SAT0320 Igg3 Autoantibodies Binding To Stathmin-4 as Marker of Polyneuropathy in Primary Sjögren Syndrome. (15th July 2016)
- Record Type:
- Journal Article
- Title:
- SAT0320 Igg3 Autoantibodies Binding To Stathmin-4 as Marker of Polyneuropathy in Primary Sjögren Syndrome. (15th July 2016)
- Main Title:
- SAT0320 Igg3 Autoantibodies Binding To Stathmin-4 as Marker of Polyneuropathy in Primary Sjögren Syndrome
- Authors:
- Ross, S.
Witte, T.
Stangel, M.
Schmidt, R.E.
Baerlecken, N.T. - Abstract:
- Abstract : Background: Primary Sjögren-syndrome (pSS) is considered as autoimmune phenomena affecting exocrine glands with various clinical phenotyps. PSS can appear with different extraglandular manifestations such as arthritis, myositis, vasculitis and peripheral or central neuropathies. 8.5–67% of patients with pSS complain about neurological symptoms. About 9% can be diagnosed having a destinct form of polyneuropathy (PNP). Objectives: Here, we investigated autoantibodies binding to stathmin-4 (STMN-4) in pSS with PNP. Methods: We screened 4 versus 4 having pSS with and without PNP for discriminating autoantibodies by using protein array technology. We identified autoantibodies binding to STMN-4 in patients with pSS and PNP. We evaluated our finding by establishing different ELISA detections for STMN-4 autoantibodies using sera of different underlying diseases (n=484). Results: Using Anti-IgG3 STMN-4, we tested the following groups. In pSS with PNP 33% had anti-IgG3 STMN-4 antibodies and 6% without PNP had anti-IgG3 STMN-4 (likelihood 5.5). Anti-IgG3 STMN is associated with PNP in pSS patiens (Fisher exact two-tailed p-value=0.016). We could not see any significant association in other diseases with PNP and metabolic or toxic induced PNP. Conclusions: Anti-IgG3 STMN is a new potential marker for PNP in patients with pSS. References: none Disclosure of Interest: S. Ross Shareholder of: none, Grant/research support from: none, Consultant for: none, Employee of: none, PaidAbstract : Background: Primary Sjögren-syndrome (pSS) is considered as autoimmune phenomena affecting exocrine glands with various clinical phenotyps. PSS can appear with different extraglandular manifestations such as arthritis, myositis, vasculitis and peripheral or central neuropathies. 8.5–67% of patients with pSS complain about neurological symptoms. About 9% can be diagnosed having a destinct form of polyneuropathy (PNP). Objectives: Here, we investigated autoantibodies binding to stathmin-4 (STMN-4) in pSS with PNP. Methods: We screened 4 versus 4 having pSS with and without PNP for discriminating autoantibodies by using protein array technology. We identified autoantibodies binding to STMN-4 in patients with pSS and PNP. We evaluated our finding by establishing different ELISA detections for STMN-4 autoantibodies using sera of different underlying diseases (n=484). Results: Using Anti-IgG3 STMN-4, we tested the following groups. In pSS with PNP 33% had anti-IgG3 STMN-4 antibodies and 6% without PNP had anti-IgG3 STMN-4 (likelihood 5.5). Anti-IgG3 STMN is associated with PNP in pSS patiens (Fisher exact two-tailed p-value=0.016). We could not see any significant association in other diseases with PNP and metabolic or toxic induced PNP. Conclusions: Anti-IgG3 STMN is a new potential marker for PNP in patients with pSS. References: none Disclosure of Interest: S. Ross Shareholder of: none, Grant/research support from: none, Consultant for: none, Employee of: none, Paid instructor for: none, Speakers bureau: none, T. Witte Shareholder of: none, Grant/research support from: none, Consultant for: none, Employee of: none, Paid instructor for: none, Speakers bureau: none, M. Stangel Shareholder of: none, Grant/research support from: none, Consultant for: none, Employee of: none, Paid instructor for: none, Speakers bureau: none, R. Schmidt Shareholder of: none, Grant/research support from: none, Consultant for: none, Employee of: none, Paid instructor for: none, Speakers bureau: none, N. Baerlecken Shareholder of: none, Grant/research support from: none, Consultant for: none, Employee of: none, Paid instructor for: none, Speakers bureau: none … (more)
- Is Part Of:
- Annals of the rheumatic diseases. Volume 75(2016)Supplement 2
- Journal:
- Annals of the rheumatic diseases
- Issue:
- Volume 75(2016)Supplement 2
- Issue Display:
- Volume 75, Issue 2 (2016)
- Year:
- 2016
- Volume:
- 75
- Issue:
- 2
- Issue Sort Value:
- 2016-0075-0002-0000
- Page Start:
- 783
- Page End:
- 783
- Publication Date:
- 2016-07-15
- Subjects:
- Rheumatism -- Periodicals
616.723005 - Journal URLs:
- http://ard.bmjjournals.com/ ↗
http://www.pubmedcentral.nih.gov/tocrender.fcgi?journal=149&action=archive ↗
http://www.bmj.com/archive ↗
http://gateway.ovid.com/server3/ovidweb.cgi?T=JS&MODE=ovid&D=ovft&PAGE=titles&SEARCH=annals+of+the+rheumatic+diseases.tj&NEWS=N ↗ - DOI:
- 10.1136/annrheumdis-2016-eular.5243 ↗
- Languages:
- English
- ISSNs:
- 0003-4967
- Deposit Type:
- Legaldeposit
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