{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T15:55:40Z","timestamp":1787241340554,"version":"build-2736575974"},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,9,12]],"date-time":"2018-09-12T00:00:00Z","timestamp":1536710400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Peripheral Nervous Sys"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:p>\n                    Antibodies to the ganglioside GD1b have been reported in various forms of immune\u2010mediated neuropathy, but their clinical relevance for diagnosis and prognosis is unknown. We investigated the prevalence of anti\u2010GD1b antibodies in acute and chronic immune\u2010mediated neuropathies, and the clinical presentation and outcome in Guillain\u2010Barr\u00e9 syndrome (GBS) and Miller Fisher\u2010GBS overlap syndrome (MF\u2010GBS). Anti\u2010GD1b, anti\u2010GM1 and anti\u2010GQ1b antibodies were tested in serum of patients with GBS (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u2009165), Miller Fisher syndrome (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200910), MF\u2010GBS (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200928), monoclonal gammopathy of unknown significance neuropathy (MGUS;\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u2009101), chronic inflammatory demyelinating polyneuropathy (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200929), paraneoplastic syndrome with anti\u2010Hu\u2010associated neuropathy (PNS;\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200911), other auto\u2010immune diseases (AID;\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200960), and healthy controls (HC;\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200960). All samples were tested by enzyme\u2010linked immunosorbent assay according to the Inflammatory Neuropathy Cause and Treatment protocol. IgM anti\u2010GD1b antibodies were found in GBS (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u20094; 2.4%), MGUS (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u20093; 3.0%), and PNS patients (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u20091; 9.1%). IgG anti\u2010GD1b antibodies were found in GBS (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200920; 12.1%) and MF\u2010GBS (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u20094; 14.3%) patients, but not in the AID and HC group. In the combined group of MF\u2010GBS and GBS patients ((MF\u2010)GBS), 14\/36 (38.9%) patients with IgG anti\u2010GD1b antibodies also had IgG anti\u2010GM1 antibodies, and IgG anti\u2010GD1b and IgG anti\u2010GQ1b antibodies were found in 3\/29 (10.3%) patients. Patients with (MF\u2010)GBS and anti\u2010GD1b without anti\u2010GM1 antibodies did not differ regarding sensory disturbances or disease severity but recovered faster regarding the ability to walk independently compared with patients without anti\u2010GD1b antibodies (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.031) and with patients with both anti\u2010GD1b and anti\u2010GM1 antibodies (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.034). In conclusion, testing for anti\u2010GD1b antibodies may identify a specific group of immune\u2010mediated neuropathies and (MF\u2010)GBS patients with only anti\u2010GD1b antibodies tend to recover faster.\n                  <\/jats:p>","DOI":"10.1111\/jns.12285","type":"journal-article","created":{"date-parts":[[2018,8,13]],"date-time":"2018-08-13T01:19:11Z","timestamp":1534123151000},"page":"227-234","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Clinical relevance of serum antibodies to GD1b in immune\u2010mediated neuropathies"],"prefix":"10.1111","volume":"23","author":[{"given":"Noor E.","family":"Taams","sequence":"first","affiliation":[{"name":"Department of Immunology, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolette C.","family":"Notermans","sequence":"additional","affiliation":[{"name":"Department of Neurology University Medical Center Utrecht  Utrecht The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Willem\u2010Jan R.","family":"Fokkink","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"},{"name":"Department of Neurology, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne P.","family":"Tio\u2010Gillen","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"},{"name":"Department of Neurology, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruth","family":"Huizinga","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC University Medical Center Rotterdam  Rotterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marco W. 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