Increased frequency of HLA-DRB1*15 in patients with multifocal motor neuropathy

N.A. Sutedja, H.G. Otten, E.A. Cats, S. Piepers, J.H. Veldink, W.L. van der Pol, L.H. van den Berg

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

OBJECTIVES: The favorable response to treatment with IV immunoglobulins and the presence of IgM antibodies to the glycolipid GM1 are indications that inflammation underlies multifocal motor neuropathy (MMN) pathogenesis. We investigated the association of MMN with human leukocyte antigen (HLA) class I and II antigens.

METHODS: HLA class I and II antigens of 74 Dutch patients with MMN and 700 controls were determined in a case-control study. Associations of HLA types with MMN disease characteristics were investigated.

RESULTS: Compared with controls, patients with MMN had higher frequencies of HLA-DRB1*15 (41 vs 24%, p = 0.0017). Disease characteristics were not associated with specific HLA types.

CONCLUSIONS: Similar associations were found in patients with multiple sclerosis and women with chronic immune-mediated demyelinating neuropathy, which may suggest that these demyelinating disorders share pathogenic mechanisms.

Original languageEnglish
Pages (from-to)828-832
Number of pages5
JournalNeurology
Volume74
Issue number10
DOIs
Publication statusPublished - 2010

Keywords

  • Adult
  • Age Factors
  • Aged
  • Brachial Plexus
  • Case-Control Studies
  • Chi-Square Distribution
  • Female
  • G(M1) Ganglioside
  • HLA-DQ Antigens
  • HLA-DQ beta-Chains
  • HLA-DR Antigens
  • HLA-DRB1 Chains
  • Humans
  • Immunoglobulin M
  • Magnetic Resonance Imaging
  • Male
  • Membrane Glycoproteins
  • Middle Aged
  • Multiple Sclerosis
  • Neural Conduction
  • Polyradiculoneuropathy, Chronic Inflammatory Demyelinating
  • Retrospective Studies
  • Journal Article
  • Research Support, Non-U.S. Gov't

Fingerprint

Dive into the research topics of 'Increased frequency of HLA-DRB1*15 in patients with multifocal motor neuropathy'. Together they form a unique fingerprint.

Cite this