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Autoimmune peripheral neuropathies.
Clin Chim Acta. 2015 Sep 20; 449:37-42.CC

Abstract

Peripheral nervous system axons and myelin have unique potential protein, proteolipid, and ganglioside antigenic determinants. Despite the existence of a blood-nerve barrier, both humoral and cellular immunity can be directed against peripheral axons and myelin. Molecular mimicry may be triggered at the systemic level, as was best demonstrated in the case of bacterial oligosaccharides. The classification of immune neuropathy has been expanded to take into account specific syndromes that share unique clinical, electrophysiological, prognostic and serological features. Guillain-Barré syndrome encompasses a classical syndrome of acute demyelinating polyradiculoneuropathy and many variants: axonal motor and sensory, axonal motor, Miller-Fisher, autonomic, and sensory. Similarly, chronic immune neuropathy is composed of classic chronic inflammatory demyelinating polyradiculoneuropathy and variants characterized as multifocal (motor or sensorimotor), sensory, distal symmetric, and syndromes associated with monoclonal gammopathy. Among putative biomarkers, myelin associated glycoprotein and several anti-ganglioside autoantibodies have shown statistically significant associations with specific neuropathic syndromes. Currently, the strongest biomarker associations are those linking Miller-Fisher syndrome with anti-GQ1b, multifocal motor neuropathy with anti-GM1, and distal acquired symmetric neuropathy with anti-MAG antibodies. Many other autoantibody associations have been proposed, but presently lack sufficient specificity and sensitivity to qualify as biomarkers. This field of research has contributed to the antigenic characterization of motor and sensory functional systems, as well as helping to define immune neuropathic syndromes with widely different clinical presentation, prognosis and response to therapy. Serologic biomarkers are likely to become even more relevant with the advent of new targeted forms of immunotherapy, such as monoclonal antibodies.

Authors+Show Affiliations

Division of Neurology, The Ottawa Hospital, 1053 Carling Avenue, Ottawa, ON K1Y 4E9, Canada.Division of Neurology, The Ottawa Hospital, 1053 Carling Avenue, Ottawa, ON K1Y 4E9, Canada; Department of Genetics, The Children's Hospital of Eastern Ontario, 401 Smyth Road, Ottawa, ON, K1H 8L1, Canada.Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC H3A 2B4, Canada.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25748038

Citation

Bourque, Pierre R., et al. "Autoimmune Peripheral Neuropathies." Clinica Chimica Acta; International Journal of Clinical Chemistry, vol. 449, 2015, pp. 37-42.
Bourque PR, Chardon JW, Massie R. Autoimmune peripheral neuropathies. Clin Chim Acta. 2015;449:37-42.
Bourque, P. R., Chardon, J. W., & Massie, R. (2015). Autoimmune peripheral neuropathies. Clinica Chimica Acta; International Journal of Clinical Chemistry, 449, 37-42. https://doi.org/10.1016/j.cca.2015.02.039
Bourque PR, Chardon JW, Massie R. Autoimmune Peripheral Neuropathies. Clin Chim Acta. 2015 Sep 20;449:37-42. PubMed PMID: 25748038.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Autoimmune peripheral neuropathies. AU - Bourque,Pierre R, AU - Chardon,Jodi Warman, AU - Massie,Rami, Y1 - 2015/03/04/ PY - 2015/02/23/received PY - 2015/02/23/accepted PY - 2015/3/10/entrez PY - 2015/3/10/pubmed PY - 2016/6/23/medline KW - Antiganglioside antibodies KW - Guillain-Barré syndrome KW - Multifocal motor neuropathy KW - Myelin KW - Neuropathy SP - 37 EP - 42 JF - Clinica chimica acta; international journal of clinical chemistry JO - Clin. Chim. Acta VL - 449 N2 - Peripheral nervous system axons and myelin have unique potential protein, proteolipid, and ganglioside antigenic determinants. Despite the existence of a blood-nerve barrier, both humoral and cellular immunity can be directed against peripheral axons and myelin. Molecular mimicry may be triggered at the systemic level, as was best demonstrated in the case of bacterial oligosaccharides. The classification of immune neuropathy has been expanded to take into account specific syndromes that share unique clinical, electrophysiological, prognostic and serological features. Guillain-Barré syndrome encompasses a classical syndrome of acute demyelinating polyradiculoneuropathy and many variants: axonal motor and sensory, axonal motor, Miller-Fisher, autonomic, and sensory. Similarly, chronic immune neuropathy is composed of classic chronic inflammatory demyelinating polyradiculoneuropathy and variants characterized as multifocal (motor or sensorimotor), sensory, distal symmetric, and syndromes associated with monoclonal gammopathy. Among putative biomarkers, myelin associated glycoprotein and several anti-ganglioside autoantibodies have shown statistically significant associations with specific neuropathic syndromes. Currently, the strongest biomarker associations are those linking Miller-Fisher syndrome with anti-GQ1b, multifocal motor neuropathy with anti-GM1, and distal acquired symmetric neuropathy with anti-MAG antibodies. Many other autoantibody associations have been proposed, but presently lack sufficient specificity and sensitivity to qualify as biomarkers. This field of research has contributed to the antigenic characterization of motor and sensory functional systems, as well as helping to define immune neuropathic syndromes with widely different clinical presentation, prognosis and response to therapy. Serologic biomarkers are likely to become even more relevant with the advent of new targeted forms of immunotherapy, such as monoclonal antibodies. SN - 1873-3492 UR - https://www.unboundmedicine.com/medline/citation/25748038/Autoimmune_peripheral_neuropathies_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-8981(15)00123-0 DB - PRIME DP - Unbound Medicine ER -