title: Neurometabolism of active neuropsychiatric lupus determined with proton MR spectroscopy.
abstract: OBJECTIVE
  To determine the neurometabolism of patients with active neuropsychiatric systemic lupus erythematosus (NPSLE) by using proton MR spectroscopy.
  
  
  METHODS
  Thirty-six patients with SLE and eight control subjects were studied with proton MR spectroscopy to measure brain metabolites. Peaks from N-acetylaspartate (NAA), creatine (Cr), choline (Cho), and at 1.3 parts per million (ppm) lipid, macromolecules, and lactate were measured. Patients were classified as having major NPSLE (seizures, psychosis, major cognitive dysfunction, delirium, stroke, or coma) (n = 15) or minor NPSLE (headache, minor affective disorder, or minor cognitive disorder) (n = 21). Patients with major NPSLE were severely ill and hospitalized.
  
  
  RESULTS
  SLE patients had lower NAA and increased metabolites at 1.3 ppm than did control subjects (NAA/Cr(SLE) = 1.90 +/- 0.35, NAA/Cr(Control) = 2.16 +/- 0.26; 1.3 ppm/Cr(SLE) = 0.49 +/- 0.41, 1.3 ppm/Cr(Control) = 0.27 +/- 0.05). NAA/Cr in patients with current or prior major NPSLE was lower than in patients without major NPSLE. Increased peaks at 1.3 ppm were present in all SLE subgroups, but particularly in patients with major NPSLE. These resonances were not evident at an echo time of 136, indicating that these signals were not lactate.
  
  
  CONCLUSIONS
  Major NPSLE, past or present, is associated with decreased levels of NAA. Elevated peaks around 1.3 ppm do not represent lactate even in severely ill patients, indicating that global ischemia is not characteristic of NPSLE. Neurochemical markers determined by MR spectroscopy may be useful for determining activity and degree of brain injury in NPSLE.
authors.affiliation: Center for Non-Invasive Diagnosis, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque 87131, USA.
authors.forename: W L
authors.initials: WL
authors.lastname: Sibbitt
authors.forename: L J
authors.initials: LJ
authors.lastname: Haseler
authors.forename: R R
authors.initials: RR
authors.lastname: Griffey
authors.forename: S D
authors.initials: SD
authors.lastname: Friedman
authors.forename: W M
authors.initials: WM
authors.lastname: Brooks
mesh_terms: D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001921:Brain / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000175:diagnosis / Q000503:physiopathology*; D002545:Brain Ischemia / Q000175:diagnosis / Q000503:physiopathology; D001931:Brain Mapping; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D050356:Lipid Metabolism; D008180:Lupus Erythematosus, Systemic / Q000175:diagnosis / Q000503:physiopathology*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D019965:Neurocognitive Disorders / Q000175:diagnosis / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology; D012016:Reference Values
chemical_list: D001224:Aspartic Acid; D019344:Lactic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline