   align="justify" >&nbsp;</P >     <P   align="justify" >&nbsp;</P >     <P   >Texto completo dispon&iacute;vel apenas em PDF.</P >     <p>Full text only available in PDF format.</p>     <P   align="justify" >&nbsp;</P >     <P   >&nbsp;</P >      <p   align="justify" ><B>REFER&Ecirc;NCIAS </b></p >    <!-- ref --><P   align="justify" ></B>1 -Thrower BW. Clinically isolated syndromes: predicting and delaying multiple sclerosis. Neurology 2007;68:S12-5. </P >    &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;[&#160;<a href="javascript:void(0);" onclick="javascript: window.open('/scielo.php?script=sci_nlinks&ref=000021&pid=S0871-3413200800030000100001&lng=','','width=640,height=500,resizable=yes,scrollbars=1,menubar=yes,');">Links</a>&#160;]<!-- end-ref --><P   align="justify" >2 -	Brettschneider J, Petzold A, Junker A, Tumani H. Axonal damage markers in the cerebrospinal &#64258;uid of patients with clinically isolated syndrome improve predicting conversion to de&#64257;nite multiple sclerosis. Mult Scler 2006;2:143-8. </P >    ]]></body>
<body><![CDATA[<P   align="justify" >3 -Motamed MR, Najimi N, Fereshtehnejad SM. The effect of interferon-beta1a on relapses and progression of disability in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis. Clin Neurol Neurosurg 2007;109:344-9. </P >       <P   align="" >4 -Miller JR. The importance of early diagnosis of multiple sclerosis. J Manag      Care Pharm 2004;10:S4-11. </P >       <P   align="" >5 -Koch M, Heersema D, Mostert J, Teelken A, De Keyser J. Cerebrospinal &#64258;uid      oligoclonal bands and progression of disability in multiple sclerosis. Eur      J Neurol 2007;14: 797-800. </P >       <P   align="justify" >6 -Doggrell SA. Is natalizumab a breakthrough in the treatment of multiple sclerosis? Expert Opin Pharmacother 2003;4:999-1001. </P >    <P   align="justify" >7 -Kieseier BC, Wiendl H, Hemmer B, Hartung HP. Treatment and treatment trials in multiple sclerosis. Curr Opin Neurol 2007;20:286-93. </P >    <P   align="justify" >8 -Lassmann H, Br&uuml;ck W, Lucchinetti C. Heterogeneity of multiple sclerosis pathogenesis: implications for diagnosis and therapy. Trends Mol Med 2001;7:115-21. </P >    <P   align="justify" >9 -McDonald WI, Compston A, Edan G. Recommended Diagnostic Criteria for Multiple Sclerosis: Guideline from the International Panel on the Diagnosis of Multiple Sclerosis. Ann Neurology 2001;50:121-7. </P >    <P   align="justify" >10 -Frohman EM, Racke MK, Raine. Multiple Sclerosis- The Plaque and Its pathogenesis. N Engl J Med 2006;354: 942-55. </P >       <P   align="justify" >11 -Berger T, Rubner P, Scautzer F et al. Antimyelin Antibodies as a Predictor      of Clinically De&#64257;nite Multiple Sclerosis after a First Demyelinating      Event. N Engl J Med 2003;349:139-45. </P >       <P   align="justify" >12 -Kerlero R, Honegger P, Lassmann H, Matthieu J. Demyelination induced in aggregating brain cell cultures by a monoclonal antibody against myelin/oligodendrocyte glycoprotein. J Neurochem 1990;55:583-7. </P >    ]]></body>
<body><![CDATA[<P   align="justify" >13 -Angelucci F, Mirabella M, Frisullo G. Serum levels of anti-myelin antibodies in relapsing-remitting multiple sclerosis patients during different phases of disease activity and immunomodulatory therapy. Dis Markers 2005;21:49-55. </P >       <P   align="justify" >14 -Lolli F, Mazzanti B, Pazzagli M. The glycopeptide CSF114(Glc) detects serum      antibodiesin multiple sclerosis. J Neuroimmunol 2005;167:131-7. </P >       <P   align="justify" >15 -Gaertner S, Graaf KL, Greve B, Weissert R. Antibodies against glycosylated      native MOG are elevated in patients with multiple sclerosis. Neurology 2004;63:2238-383.</P >       <P   align="justify" >16 -Lalive PH, Menge T, Delarasse C, Gaspera BD, Pham-Dinh D, Villoslada P. Antibodies      to native myelin oligodendrocyte glycoprotein are serologic markers of early      inflammation in multiple sclerosis. Proc Natl Acad Sci USA 2006;103: 2280-5.    </P >       <P   align="justify" >17 -Khalil M, Reindl M, Luterotti A, Kuenz B, Ehling R, Gneiss C et al, Epitope      specificity of serum antibodies against the extracelular domain of myelin      oligodendrocyte glycoprotein: Influence of relapses and immunomodulatory treatments.      J Neuroimmunol 2006;174:147-56. </P >       <P   align="justify" >18 -Breij ECW, Heijen P, van der Goes A, Teunissen CE, Polman CH, Dijkstra .      Myelin flow citometry assay detects enhanced levels of antibodies to human      whole myelin in a subpopulation of multiple sclerosis patients. J Neuroimmunol      2006;176:106-14. </P >       <P   align="justify" >19 -Mantegazza R, Cristaldini P, Bernasconi, P. Anti-MOG autoantibodies in Italian      multiple sclerosis patients: specificity, sensitivity and clinical association.      Int Immunol 2004;16: 559-65. </P >       <P   align="justify" >20 -Lim ET, Berger T, Reidl M. Anti-myelin antibodies do not allow earlier diagnosis      of multiple sclerosis. Mul Scler 2005;11:492-4.</P >       <P   align="justify" >21 -Zadro I, Brinar V, Horvat G, Brinar M. Clinical Relevance of antibodies against      myelin oligodendrocyte glycoprotein in different clinical types of multiple      sclerosis. Clin Neurol Neurosurg 2007;109:23-6.</P >       <P   align="justify" >22 -Zadro I, Brinar V, Horvat G, Brinar M. Clinical Relevance of antibodies against      myelin oligodendrocyte glycoprotein in different clinical types of multiple      sclerosis. Clin Neurol Neurosurg 2007;109:23-6. </P >       ]]></body>
<body><![CDATA[<P   align="justify" >23 -Lampsona V, Franciotta D, Furlan R . Similar low frequency of anti-MOG IgG      and IgM in MS patients and healthy subjects. Neurology 2004;62:2092-4. </P >       <P   align="justify" >24 -Marta CM, Oliver AR, Sweet RA. Pathogenic myelin oligodendrocyte glycoprotein      antibodies recognize glycosilated epitopes and perturb oligodendrocyte physiology.      Proc Natl Acad Sci USA 2005;102:13992-7. </P >       <P   align="justify" >25 -Reindl M, Khalil M, Berger T. Antibodies as biological markers for pathophysiological      processes in MS. J Neuroimmunol 2006;180:50-62.</P >       <P   align="justify" >26 -Robinson W H, Fontoura P, Lee B J et al. Protein microarrays guide tolerizing      DNA vaccine treatment of autoimmune encephalomyelitis. Nat Biotechnol 2003;21:1033-9.</P >       <P   align="justify" >&nbsp;</P >       <P   align="justify" ><b>Correspond&ecirc;ncia:</b></P >       <P   align="justify" > Dr. Eduardo Lima </P >       <P   align="justify" >Laborat&oacute;rio de Imunologia </P >       <P   align="justify" >Hospital de S&atilde;o Jo&atilde;o </P >       <P   align="justify" >Alameda Prof. Hern&acirc;ni Monteiro </P >       ]]></body>
<body><![CDATA[<P   align="justify" >4200-319 Porto</P >       <P   align="justify" > e-mail: <a href="mailto:edlima1982@hotmail.com">edlima1982@hotmail.com</a></P >       ]]></body><back>
<ref-list>
<ref id="B1">
<nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Thrower]]></surname>
<given-names><![CDATA[BW]]></given-names>
</name>
</person-group>
<article-title xml:lang="en"><![CDATA[Clinically isolated syndromes: predicting and delaying multiple sclerosis]]></article-title>
<source><![CDATA[Neurology]]></source>
<year>2007</year>
<volume>68</volume>
<page-range>S12-5</page-range></nlm-citation>
</ref>
</ref-list>
</back>
</article>
