title: Neurometabolite markers of cerebral injury in the antiphospholipid antibody syndrome of systemic lupus erythematosus.
abstract: OBJECTIVE
  To determine the neurometabolic patterns of brain injury in systemic lupus erythematosus with antiphospholipid antibody syndrome (SLE-aPLS).
  
  
  METHODS
  Forty-nine SLE patients (12 SLE-aPLS) and 23 control subjects were studied using magnetic resonance imaging and spectroscopy. N-Acetylaspartate/creatine (NAA/Cre) and choline/Cre (Cho/Cre) were measured in normal-appearing tissue. IgG and IgM antiphospholipid antibodies (aPL) were measured by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Stroke, epilepsy, and elevated IgG-aPL were more common in SLE-aPLS patients than in SLE patients (P<0.001). NAA/Cre was lower (P<0.05) and Cho/Cre higher (P<0.001) in SLE-aPLS patients than in SLE patients without aPLS. Regression models showed NAA/Cre was most related to injury seen by imaging (P<0.01), disease duration (P<0. 05), and prior neuropsychiatric SLE (NPSLE) (P=0.07). Reduced NAA/Cre was more closely related to IgG-aPL (P<0.01) than the presence of stroke or aPLS. When adjusted for all factors, Cho/Cre was most associated with the presence of aPLS (P=0.05).
  
  
  CONCLUSIONS
  SLE and SLE-aPLS are actually a clinical continuum describing brain injury in SLE, with SLE-aPLS being characterized by increased aPL, NPSLE, stroke, epilepsy, and disturbed neurochemistry. An elevated IgG-aPL level is a potent risk factor for brain injury as measured by NAA/Cre in SLE that is independent of stroke and aPLS. However, thrombotic phenomena and the presence of aPL (aPLS) are most closely associated with increased Cho/Cre in SLE. These results suggest that aPLs exacerbate SLE, resulting in increased thrombotic and nonthrombotic brain injuries. Spectroscopy detects brain injury in SLE and may permit better understanding of the neurological consequences of SLE and SLE-aPLS.
authors.affiliation: Clinical and Magnetic Resonance Research System, Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
authors.forename: A
authors.initials: A
authors.lastname: Sabet
authors.forename: W L
authors.initials: WL
authors.lastname: Sibbitt
authors.forename: C A
authors.initials: CA
authors.lastname: Stidley
authors.forename: J
authors.initials: J
authors.lastname: Danska
authors.forename: W M
authors.initials: WM
authors.lastname: Brooks
mesh_terms: D000328:Adult; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000276:immunology / Q000378:metabolism*; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000032:analysis / Q000378:metabolism; D015415:Biomarkers; D001923:Brain Chemistry / Q000276:immunology; D001927:Brain Diseases / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism*; D002544:Cerebral Infarction / Q000209:etiology / Q000378:metabolism; D005260:Female; D006801:Humans; D016014:Linear Models; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology / Q000378:metabolism*; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D011522:Protons
chemical_list: D015415:Biomarkers; D011522:Protons; D001224:Aspartic Acid; C000179:N-acetylaspartate