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Your search keyword '"W. Ludo van der Pol"' showing total 4 results
Start Over Author "W. Ludo van der Pol" Journal journal of neurology, neurosurgery, and psychiatry
4 results on '"W. Ludo van der Pol"'

1. High prevalence of the MYD88 L265P mutation in IgM anti-MAG paraprotein-associated peripheral neuropathy

Author

Steven T. Pals, Josephine M.I. Vos, Mary M. Reilly, Rajeev Gupta, Monique C. Minnema, Jane Chalker, Michael P. Lunn, Marie José Kersten, Willem Kraan, Nicolette C. Notermans, Shirley D'Sa, W. Ludo van der Pol, Pathology, and Clinical Haematology

Subjects
biology, business.industry, Cold agglutinin disease, medicine.disease, Malignancy, Asymptomatic, IgM Monoclonal Gammopathy, 03 medical and health sciences, Psychiatry and Mental health, 0302 clinical medicine, medicine.anatomical_structure, Peripheral neuropathy, Immunoglobulin M, hemic and lymphatic diseases, Immunology, biology.protein, Medicine, Surgery, Neurology (clinical), Bone marrow, medicine.symptom, business, 030217 neurology & neurosurgery, Multiple myeloma, 030215 immunology
Abstract

Immunoglobulin M (IgM) anti-myelin-associated glycoprotein (MAG) paraprotein-associated peripheral neuropathy (anti-MAG PN) is the most frequent type of paraprotein-associated neuropathy. It typically presents as a chronic demyelinating disorder with progressive ataxia, tremor and sensory disturbance.1 By definition, IgM paraproteinaemia and high-titre anti-MAG antibodies are present. Up to 50% of patients develop significant disability. Progressive disease-related disability is considered an indication to start treatment. However, there is no consensus on the optimal treatment approach and a high clinical need for effective therapies.1 IgM paraproteinaemia is the hallmark of Waldenstrom’s macroglobulinaemia (WM) and IgM monoclonal gammopathy of unknown significance (MGUS). WM is an indolent B-cell malignancy with lymphoplasmacytic differentiation typically localised in the bone marrow (BM), while IgM MGUS is considered a premalignant condition, defined as asymptomatic IgM paraproteinaemia with 90%) of patients with WM and approximately 50% of patients with IgM MGUS. The mutation is absent in healthy donors, multiple myeloma and non-IgM MGUS.3 MYD88 is an adaptor protein of the interleukin-1R and toll-like receptor signalling pathways that ultimately lead to activation of nuclear factor …

Published
2018

2. High prevalence of the

Author

Josephine Mathilde, Vos, Nicolette C, Notermans, Shirley, D'Sa, Michael P, Lunn, W Ludo, van der Pol, Willem, Kraan, Mary M, Reilly, Jane, Chalker, Rajeev, Gupta, Marie-José, Kersten, Steven T, Pals, and Monique C, Minnema

Subjects
Adult, Cohort Studies, Male, Myelin-Associated Glycoprotein, Immunoglobulin M, Mutation, Myeloid Differentiation Factor 88, Prevalence, Humans, Peripheral Nervous System Diseases, Female, Middle Aged, Aged
Published
2017

3. Clonality of anti-GM1 IgM antibodies in multifocal motor neuropathy and the Guillain-Barré syndrome

Author

Leonard H. van den Berg, Anne P Tio-Gillen, W-Ludo van der Pol, Elisabeth A. Cats, Bart C. Jacobs, Frank P. Diekstra, Immunology, and Neurology

Subjects
Pathology, medicine.medical_specialty, Clinical Neurology, Mismatch negativity, G(M1) Ganglioside, Immunoglobulin light chain, medicine.disease_cause, Guillain-Barre Syndrome, behavioral disciplines and activities, Immunoglobulin kappa-Chains, Polyneuropathies, Arts and Humanities (miscellaneous), Immunoglobulin lambda-Chains, medicine, Humans, Autoantibodies, B-Lymphocytes, Ganglioside, biology, Guillain-Barre syndrome, business.industry, medicine.disease, Molecular mimicry, Psychiatry and Mental health, Immunoglobulin M, Polyclonal antibodies, Case-Control Studies, Immunology, biology.protein, Surgery, Neurology (clinical), Antibody, business, psychological phenomena and processes, Multifocal motor neuropathy
Abstract

Objective Multifocal motor neuropathy ( MMN) and the Guillain-Barre syndrome ( GBS) are immune-mediated motor neuropathies with antibodies against the ganglioside GM1. In GBS, these antibodies are induced by molecular mimicry, but in MMN their origin is elusive. Methods We compared the light-chain use of anti-GM1 IgM antibodies in serum from 42 patients with MMN and 23 patients with GBS by ELISA. Results Exclusive use of either. or. light chains was found in 38 ( 90%) patients with MMN and 9 ( 39%) with GBS ( p

Published
2014

4. Serum IgG levels in IV immunoglobulin treated chronic inflammatory demyelinating polyneuropathy

Author

Teun van Gelder, Pieter A. van Doorn, Anne P. Tio-Gillen, Nicolette C. Notermans, Krista Kuitwaard, Leonard H. van den Berg, Anneke J. van der Kooi, W-Ludo van der Pol, Marinus Vermeulen, Esther Brusse, Bart C. Jacobs, Wouter van Rijs, Ivo N. van Schaik, Amsterdam Neuroscience, Neurology, Amsterdam institute for Infection and Immunity, 05 Neurology and psychiatry, and Pharmacy

Subjects
Neuromuscular disease, biology, Dose-Response Relationship, Drug, business.industry, Coefficient of variation, Immunoglobulins, Intravenous, Chronic inflammatory demyelinating polyneuropathy, medicine.disease, Fixed dose, Psychiatry and Mental health, Stable Disease, Pharmacokinetics, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating, Immunoglobulin G, Immunology, biology.protein, Medicine, Humans, Surgery, In patient, Neurology (clinical), Antibody, business
Abstract

Objective: To determine the variability of serum IgG in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Methods: All 25 CIDP patients had active but stable disease and were treated with individually optimised fixed dose IVIg regimens. IgG was measured by turbidimetry and variability was defined as coefficient of variation (CV). Results: The intra-patient variability of the pre-treatment IgG levels, post-treatment levels and increase in serum IgG shortly after IVIg (ΔIgG) was low (mean CV=3%, 4%, 10%). The inter-patient variability between patients treated with the same dose and interval was low in pre-treatment, post-treatment and ΔIgG level (mean CV=13%, 11%, 20%). The ΔIgG levels were associated with IVIg dosage (rs=0.78, p

Published
2013

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