title: Autoantibodies and neuropsychiatric events at the time of systemic lupus erythematosus diagnosis: results from an international inception cohort study.
abstract: OBJECTIVE
  To examine, in an inception cohort of systemic lupus erythematosus (SLE) patients, the association between neuropsychiatric (NP) events and anti-ribosomal P (anti-P), antiphospholipid (lupus anticoagulant [LAC], anticardiolipin), anti-beta2-glycoprotein I, and anti-NR2 glutamate receptor antibodies.
  
  
  METHODS
  NP events were identified using the American College of Rheumatology case definitions and clustered into central/peripheral and diffuse/focal events. Attribution of NP events to SLE was determined using decision rules of differing stringency. Autoantibodies were measured without knowledge of NP events or their attribution.
  
  
  RESULTS
  Four hundred twelve patients were studied (87.4% female; mean +/- SD age 34.9 +/- 13.5 years, mean +/- SD disease duration 5.0 +/- 4.2 months). There were 214 NP events in 133 patients (32.3%). The proportion of NP events attributed to SLE varied from 15% to 36%. There was no association between autoantibodies and NP events overall. However, the frequency of anti-P antibodies in patients with central NP events attributed to SLE was 4 of 20 (20%), versus 3 of 107 (2.8%) in patients with other NP events and 24 of 279 (8.6%) in those with no NP events (P = 0.04). Among patients with diffuse NP events, 3 of 11 had anti-P antibodies (27%), compared with 4 of 111 patients with other NP events (3.6%) and 24 of 279 of those with no NP events (8.6%) (P = 0.02). Specific clinical-serologic associations were found between anti-P and psychosis attributed to SLE (P = 0.02) and between LAC and cerebrovascular disease attributed to SLE (P = 0.038). There was no significant association between other autoantibodies and NP events.
  
  
  CONCLUSIONS
  Clinically distinct NP events attributed to SLE and occurring around the time of diagnosis were found to be associated with anti-P antibodies and LAC. This suggests that there are different autoimmune pathogenetic mechanisms, although low sensitivity limits the clinical application of testing for these antibodies.
authors.affiliation: Division of Rheumatology, Nova Scotia Rehabilitation Centre (2nd floor), Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia, Canada. john.hanly@cdha.nshealth.ca
authors.forename: J G
authors.initials: JG
authors.lastname: Hanly
authors.forename: M B
authors.initials: MB
authors.lastname: Urowitz
authors.forename: F
authors.initials: F
authors.lastname: Siannis
authors.forename: V
authors.initials: V
authors.lastname: Farewell
authors.forename: C
authors.initials: C
authors.lastname: Gordon
authors.forename: S C
authors.initials: SC
authors.lastname: Bae
authors.forename: D
authors.initials: D
authors.lastname: Isenberg
authors.forename: M A
authors.initials: MA
authors.lastname: Dooley
authors.forename: A
authors.initials: A
authors.lastname: Clarke
authors.forename: S
authors.initials: S
authors.lastname: Bernatsky
authors.forename: D
authors.initials: D
authors.lastname: Gladman
authors.forename: P R
authors.initials: PR
authors.lastname: Fortin
authors.forename: S
authors.initials: S
authors.lastname: Manzi
authors.forename: K
authors.initials: K
authors.lastname: Steinsson
authors.forename: I N
authors.initials: IN
authors.lastname: Bruce
authors.forename: E
authors.initials: E
authors.lastname: Ginzler
authors.forename: C
authors.initials: C
authors.lastname: Aranow
authors.forename: D J
authors.initials: DJ
authors.lastname: Wallace
authors.forename: R
authors.initials: R
authors.lastname: Ramsey-Goldman
authors.forename: R
authors.initials: R
authors.lastname: van Vollenhoven
authors.forename: G
authors.initials: G
authors.lastname: Sturfelt
authors.forename: O
authors.initials: O
authors.lastname: Nived
authors.forename: J
authors.initials: J
authors.lastname: Sanchez-Guerrero
authors.forename: G S
authors.initials: GS
authors.lastname: Alarcón
authors.forename: M
authors.initials: M
authors.lastname: Petri
authors.forename: M
authors.initials: M
authors.lastname: Khamashta
authors.forename: A
authors.initials: A
authors.lastname: Zoma
authors.forename: J
authors.initials: J
authors.lastname: Font
authors.forename: K
authors.initials: K
authors.lastname: Kalunian
authors.forename: J
authors.initials: J
authors.lastname: Douglas
authors.forename: Q
authors.initials: Q
authors.lastname: Qi
authors.forename: K
authors.initials: K
authors.lastname: Thompson
authors.forename: J T
authors.initials: JT
authors.lastname: Merrill
mesh_terms: D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood; D001323:Autoantibodies / Q000097:blood*; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007391:International Cooperation; D016682:Lupus Coagulation Inhibitor / Q000276:immunology*; D020945:Lupus Vasculitis, Central Nervous System / Q000175:diagnosis / Q000276:immunology* / Q000523:psychology*; D008297:Male; D008875:Middle Aged; D017470:Receptors, Glutamate / Q000276:immunology; D012269:Ribosomal Proteins / Q000276:immunology; D053482:beta 2-Glycoprotein I / Q000276:immunology
chemical_list: D017153:Antibodies, Anticardiolipin; D001323:Autoantibodies; D016682:Lupus Coagulation Inhibitor; D017470:Receptors, Glutamate; D012269:Ribosomal Proteins; D053482:beta 2-Glycoprotein I