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array:24 [ "pii" => "S2387020619304395" "issn" => "23870206" "doi" => "10.1016/j.medcle.2019.06.015" "estado" => "S300" "fechaPublicacion" => "2019-11-15" "aid" => "4926" "copyright" => "Elsevier España, S.L.U.. All rights reserved" "copyrightAnyo" => "2019" "documento" => "article" "crossmark" => 1 "subdocumento" => "rev" "cita" => "Med Clin. 2019;153:360-7" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "Traduccion" => array:1 [ "es" => array:19 [ "pii" => "S0025775319304488" "issn" => "00257753" "doi" => "10.1016/j.medcli.2019.06.007" "estado" => "S300" "fechaPublicacion" => "2019-11-15" "aid" => "4926" "copyright" => "Elsevier España, S.L.U." "documento" => "article" "crossmark" => 1 "subdocumento" => "rev" "cita" => "Med Clin. 2019;153:360-7" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 24 "formatos" => array:2 [ "HTML" => 10 "PDF" => 14 ] ] "es" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Revisión</span>" "titulo" => "Autoanticuerpos en neuropatías inflamatorias inmunomediadas" "tienePdf" => "es" "tieneTextoCompleto" => "es" "tieneResumen" => array:2 [ 0 => "es" 1 => "en" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "360" "paginaFinal" => "367" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Autoantibodies in immune-mediated inflammatory neuropathies" ] ] "contieneResumen" => array:2 [ "es" => true "en" => true ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figura 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 2832 "Ancho" => 2083 "Tamanyo" => 329308 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Estructura de los gangliósidos y mimetismo molecular. La presencia de una estructura de lipooligosacárido de membrana bacteriana en <span class="elsevierStyleItalic">Campylobacter</span> similar a los gangliósidos GM1, GD1a o GQ1b puede determinar reacción cruzada por anticuerpos contra el nervio periférico.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Lorena Martín-Aguilar, Elba Pascual-Goñi, Luis Querol" "autores" => array:3 [ 0 => array:2 [ "nombre" => "Lorena" "apellidos" => "Martín-Aguilar" ] 1 => array:2 [ "nombre" => "Elba" "apellidos" => "Pascual-Goñi" ] 2 => array:2 [ "nombre" => "Luis" "apellidos" => "Querol" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2387020619304395" "doi" => "10.1016/j.medcle.2019.06.015" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020619304395?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775319304488?idApp=UINPBA00004N" "url" => "/00257753/0000015300000009/v1_201910300628/S0025775319304488/v1_201910300628/es/main.assets" ] ] "itemSiguiente" => array:19 [ "pii" => "S2387020619304371" "issn" => "23870206" "doi" => "10.1016/j.medcle.2019.04.022" "estado" => "S300" "fechaPublicacion" => "2019-11-15" "aid" => "4889" "copyright" => "Elsevier España, S.L.U." "documento" => "article" "crossmark" => 1 "subdocumento" => "sco" "cita" => "Med Clin. 2019;153:368-71" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Special article</span>" "titulo" => "Bullous pemphigoid and DPP4 inhibitors" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "368" "paginaFinal" => "371" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Penfigoide ampolloso e inhibidores de la DPP4" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1937 "Ancho" => 4445 "Tamanyo" => 1106149 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">82-year-old female patient with type 2 diabetes mellitus in therapy with linagliptin. Three and a half months after the start of treatment, blistering and erosive lesions begin to appear (left). Confirmed diagnosis of bullous pemphigoid; refractory to doses of prednisone of up to 2 mg/kg/day and intensified topical cures (applied poultice using zinc sulfate and betamethasone valerate gentamicin sulfate every 6 h). On suspicion of BP associated with iDPP-4, linagliptin is withdrawn and replaced with insulin. After eight days (centre), the patient undergoes a significant clinical improvement, with partial epithelialization of the lesions, without modifications in the treatment of BP. We decided to reduce the doses of prednisone to 1 mg/kg/day. In fewer than 30 days, medium-sized lesions completely epithelized and large lesions had a very favourable evolution (right). The glucocorticoid regime is gradually decreased with complete healing one and a half months after withdrawal of iDPP-4.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Rubén García Castro, Elena Godoy Gijón, Ana María González Pérez, Concepción Román Curto" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Rubén" "apellidos" => "García Castro" ] 1 => array:2 [ "nombre" => "Elena" "apellidos" => "Godoy Gijón" ] 2 => array:2 [ "nombre" => "Ana María" "apellidos" => "González Pérez" ] 3 => array:2 [ "nombre" => "Concepción" "apellidos" => "Román Curto" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775319304075" "doi" => "10.1016/j.medcli.2019.04.031" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775319304075?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020619304371?idApp=UINPBA00004N" "url" => "/23870206/0000015300000009/v1_201911071124/S2387020619304371/v1_201911071124/en/main.assets" ] "itemAnterior" => array:19 [ "pii" => "S238702061930436X" "issn" => "23870206" "doi" => "10.1016/j.medcle.2019.03.018" "estado" => "S300" "fechaPublicacion" => "2019-11-15" "aid" => "4839" "copyright" => "Elsevier España, S.L.U." "documento" => "article" "crossmark" => 1 "subdocumento" => "sco" "cita" => "Med Clin. 2019;153:357-9" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial</span>" "titulo" => "Map of ethical conflicts of the CRISPR-Cas9 gene edition technique" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "357" "paginaFinal" => "359" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Mapa de conflictos éticos de la técnica de edición genética CRISPR-Cas9" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "David Lorenzo, Montse Esquerda" "autores" => array:3 [ 0 => array:2 [ "nombre" => "David" "apellidos" => "Lorenzo" ] 1 => array:2 [ "nombre" => "Montse" "apellidos" => "Esquerda" ] 2 => array:1 [ "colaborador" => "Grupo Interdisciplinar en Bioética" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775319302532" "doi" => "10.1016/j.medcli.2019.03.024" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775319302532?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S238702061930436X?idApp=UINPBA00004N" "url" => "/23870206/0000015300000009/v1_201911071124/S238702061930436X/v1_201911071124/en/main.assets" ] "en" => array:20 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "Autoantibodies in immune-mediated inflammatory neuropathies" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "360" "paginaFinal" => "367" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Lorena Martín-Aguilar, Elba Pascual-Goñi, Luis Querol" "autores" => array:3 [ 0 => array:2 [ "nombre" => "Lorena" "apellidos" => "Martín-Aguilar" ] 1 => array:2 [ "nombre" => "Elba" "apellidos" => "Pascual-Goñi" ] 2 => array:4 [ "nombre" => "Luis" "apellidos" => "Querol" "email" => array:1 [ 0 => "lquerol@santpau.cat" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Unidad de Enfermedades Neuromusculares, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Autoanticuerpos en neuropatías inmunomediadas" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 2962 "Ancho" => 2167 "Tamanyo" => 363277 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Ganglioside and molecular mimicry structure. The presence of a lipooligosaccharide structure of bacterial membrane in <span class="elsevierStyleItalic">Campylobacter</span> which is similar to the GM1, GD1a or GQ1b gangliosides can determine a cross-reaction by antibodies against the peripheral nerve.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Inflammatory neuropathies are a heterogeneous group of rare diseases of the peripheral nervous system. They are characterized by motor and sensory symptoms that are usually disabling and that generally improve with immunomodulatory and immunosuppressive treatments.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The diagnosis of these diseases is based on clinical and electrophysiological criteria, which determines a great heterogeneity in its clinical spectrum. There are acute forms encompassed in the Guillain-Barré syndrome (GBS) and its variants, as well as chronic forms such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multifocal motor neuropathy (MMN) or demyelinating neuropathy associated with monoclonal gammopathy of uncertain significance (D-MGUS). The presence of inflammatory infiltrates in nerves and nerve roots<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> support the autoimmune pathogenesis of these diseases. Although the exact immunopathogenic mechanisms of these diseases are largely unknown, the response to immunomodulatory treatment with intravenous immunoglobulins (IVIg) or plasma exchange suggests that autoantibodies play a key role in their development.</p><p id="par0010" class="elsevierStylePara elsevierViewall">In recent years, papers have described several autoantibodies that recognize different antigens located in the peripheral nerve and that are associated with specific clinical phenotypes, including treatment response profiles that differ from the variants not associated with autoantibodies. A paradigmatic example is the description of autoantibodies directed against paranodal antigens and the node of Ranvier in the CIDP. These are neurofascin-155 (NF155),<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> nodal neurofascin (NF140/186),<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> contactin-1 (CNTN1)<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> and contactin-associated protein 1 (Caspr1),<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> which are present in 5–10% of patients. The description of these autoantibodies has been a boost in the field of immunomediated neuropathies, not only because of its direct usefulness in clinical practice as diagnostic biomarkers, but also because, for the first time, the existence of different subtypes of disease with antigenic targets and various immunopathogenic mechanisms is shown. In this review we will provide deeper knowledge regarding the autoantibodies and their clinical relevance in acute and chronic immunomediated neuropathies.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Guillain Barre syndrome</span><p id="par0015" class="elsevierStylePara elsevierViewall">GBS is characterized by a symmetrical and ascending weakness with hyporeflexia or areflexia, of acute and single phase course, when the nadir of weakness is reached in about four weeks. Although the predominant symptoms are motor symptoms; sensitivity symptoms such as paraesthesia or hypoaesthesia, are quite common in typical GBS and generally occur distally and symmetrically. It is the most frequent and most severe acute paralytic neuropathy, affecting approximately 100,000 people per year worldwide.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Its treatment is based on IVIg and plasma exchange.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Its classic diagnostic criteria are well defined and the clinical suspicion is based on albuminocytologic dissociation in cerebrospinal fluid (CSF) and electrophysiological criteria,<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> its presentation, clinical course and prognosis differs considerably from patient to patient. In addition, the differential diagnosis is broad with other causes of acute weakness, so having specific biomarkers such as antibodies may be key to confirming the diagnosis. Within this syndrome, several clinical and electrophysiological forms with different prognoses have been described. The most common subtypes of GBS are acute demyelinating inflammatory polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). There are other less frequent clinical variants, such as acute sensory ataxic neuropathy, characterized by the predominance of ataxia with positive Romberg sign and the positivity of antibodies against the disialosyl epitopes<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a>; Miller Fisher syndrome (MFS), characterized by ophthalmoplegia, ataxia and areflexia with positive anti-GQ1b antibodies<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a>; or Bickerstaff encephalitis, clinically similar to MFS plus drowsiness and long tract signs involvement, also associated with anti-GQ1b.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> Finally, the pharyngeal-cervical-brachial (PCB) variant, which occurs in the form of acute bulbar paralysis and proximal weakness of the upper extremities, and is associated with anti-GT1a antibodies.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Immunopathogenesis</span><p id="par0025" class="elsevierStylePara elsevierViewall">The immunopathogenesis of GBS is relatively unknown and most of the findings described are based on the animal model of acute experimental neuritis. There are also several studies of necropsies in patients with GBS, which describe edema, segmental demyelination, axonal damage and inflammatory infiltrates, with a more important involvement of the root when the segment analyzed is more proximal. The most specific finding of inflammatory neuropathies is the presence of inflammatory infiltrates in the endoneurial space. In some patients with GBS the existence of complement deposition in the peripheral nerve membrane has been demonstrated,<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> so it is postulated that complement activation mediated by the binding of specific antibodies directed against Schwann cell epitopes would be decisive in the appearance of demyelination.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> Among the different immunopathogenic mechanisms proposed in the AMAN variants of GBS is the autoantibody-mediated attack directed against node of Ranvier structures. In these patients there is no demyelination or peripheral inflammatory infiltrates, but IgG and complement depositions appear in the motor fibre axolemma.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> These changes may be initially reversible, which explains the rapid recovery of some patients.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Recently, a new concept has been introduced in the pathophysiology of immunomediated neuropathies: nodopathy.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> This concept stems from the discovery of the involvement of the nodal region in the pathophysiology of immunomediated neuropathies, and from the need to reformulate the classification of neuropathies as demyelinating or axonal in those patients in which there is no clear demyelinating involvement nor denervation in the needle electromyogram, but the neurography shows a drop in the amplitude of the motor potentials, suggesting a motor conduction failure which is reversible when the disease improves.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Antiganglioside antibodies and molecular mimicry</span><p id="par0035" class="elsevierStylePara elsevierViewall">Approximately 2 thirds of patients with GBS report having presented infectious symptoms six weeks before the onset of symptoms<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a>; typically after a gastrointestinal or respiratory infection, in which the immune response generates antibodies that cross-react with the gangliosides in nerve membranes. This autoimmune response causes nerve damage or a functional nerve conduction block. The preceding type of infection and the specificity of the antiganglioside antibodies largely determine the subtype and the clinical development of the GBS. The most common pathogen that precedes GBS in 30–40% of cases is <span class="elsevierStyleItalic">Campylobacter jejuni (C. jejuni)</span>, associated with the AMAN subtype, although other pathogens such as <span class="elsevierStyleItalic">Mycoplasma, Haemophilus</span>, <span class="elsevierStyleItalic">Cytomegalovirus</span> and, more recently, the Zika virus<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> and hepatitis E<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> have been associated with GBS. The history of prior vaccination has also been associated with the development of GBS.</p><p id="par0040" class="elsevierStylePara elsevierViewall">This direct relationship with a previous infection has led to propose the theory of molecular mimicry between antigens of the infectious agent and the peripheral nerve. Infection by <span class="elsevierStyleItalic">C. jejuni</span> determines the appearance of antibodies against bacteria cell wall lipooligosaccharides, which are structurally similar to the GM1 and GD1a gangliosides, present in the nerve and neuromuscular junction<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">Antiganglioside antibodies are oligoclonal antibodies that activate the complement and affect the function of the node of Ranvier in the motor axons.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> The description of the appearance of a motor GBS in 7 patients after parenteral injection of ganglioside<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a> supports its role in the pathogenesis of the disease. The main gangliosides of the nervous system include GM1, GM2, GD1a, GD1b, GT1a, GT1b and GQ1b, and they have specific locations in the peripheral nerve immunohistochemistry: for example, the GD1a ganglioside is located in the motor fibers and GD1b in the dorsal spinal ganglia.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> Thus, the presence of the GQ1b epitope in the nerves of the extrinsic ocular muscles would explain ophthalmoparesis in the MFS and its presence in the dorsal spinal ganglia would explain the associated ataxia. The association of each ganglioside subtype with the GBS phenotype is detailed in <a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Chronic inflammatory demyelinating polyradiculoneuropathy</span><p id="par0050" class="elsevierStylePara elsevierViewall">CIDP is the most frequent chronic inflammatory neuropathy. Its typical form of presentation (in 75% of cases) is characterized by predominantly proximal muscle weakness and distal sensory symptoms in the 4 limbs, which develops over at least an 8-week period. In some patients the onset of symptoms is acute, so they may be mistakenly diagnosed with GBS. The CIDP spectrum also includes atypical variants with weakness of distal predominance (DADS variant), asymmetric or focal forms of presentation (Lewis-Sumner syndrome) and purely motor, sensory or ataxic forms. In all cases the diagnosis is made based on clinical and electrophysiological criteria,<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> whose objective is to detect all those patients who would benefit from immunomodulatory treatment. This determines a great clinical heterogeneity in patients who, despite sharing the same diagnosis, may differ in the clinical phenotype, response to treatment and immunopathogenic mechanism of their disease.</p><p id="par0055" class="elsevierStylePara elsevierViewall">The pathogenesis of CIDP is mediated by cellular and humoral immunity.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> The characteristic pathological finding of the CIDP is segmental demyelination with a variable presence of inflammatory infiltrates of monocytic predominance, but also of CD4+ and CD8 + T lymphocytes. In addition, the presence of immunoglobulin and complement deposits in sural nerve biopsy samples implicate the humoral immunity in the CIDP.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Treatment consists of IVIg or subcutaneous immunoglobulins, oral glucocorticoids (1 mg/kg/day) or in intravenous pulse therapy and plasma exchange.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Autoantibodies in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)</span><p id="par0060" class="elsevierStylePara elsevierViewall">The good and rapid response of the CIDP to treatment with IVIg or plasma exchange, as well as the presence of immunoglobulin and complement deposits in the sural nerve biopsies of patients, led to the hypothesis that the disease was mediated by autoantibodies. In addition, several groups described the disruption of the node of Ranvier in biopsies of patients with CIDP.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> Recently, several groups, including ours, have described the presence of autoantibodies directed against proteins of the node of Ranvier and paranodes in up to 5–10% of patients with CIDP (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). These antigens are NF155, CNTN1, NF140/186 and Caspr1. They are extracellular proteins anchored to the myelin or the axon, which are involved in the cell adhesion and are key to myelination, the molecular organization of the node of Ranvier and, therefore the preservation of the saltatory conduction. Interestingly, the autoantibodies described are predominantly of the IgG4 isotype, which gives them unique characteristics: they are not capable of activating complement nor cell-mediated cytotoxicity, and they have a high antigenic affinity, so they interfere in the interactions between the antigens and their ligands.<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a> By disrupting the anatomy of the node of Ranvier and its function, they hinder saltatory conduction. In patients with CIDP and IgG4 autoantibodies, a poor response to IVIgs has been reported, although the mechanisms causing this to occur are unknown. However, anti-CD20 therapy  has been shown to be very effective in these subgroups of patients.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> Therefore, the detection of these autoantibodies does not only have diagnostic implications, but it also affects prognosis and treatment choice.</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Anti-neurofascin 155 antibodies (NF155)</span><p id="par0065" class="elsevierStylePara elsevierViewall">About 5% of patients with CIDP have anti-NF155 antibodies.<a class="elsevierStyleCrossRefs" href="#bib0135"><span class="elsevierStyleSup">27,28</span></a> These patients present a unique phenotype which is different from that of the typical CIDP. It is characterized by predominantly distal motor symptoms, disabling tremor and cerebellar ataxia.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> The sural nerve biopsies of these patients are characterized by the disappearance of the junction between the paranodal loops of the Schwann cells and the axon without inflammatory infiltrates.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> On the other hand, patients with CIDP NF155+ are carriers with a high frequency of the class II allele HLA-DRB1*15.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a> Finally, these patients do not usually respond to IVIg treatment, however they may respond to glucocorticoids and B-cell depletion therapies.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> All these peculiarities add weight to the idea that the CIDP NF155+ is a different entity to the typical CIDP.</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Anti-contactin-1 antibodies (CNTN1)</span><p id="par0070" class="elsevierStylePara elsevierViewall">Our group described for the first time the presence of anti-CNTN1 IgG4 antibodies in 2 patients with aggressive CIDP, with acute onset and predominantly motor with denervation in the electromyography.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> These patients had a poor response to IVIg probably because the autoantibodies were of the IgG4 isotype, and yet they responded to B-cell depletion treatment with rituximab.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> Other groups confirmed the presence of anti-CNTN1 antibodies and phenotypic associations similar to those described in our patients in their cohorts of patients with CIDP.<a class="elsevierStyleCrossRefs" href="#bib0155"><span class="elsevierStyleSup">31,32</span></a> The sural nerve biopsy in CIDP anti-CNTN1+ also detects the presence of paranodal axoglial junction dissection, in the absence of inflammatory infiltrates.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Recently there have been reports of patients with anti-CNTN1 + CIDP and associated nephrotic syndrome.<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">34,35</span></a> These patients presented proteinuria in the nephrotic range, hypoalbuminemia, variable alteration of the glomerular filtration rate and glomerulonephritis with IgG4 deposits, without complement. The mechanism by which the presence of anti-CNTN1 antibodies is associated with glomerulonephritis is unknown, but it could be due to their binding to the CNTN1 expressed in the podocytes.</p><p id="par0080" class="elsevierStylePara elsevierViewall">Anti-CNTN1 IgG4 antibodies have demonstrated their pathogenicity both <span class="elsevierStyleItalic">in vitro</span> as well as <span class="elsevierStyleItalic">in vivo</span>, becoming the first pathogenic antibodies described in CIDP.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a> Once again, the anti-CNTN1 demonstrate that the detection of specific antibodies is essential to optimize diagnosis and management in these patients.</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Antibodies against contactin-associated protein 1 (Caspr1)</span><p id="par0085" class="elsevierStylePara elsevierViewall">Anti-Caspr1 antibodies were described in 2 patients, one with CIDP and one with GBS.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In both, IgG deposition was detected in the paranodes of sural nerve fibre preparations. The skin biopsy of these patients showed a disruption of the paranode architecture, and the sural nerve biopsy showed IgG deposits in the paranode. In these patients, pain was one of the predominant symptoms, possibly due to the binding of IgG to the neurons of the dorsal spinal ganglia. These findings have not been replicated to date in other cohorts of patients with immunomediated neuropathies.</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Anti-neurofascin 140/186 antibodies (NF40/86)</span><p id="par0090" class="elsevierStylePara elsevierViewall">Recently identified are autoantibodies directed against the isoforms <span class="elsevierStyleItalic">NF140/186</span><a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> of neurofascin (located in the node of Ranvier) in patients with CIDP. These patients shared a severe phenotype of subacute onset, with sensory ataxia and in some cases cranial involvement. In addition, 2 of the patients presented a nephrotic syndrome. The electrophysiological study highlighted conduction blocks or decreased distal motor amplitudes, which recovered after clinical remission. These findings, indicative of nodopathy, were later corroborated by the description of a patient with antibodies against nodal neurofascin whose sural nerves exhibited an alteration of the node structure with disappearance of the Schwann cell microvilli.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">37</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Other autoantibodies in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)</span><p id="par0095" class="elsevierStylePara elsevierViewall">In studies of systematic autoantibody screening, some patients with CIDP have presented reactivity against Schwann cells, which indicates the presence of autoantibodies directed against myelin structures.<a class="elsevierStyleCrossRefs" href="#bib0190"><span class="elsevierStyleSup">38,39</span></a> In our cohort of patients with CIDP, 18% had ELISA-tested antiganglioside antibodies, among which 4 patients stood out due to with high-titre IgM anti-GM1.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">39</span></a> However, these studies did not include the clinical phenotype of these patients.</p></span></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Multifocal motor neuropathy</span><p id="par0100" class="elsevierStylePara elsevierViewall">MMN is a focal and asymmetric motor neuropathy, with a homogeneous clinical and electrophysiological pattern, characterized by the absence of sensory involvement and the presence of conduction blocks in the neurographs. Its etiology is presumed autoimmune, since the patients respond to treatment with IVIg and 50% present IgM antibodies against the GM1 ganglioside.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a> In contrast, patients with MMN do not respond to plasmapheresis treatment and may worsen with corticosteroid treatment.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a></p><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Multifocal motor neuropathy and anti-GM1</span><p id="par0105" class="elsevierStylePara elsevierViewall">The anti-GM1 antibodies are highly sensitive and specific for MMN and, although their presence is not required by diagnostic criteria, they support diagnosis in patients with compatible clinical features.</p><p id="par0110" class="elsevierStylePara elsevierViewall">Several studies indicate that the diagnostic performance of anti-GM1 in patients with MMN improves when the reactivity of the antibodies to the GM1/galactocerebroside complexes is also evaluated,<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">42</span></a> raising its positivity up to 70% without compromising its specificity in the diagnosis.</p><p id="par0115" class="elsevierStylePara elsevierViewall">IgM anti-GM1 antibodies are pathogenic via complement activation and their pathogenicity is nullified by complement inactivation or the block of GM1.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">43</span></a> In one study, the plasma complement activity of patients with MMN was positively correlated with the anti-GM1 IgM antibody titres and, most importantly, with the severity of the disease.<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">44</span></a> These findings suggest that the complement inhibitors could be an effective treatment for MMN, but the results of a small open trial of the complement inhibitor eculizumab in 13 patients with MMN were considered negative, since the addition of eculizumab did not cause changes in the dosing frequency in the 10 patients who received maintenance IVIg.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a></p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Clinical utility of the detection of anti-GM1 antibodies in multifocal motor neuropathy (MMN)</span><p id="par0120" class="elsevierStylePara elsevierViewall">The key diagnostic feature of MMN is the presence of conduction blocks in the motor neurographs outside the usual compression sites. The use of standardized criteria allows easy diagnosis of patients who have a typical form of the syndrome.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a> However, there is a subgroup of patients in whom there are no obvious conduction blocks and who respond to treatment with IVIg; being, therefore, included in the diagnosis of an MMN without conduction blocks.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a> In these patients in whom the disease occurs in its atypical form; the diagnosis is more complicated, since the differential diagnosis should include amyotrophic lateral sclerosis and other secondary motor neuron syndromes,<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a> for which there is no treatment and whose prognosis is much worse. Thus, the existence of some patients with MMN who do not show conduction blocks or who do not have an IVIg response makes the search for biomarkers, that may be useful in the diagnosis and management of patients with MMN, important for daily clinical practice.</p><p id="par0125" class="elsevierStylePara elsevierViewall">Requesting antibodies against gangliosides is of particular interest in those patients who have clinical syndromes that do not meet the classic diagnostic criteria of MMN, since the presence of anti-GM1 IgM antibodies could identify a subset of patients with atypical MMN. This then could respond to IVIg treatment — despite the lack of evidence of conduction blocks or demyelinating characteristics in the electromyogram.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a> In addition, the proper use of anti GM1 IgM antibodies could also prevent misdiagnosis and excessive treatment of patients who actually have a degenerative lower motor neuron syndrome, instead of an atypical MMN.</p></span></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Polyneuropathy associated with monoclonal gammopathy of uncertain significance</span><p id="par0130" class="elsevierStylePara elsevierViewall">Neuropathies that present in the context of monoclonal gammopathy have traditionally called paraproteinemic polyneuropathies. Although they may present in the context of malignant lymphoid neoplasms such as Waldenström macroglobulinemia or myeloma, most of these neuropathies are associated to the presence of a MGUS. Demyelinating neuropathies associated to MGUS are usually of the IgM type and are called D-MGUS. 50% of patients with IgM-MGUS will develop peripheral neuropathy. The D-IgM-MGUS has clinicopathological characteristics different from those of the CIDP. In contrast, patients with demyelinating polyneuropathies associated with IgG- or IgA-MGUS generally have a clinical phenotype superimposable on the typical CIDP. In these cases it is not clear whether there is a causal relationship between IgG- or IgA-MGUS and the neuropathy, since the MGUS could be an incidental finding not related to the development of the neuropathy.</p><p id="par0135" class="elsevierStylePara elsevierViewall">The clinical spectrum of D-MGUS is very wide. The most common form of presentation is characterized by distal sensory symptoms in hands or feet which slowly progress over months or even years, to which can be added sensory ataxia of the gait, postural tremor and mild distal weakness. In a small percentage of patients the symptoms begin subacutely in the form of disabling sensory and motor symptoms, which may resemble a typical CIDP. Electrophysiological studies show slow conduction velocities and typically elongated motor distal latencies that are indicative of distal demyelination.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">49</span></a> Electrophoresis and protein immunofixation studies show an IgM monoclonal peak and the total IgM levels are usually increased. The CSF study usually shows high protein levels. More than 50% of patients with D-MGUS have autoantibodies directed against myelin-associated glycoprotein (MAG).<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a> In addition, some patients have autoantibodies directed against sulfates<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a> or against gangliosides with disialosyl groups.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a> The sural nerve biopsy of these patients shows a loss of myelinated thick fibers and IgM deposits, and complement in the paranodes and in the Schmidt-Lanterman incisures. The findings in the electron microscopy are very characteristic and consist in an increase in the spaces between the myelin terminal loops adjacent to the node of Ranvier, in the same location as the IgM deposits.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">The presence of deposits of IgM and complement in the patients' nerves, as well as the studies of transferring human anti-MAG antibodies to animal models that trigger demyelinating neuropathy,<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">54</span></a> suggest a pathogenic effect of the IgM antibodies. Based on these findings, multiple immunomodulatory or immunosuppressive treatments have been tested. However, the response has been limited. Some studies have shown beneficial effects of IVIg,<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> rituximab<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a> and cyclophosphamide.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> Taking into account that these effects are partial or transitory and that the treatments are not harmless, they are usually reserved for aggressive D-MGUS. On the other hand, patients with MGUS are at risk of developing malignant neoplasms of plasma cells. Therefore, at the time of diagnosis of the monoclonal gammopathy it is mandatory to perform a malignancy screening. In addition, an annual follow-up that includes electrophoresis, protein immunofixation and immunoglobulin levels should be performed in order to detect possible malignancy.</p><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Antibodies against myelin-associated glycoprotein (anti-MAG)</span><p id="par0145" class="elsevierStylePara elsevierViewall">Approximately 50% of patients with D-MGUS have IgM antibodies directed against MAG, a transmembrane glycoprotein located in the Schwann cells that participates in the adhesion between the myelin loops, contributing to its maintenance. The technique of choice for detecting the anti-MAG antibodies in serum is ELISA. The presence of these autoantibodies is associated with a relatively homogeneous clinical phenotype characterized by predominantly sensory distal symptoms that are slowly progressive, along with gait ataxia and tremor. Therefore, the anti-MAG antibodies are highly sensitive and specific for the diagnosis of anti-MAG + D-MGUS. On the contrary, its use is not recommended to monitor the therapeutic response or for prognostic purposes, since the titres do not always correlate with the severity of the symptoms.</p></span><span id="sec0085" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">IgM antiganglioside antibodies</span><p id="par0150" class="elsevierStylePara elsevierViewall">A percentage of patients with anti-MAG D-MGUS negative have presented IgM reactivity against gangliosides containing disialosyl epitopes. Some patients may present chronic ataxic neuropathy with bulbar involvement, which is associated with the presence of IgM antibodies against NeuNAc(〈2-3)Gal epitopes shared by GM3, GD1a and GT1b gangliosides.<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a> A few patients with IgM-MGUS present chronic ataxic sensory neuropathy with a characteristic phenotype called CANOMAD syndrome. This includes chronic ataxic neuropathy with ophthalmoplegia, trigeminal involvement, facial and bulbar weakness, IgM monoclonal protein, cold agglutinin disease and IgM antiganglioside antibodies containing disialosyl epitopes (GD1b, GD3, GT1b and GQ1b).<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a></p></span><span id="sec0090" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Antisulphatide antibodies</span><p id="par0155" class="elsevierStylePara elsevierViewall">Some patients with D-MGUS present IgM reactivity against sulphatide (3<span class="elsevierStyleGlyphsbnd"></span>O<span class="elsevierStyleGlyphsbnd"></span>sulfogalactosylceramide), a type of galactolipid involved in the maturation of the myelin whose presence in the node and paranode is key to the compaction and stability of myelin. These antibodies are associated with heterogeneous clinical conditions with variable neurophysiological and pathological characteristics.<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a> Therefore, its clinical relevance is not well established.</p></span></span><span id="sec0095" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Conclusions</span><p id="par0160" class="elsevierStylePara elsevierViewall">The autoantibodies have been used classically as diagnostic biomarkers in different autoimmune diseases. In many cases, the discovery of the target antigens has allowed their clinical application to be improved, not only for the diagnosis, but also for the treatment.</p><p id="par0165" class="elsevierStylePara elsevierViewall">In the case of the immunomediated neuropathies, its traditional diagnosis is based on clinical symptoms and electrophysiology and this makes the heterogeneity of patients very high and the diagnosis is often incorrect.<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">59</span></a> The discovery of new autoantibodies has allowed a better phenotypic characterization, it has decreased the clinical heterogeneity and it has provided a better treatment choice. The paradigm of this better characterization has been the CIDP, in which the recent discovery of new autoantibodies has allowed the establishment of small subgroups of patients with phenotype, pathophysiological mechanisms and specific therapeutic response.</p><p id="par0170" class="elsevierStylePara elsevierViewall">Thus, the detection of specific antigens involved in autoimmune diseases, including immunomediated neuropathies, is a key element in the understanding of their pathogenesis, clinical characterization and treatment.</p></span><span id="sec0100" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Funding</span><p id="par0175" class="elsevierStylePara elsevierViewall">This project has been funded by the <span class="elsevierStyleGrantSponsor" id="gs0005">Fondo de Investigaciones Sanitarias [Health Research Fund] (FIS)</span>, <span class="elsevierStyleGrantSponsor" id="gs0010">Carlos III Health Institute, Spain</span>, and <span class="elsevierStyleGrantSponsor" id="gs0015">FEDER</span> with the <span class="elsevierStyleGrantNumber" refid="gs0015">FIS16/00627</span> grant, and a personal grant <span class="elsevierStyleGrantNumber" refid="gs0020">SLT006/17/00131</span> from the <span class="elsevierStyleGrantSponsor" id="gs0020">Pla Estratègic de Recerca i Innovació en Salut [Strategic Health Research and Innovation Plan] (PERIS)</span>, Department of Health, Generalitat de Catalunya, PI Luis Querol.</p></span><span id="sec0105" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Conflict of interests</span><p id="par0180" class="elsevierStylePara elsevierViewall">LQ has provided expert testimony for Grifols, Genzyme, Roche, Merck and CSL Behring, and he has received research funds from Novartis Spain, Genzyme and Grifols (Spin Award and ISR). The other authors have no conflicts to declare.</p></span><span id="sec0110" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Thanks</span><p id="par0185" class="elsevierStylePara elsevierViewall">The authors would like to thank Professor Isabel Illa and Dr. René Robles-Cedeño for the assignment of the images used in this review.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:14 [ 0 => array:3 [ "identificador" => "xres1263106" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1169540" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1263107" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1169539" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:3 [ "identificador" => "sec0010" "titulo" => "Guillain Barre syndrome" "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0015" "titulo" => "Immunopathogenesis" ] 1 => array:2 [ "identificador" => "sec0020" "titulo" => "Antiganglioside antibodies and molecular mimicry" ] ] ] 6 => array:3 [ "identificador" => "sec0025" "titulo" => "Chronic inflammatory demyelinating polyradiculoneuropathy" "secciones" => array:6 [ 0 => array:2 [ "identificador" => "sec0030" "titulo" => "Autoantibodies in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)" ] 1 => array:2 [ "identificador" => "sec0035" "titulo" => "Anti-neurofascin 155 antibodies (NF155)" ] 2 => array:2 [ "identificador" => "sec0040" "titulo" => "Anti-contactin-1 antibodies (CNTN1)" ] 3 => array:2 [ "identificador" => "sec0045" "titulo" => "Antibodies against contactin-associated protein 1 (Caspr1)" ] 4 => array:2 [ "identificador" => "sec0050" "titulo" => "Anti-neurofascin 140/186 antibodies (NF40/86)" ] 5 => array:2 [ "identificador" => "sec0055" "titulo" => "Other autoantibodies in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)" ] ] ] 7 => array:3 [ "identificador" => "sec0060" "titulo" => "Multifocal motor neuropathy" "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0065" "titulo" => "Multifocal motor neuropathy and anti-GM1" ] 1 => array:2 [ "identificador" => "sec0070" "titulo" => "Clinical utility of the detection of anti-GM1 antibodies in multifocal motor neuropathy (MMN)" ] ] ] 8 => array:3 [ "identificador" => "sec0075" "titulo" => "Polyneuropathy associated with monoclonal gammopathy of uncertain significance" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0080" "titulo" => "Antibodies against myelin-associated glycoprotein (anti-MAG)" ] 1 => array:2 [ "identificador" => "sec0085" "titulo" => "IgM antiganglioside antibodies" ] 2 => array:2 [ "identificador" => "sec0090" "titulo" => "Antisulphatide antibodies" ] ] ] 9 => array:2 [ "identificador" => "sec0095" "titulo" => "Conclusions" ] 10 => array:2 [ "identificador" => "sec0100" "titulo" => "Funding" ] 11 => array:2 [ "identificador" => "sec0105" "titulo" => "Conflict of interests" ] 12 => array:2 [ "identificador" => "sec0110" "titulo" => "Thanks" ] 13 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2019-03-14" "fechaAceptado" => "2019-06-04" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1169540" "palabras" => array:6 [ 0 => "Immune-mediated neuropathies" 1 => "Guillain-Barré syndrome" 2 => "CIDP" 3 => "Multifocal motor neuropathy" 4 => "MGUS-P" 5 => "Autoantibodies" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1169539" "palabras" => array:6 [ 0 => "Neuropatías inmunomediadas" 1 => "Síndrome de Guillain-Barré" 2 => "CIDP" 3 => "Neuropatía motora multifocal" 4 => "GMSI-P" 5 => "Autoanticuerpos" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Inflammatory neuropathies are a rare and heterogeneous group of diseases of the nervous system characterized by the dysfunction and damage of different structures of the peripheral nerves. This group includes Guillain-Barré syndrome, chronic demyelinating inflammatory polyradiculoneuropathy, multifocal motor neuropathy or neuropathies associated with monoclonal gammopathy. The aetiology of these diseases is unknown, but B cells and autoantibodies play a key role in their pathogenesis. Autoantibodies against peripheral nerve molecules such as gangliosides, proteins of the Ranvier node or myelin-associated glycoprotein have been described, allowing the identification of subgroups of patients with specific clinical phenotypes. For all these reasons, these antibodies are useful in clinical practice. This review focuses on the diagnostic and therapeutic relevance of autoantibodies in inflammatory neuropathies.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Las neuropatías inflamatorias son un grupo heterogéneo de enfermedades raras del sistema nervioso caracterizadas por la disfunción y el daño de diferentes estructuras de los nervios periféricos. Este grupo incluye el síndrome de Guillain-Barré, la polirradiculoneuropatía inflamatoria desmielinizante crónica, la neuropatía motora multifocal o las neuropatías asociadas a gammapatía monoclonal. La inmunopatogenia de estas enfermedades no es bien conocida, pero las células B y los autoanticuerpos parecen tener un papel clave en su desarrollo. Se han descrito autoanticuerpos dirigidos contra estructuras del nervio periférico como los gangliósidos, los anticuerpos dirigidos contra proteínas del nodo de Ranvier o la glucoproteína asociada a la mielina, que permiten identificar subgrupos de pacientes con fenotipos clínicos específicos asociados a dichos autoanticuerpos. Por todo ello, estos anticuerpos son de gran utilidad en la práctica clínica. Esta revisión se centra en la relevancia diagnóstica y terapéutica de los autoanticuerpos en las neuropatías inmunomediadas.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Martín-Aguilar L, Pascual-Goñi E, Querol L. Autoanticuerpos en neuropatías inmunomediadas. Med Clin (Barc). 2019;153:360–367.</p>" ] ] "multimedia" => array:3 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 2962 "Ancho" => 2167 "Tamanyo" => 363277 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Ganglioside and molecular mimicry structure. The presence of a lipooligosaccharide structure of bacterial membrane in <span class="elsevierStyleItalic">Campylobacter</span> which is similar to the GM1, GD1a or GQ1b gangliosides can determine a cross-reaction by antibodies against the peripheral nerve.</p>" ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1227 "Ancho" => 2490 "Tamanyo" => 176851 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Node of Ranvier and autoantibodies. The myelinated fibers are organized in different domains: the node, the paranode, the juxtaparanode and the internode. In the node, the myelin is interrupted and the axolemma is in direct contact with the extracellular fluid, although it is covered by the Schwann cell microvilli. In the paranode, the loops of the non-compacted myelin are strongly bound to the axolema, and in the internodes the axons are wrapped by compact myelin. CNTN1 and Caspr1 express themselves in the neurons and form a complex that binds to NF155 (its glial counterpart) in paranodal loops. This complex allows the compartmentalization of the voltage-gated sodium channels in the nodes and the voltage-gated potassium channels in the juxtaparanodes. In the CIDP, the IgG4 antibodies bind to CNTN1 or NF155, interfering in the axoglial junction between CNTN1 and Caspr1 (axonals) with NF155 (glial), destructuring the paranode and altering the saltatory conduction.</p>" ] ] 2 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0015" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">AMAN: acute motor axonal neuropathy; AMSAN: acute motor-sensory axonal neuropathy; ASAN: acute sensory ataxic neuropathy; Caspr-1: contactin associated protein 1; CIDP: chronic inflammatory demyelinating polyradiculoneuropathy; CJ: <span class="elsevierStyleItalic">Campylobacter jejuni</span>; CNTN-1: contactin-1; EMG: electromyogram; D-MGUS: demyelinating neuropathy associated with monoclonal gammopathy of uncertain significance; IgG: Immunoglobulin G; IVIg: intravenous immunoglobulins; IgM: immunoglobulin M; CSF: cerebrospinal fluid; MAG: myelin-associated glycoprotein; NF140/186: neurofascin-140/186; NF155: neurofascin-155; MMN: multifocal motor neuropathy; GBS: Guillain-Barré syndrome; MFS: Miller Fisher syndrome.</p>" "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Neuropathy \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Autoantibody \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Clinical phenotype \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Frequency \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " colspan="4" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">GBS</span></td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-GM1 IgG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">AMAN \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">30% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-GD1a IgG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">AMSAN \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">GD1b IgG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Sensory GBS \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Unknown \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">IgG disialosyl \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">ASAN \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Unknown \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">GQ1b IgG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Miller Fisher syndrome: ophthalmoplegia, ataxia and arreflexia \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">95% MFS \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">GT1a IgG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Pharyngeal-cervical-brachial paralysis: oropharynx, neck and proximal upper limb involvement \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">50% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " colspan="4" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">CIDP</span></td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-NF155 IgG4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Distal motor deficit, tremor, cerebellar ataxia, poor IVIg response \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5–10% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-NF140/186 IgG4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Subacute and aggressive onset, conduction blocks, associated nephrotic syndrome \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">2% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " rowspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"></td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " rowspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-CNTN-1 IgG4</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Neuropathy of acute and aggressive onset, poor IVIg response \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " rowspan="2" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5%</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Associated nephrotic syndrome \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-CASPR-1 IgG4 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Demyelinating neuropathy with severe pain \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><1% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-GM1 IgM \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Phenotype not described \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">6% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " colspan="4" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">MMN</span></td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-GM1 IgM \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Focal and asymmetric motor neuropathy without sensory involvement and with or without conduction blocks in the EMG \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">50% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " colspan="4" align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"><span class="elsevierStyleItalic">D-MGUS</span></td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Anti-MAG IgM \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Predominantly distal sensory involvement, mild distal motor involvement, ataxia, tremor \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">50% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">IgM Antisulphate \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Variable phenotype \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1% \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Antidisialosyl IgM \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Ataxia, ophthalmoparesis, bulbar involvement \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">1% \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2160539.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Autoantibodies in the immunomediated neuropathies and associated clinical phenotypes.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:59 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Advances in the diagnosis, pathogenesis and treatment of CIDP" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "M.C. 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