Volume 23, Issue 4 pp. 227-234
RESEARCH REPORT

Clinical relevance of serum antibodies to GD1b in immune-mediated neuropathies

Noor E. Taams

Noor E. Taams

Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

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Nicolette C. Notermans

Nicolette C. Notermans

Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands

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Willem-Jan R. Fokkink

Willem-Jan R. Fokkink

Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

Department of Neurology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

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Anne P. Tio-Gillen

Anne P. Tio-Gillen

Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

Department of Neurology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

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Ruth Huizinga

Ruth Huizinga

Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

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Marco W. J. Schreurs

Marco W. J. Schreurs

Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

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Bart C. Jacobs

Corresponding Author

Bart C. Jacobs

Department of Immunology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

Department of Neurology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

Correspondence

Bart C. Jacobs, Department of Neurology and Immunology, Erasmus MC, University Medical Center Rotterdam, PO Box 2040, 3000 CA Rotterdam, The Netherlands.

Email: [email protected]

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First published: 12 August 2018
Citations: 11

Abstract

Antibodies to the ganglioside GD1b have been reported in various forms of immune-mediated neuropathy, but their clinical relevance for diagnosis and prognosis is unknown. We investigated the prevalence of anti-GD1b antibodies in acute and chronic immune-mediated neuropathies, and the clinical presentation and outcome in Guillain-Barré syndrome (GBS) and Miller Fisher-GBS overlap syndrome (MF-GBS). Anti-GD1b, anti-GM1 and anti-GQ1b antibodies were tested in serum of patients with GBS (N = 165), Miller Fisher syndrome (N = 10), MF-GBS (N = 28), monoclonal gammopathy of unknown significance neuropathy (MGUS; N = 101), chronic inflammatory demyelinating polyneuropathy (N = 29), paraneoplastic syndrome with anti-Hu-associated neuropathy (PNS; N = 11), other auto-immune diseases (AID; N = 60), and healthy controls (HC; N = 60). All samples were tested by enzyme-linked immunosorbent assay according to the Inflammatory Neuropathy Cause and Treatment protocol. IgM anti-GD1b antibodies were found in GBS (N = 4; 2.4%), MGUS (N = 3; 3.0%), and PNS patients (N = 1; 9.1%). IgG anti-GD1b antibodies were found in GBS (N = 20; 12.1%) and MF-GBS (N = 4; 14.3%) patients, but not in the AID and HC group. In the combined group of MF-GBS and GBS patients ((MF-)GBS), 14/36 (38.9%) patients with IgG anti-GD1b antibodies also had IgG anti-GM1 antibodies, and IgG anti-GD1b and IgG anti-GQ1b antibodies were found in 3/29 (10.3%) patients. Patients with (MF-)GBS and anti-GD1b without anti-GM1 antibodies did not differ regarding sensory disturbances or disease severity but recovered faster regarding the ability to walk independently compared with patients without anti-GD1b antibodies (P = 0.031) and with patients with both anti-GD1b and anti-GM1 antibodies (P = 0.034). In conclusion, testing for anti-GD1b antibodies may identify a specific group of immune-mediated neuropathies and (MF-)GBS patients with only anti-GD1b antibodies tend to recover faster.

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