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Inflammatory neuropathies: all shapes and sizes
  1. Nidhi Garg1,2,
  2. Susanna B Park1,
  3. Matthew C Kiernan1,2
  1. 1 Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia
  2. 2 Institute of Clinical Neurosciences, Royal Prince Alfred Hospital, Sydney, New South Waes, Australia
  1. Correspondence to Dr Nidhi Garg, Brain and Mind Centre, The University of Sydney, Sydney, NSW 2050, Australia; nidhi.garg{at}sydney.edu.au

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One small step for precision medicine in inflammatory neuropathy

Appreciation of the importance of nodal and paranodal regions in the pathophysiology of demyelinating autoimmune neuropathies has been a major recent milestone in the delineation of peripheral autoimmune disorders.1 In the JNNP paper by Doppler et al 2, 140 patients with inflammatory neuropathy were screened for IgM antibodies targeting the paranodal proteins, neurofascin-155 and contactin-1 and the nodal protein, neurofascin-186. While IgG antibodies (most of the IgG4 isotype) against these proteins have been detected in a proportion of patients with inflammatory neuropathy,3 the presence of IgM antibodies has not yet been thoroughly explored. Doppler and colleagues2 report five patients with IgM antibodies against neurofascin-155, four with a clinical diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) and one …

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Footnotes

  • Contributors NG, SBP and MCK drafted the manuscript. All authors revised the manuscript critically for important intellectual content and gave final approval of the version to be published.

  • Funding This work was supported by a National Health and Medical Research Council of Australia Project grant (no: 1107749), funding to Forefront Program Grant (no: 1037746) from the National Health and Medical Research Council of Australia.

  • Competing interests MCK is Editor-in-Chief of JNNP.

  • Patient consent Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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