<?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>1688-0390</journal-id>
<journal-title><![CDATA[Revista Médica del Uruguay]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. Méd. Urug.]]></abbrev-journal-title>
<issn>1688-0390</issn>
<publisher>
<publisher-name><![CDATA[Sindicato Médico del Uruguay]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1688-03902025000401702</article-id>
<article-id pub-id-type="doi">10.29193/rmu.41.4.11</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Neuropatía distal adquirida desmielinizante y simétrica anti-myelin-associated glycoprotein: a propósito de un caso clínico]]></article-title>
<article-title xml:lang="en"><![CDATA[Anti&#8211;Myelin-Associated Glycoprotein (MAG) Neuropathy: Case Report]]></article-title>
<article-title xml:lang="pt"><![CDATA[Neuropatia Anti&#8211;Myelin-Associated Glycoprotein (MAG): Relato de Caso]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rocha Pagés]]></surname>
<given-names><![CDATA[Valeria]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hackembruch]]></surname>
<given-names><![CDATA[Heber]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Muxi]]></surname>
<given-names><![CDATA[Pablo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Medicina Personalizada y Hospital Británico  ]]></institution>
<addr-line><![CDATA[Montevideo ]]></addr-line>
<country>Uruguay</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Clínica de Neurofisiología Charcot  ]]></institution>
<addr-line><![CDATA[Montevideo ]]></addr-line>
<country>Uruguay</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2025</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2025</year>
</pub-date>
<volume>41</volume>
<numero>4</numero>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.edu.uy/scielo.php?script=sci_arttext&amp;pid=S1688-03902025000401702&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.edu.uy/scielo.php?script=sci_abstract&amp;pid=S1688-03902025000401702&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.edu.uy/scielo.php?script=sci_pdf&amp;pid=S1688-03902025000401702&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La neuropatía anti-myelin-associated glycoprotein (MAG) es una neuropatía desmielinizante crónica, caracterizada por desmielinización distal del nervio periférico. Se manifiesta principalmente con parestesias y ataxia progresiva. Presentamos el caso clínico de un hombre de 83 años, diabético, quien desde hace 4 años presentaba parestesias en miembros inferiores (MMII), de caracter estable. En el último año se añadieron parestesias en manos e inestabilidad en la marcha. Al examen, se constató temblor postural de manos, fuerza conservada, arreflexia generalizada, hipoestesia distal y pallestesia en MMII con patrón largo dependiente. Estática inestable y Romberg sin latencia. Ante un síndrome sensitivo simétrico distal, con ataxia propioceptiva, se plantea una neuropatía sensitiva con un cambio clínico-evolutivo. Se realiza neuroconducción que evidencia potenciales sensitivos ausentes. Potenciales motores con velocidades de conducción levemente reducidas pero con latencias distales muy aumentadas (desmielinización distal). El líquido cefalorraquídeo evidenció proteinorraquia sin células. Además, presentó un componente monoclonal IgM y anticuerpo anti-MAG positivo. Se descartaron linfopatías malignas, amiloidosis y POEMS. La neuropatía anti-MAG es una neuropatía inflamatoria crónica asociada a gammapatías monoclonales. Clínicamente, se caracteriza por parestesias distales y la ataxia sensitiva que progresan con patrón largo dependiente, y la neuroconducción detecta una desmielinización distal. Los anticuerpos anti-MAG son fundamentales, dado que su reacción contra las glicoproteínas del sector distal del nervio periférico explica el cuadro. La neuropatía anti-MAG debe ser sospechada en pacientes con clínica sugerente. El estudio eléctrico y la serología, asociados al componente monoclonal, permiten su correcto diagnóstico.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Anti&#8211;myelin-associated glycoprotein (MAG) neuropathy is a chronic demyelinating neuropathy characterised by distal demyelination of the peripheral nerve. It manifests mainly with paraesthesias and progressive ataxia. We present the clinical case of an 83-year-old man with diabetes, who had been experiencing paraesthesias in the lower limbs (LL) for four years, of a stable nature. During the past year, paraesthesias in the hands and gait instability were added. On examination, postural tremor of the hands, preserved strength, generalised areflexia, distal hypoesthesia, and pallesthesia in the LL with a length-dependent pattern were observed. He also presented with unsteady stance and a Romberg sign without latency. Given the presence of a distal symmetric sensory syndrome with proprioceptive ataxia, a sensory neuropathy with a clinical-evolutionary change was considered. Nerve conduction studies showed absent sensory potentials. Motor potentials displayed slightly reduced conduction velocities but markedly increased distal latencies (distal demyelination). Cerebrospinal fluid revealed proteinorrachia without cells. In addition, a monoclonal IgM component and positive anti-MAG antibodies were detected. Malignant lymphoproliferative disorders, amyloidosis, and POEMS were ruled out. Anti-MAG neuropathy is a chronic inflammatory neuropathy associated with monoclonal gammopathies. Clinically, it is characterised by distal paraesthesias and sensory ataxia that progress in a length-dependent pattern, while nerve conduction studies detect distal demyelination. Anti-MAG antibodies are fundamental, as their reaction against glycoproteins in the distal segment of the peripheral nerve explains the condition. Anti-MAG neuropathy should be suspected in patients with suggestive clinical features. Electrophysiological studies and serology, in association with the monoclonal component, allow an accurate diagnosis.]]></p></abstract>
<abstract abstract-type="short" xml:lang="pt"><p><![CDATA[Resumo A neuropatia anti&#8211;myelin-associated glycoprotein (MAG) é uma neuropatia desmielinizante crônica, caracterizada por desmielinização distal do nervo periférico. Manifesta-se principalmente com parestesias e ataxia progressiva. Apresentamos o caso clínico de um homem de 83 anos, diabético, que há 4 anos apresentava parestesias em membros inferiores (MMII), de caráter estável. No último ano acrescentaram-se parestesias nas mãos e instabilidade da marcha. Ao exame, constatou-se tremor postural das mãos, força preservada, arreflexia generalizada, hipoestesia distal e palestesia em MMII com padrão comprimento-dependente. Estática instável e sinal de Romberg sem latência. Diante de uma síndrome sensitiva simétrica distal, com ataxia proprioceptiva, levantou-se a hipótese de uma neuropatia sensitiva com mudança clínico-evolutiva. O estudo de condução nervosa evidenciou potenciais sensitivos ausentes. Os potenciais motores apresentaram velocidades de condução levemente reduzidas, mas com latências distais muito aumentadas (desmielinização distal). O líquido cefalorraquidiano mostrou proteinorraquia sem células. Além disso, apresentou componente monoclonal IgM e anticorpo anti-MAG positivo. Foram descartadas linfopatias malignas, amiloidose e POEMS. A neuropatia anti-MAG é uma neuropatia inflamatória crônica associada a gamopatias monoclonais. Clinicamente, caracteriza-se por parestesias distais e ataxia sensitiva que progridem com padrão comprimento-dependente, enquanto o estudo de condução nervosa detecta desmielinização distal. Os anticorpos anti-MAG são fundamentais, dado que sua reação contra as glicoproteínas do setor distal do nervo periférico explica o quadro. A neuropatia anti-MAG deve ser suspeitada em pacientes com clínica sugestiva. O estudo eletrofisiológico e a sorologia, associados ao componente monoclonal, permitem o diagnóstico correto.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Neuropatía anti-MAG]]></kwd>
<kwd lng="es"><![CDATA[Neuropatía desmielinizante crónica]]></kwd>
<kwd lng="es"><![CDATA[Myelin-associated glycoprotein]]></kwd>
<kwd lng="en"><![CDATA[Anti-MAG neuropathy]]></kwd>
<kwd lng="en"><![CDATA[Chronic demyelinating neuropathy]]></kwd>
<kwd lng="en"><![CDATA[Myelin-associated glycoprotein]]></kwd>
<kwd lng="pt"><![CDATA[Neuropatia anti-MAG]]></kwd>
<kwd lng="pt"><![CDATA[Neuropatia desmielinizante crônica]]></kwd>
<kwd lng="pt"><![CDATA[Myelin-associated glycoprotein]]></kwd>
</kwd-group>
</article-meta>
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