NDLI: Terminal complement activation is increased and associated with disease severity in CIDP

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Terminal complement activation is increased and associated with disease severity in CIDP

Content Provider	Semantic Scholar
Author	Quast, Isaak Keller, Ch. Hiepe, Falk Tackenberg, Bjoern Lünemann, Jan D.
Copyright Year	2016
Abstract	Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common chronic autoimmune neuropathy. While both cell-mediated and humoral mechanisms contribute to its pathogenesis, the rapid clinical response to plasmapheresis implicates a circulating factor responsible for peripheral nerve injury. We report that treatment-naïve patients with CIDP show increased serum and CSF levels of the anaphylatoxin C5a and the soluble terminal complement complex (sTCC). Systemic terminal complement activation correlates with clinical disease severity as determined by the Inflammatory Neuropathy Cause and Treatment (INCAT) disability scale. These data indicate that complement activation contributes to peripheral nerve injury and suggest that complement inhibition should be explored for its potential therapeutic merit in CIDP.
Starting Page	730
Ending Page	735
Page Count	6
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://edocs.fu-berlin.de/docs/servlets/MCRFileNodeServlet/FUDOCS_derivate_000000007306/acn3331.pdf
PubMed reference number	5018585
Alternate Webpage(s)	https://doi.org/10.1002/acn3.331
DOI	10.1002/acn3.331
Journal	Annals of clinical and translational neurology
Volume Number	3
Language	English
Access Restriction	Open
Subject Keyword	Anaphylatoxin Autoimmune Diseases Complement Activation Complement System Proteins Demyelinating peripheral neuropathy Patients Peripheral Nerve Injuries Peripheral Nerves Plasmapheresis Polyneuropathy Polyradiculoneuropathy, Chronic Inflammatory Demyelinating membrane attack complex location nerve injury nervous system disorder
Content Type	Text
Resource Type	Article

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