title: Cerebral magnetic resonance imaging in patients with or without antiphospholipid antibodies.
abstract: OBJECTIVE
  To determine in patients with systemic lupus erythematosus (SLE) or with primary antiphospholipid syndrome (PAPS) the prevalence of cerebral magnetic resonance imaging changes (MRI) and the relationship with antiphospholipid antibodies.
  
  
  METHODS
  Twenty-nine consecutive SLE patients, 24 PAPS patients and 31 healthy controls were prospectively included in the study and underwent MRI Scan over a 1-year period. MRI scans were analyzed separately by a neuroradiologist for white matter changes [periventricular hyperintensity (PVH) (0-6 scale), deep white matter hyperintensity (WMH) (0-24 scale)], and one neurologist for cerebral atrophy (0-39 scale) and stroke subtypes. Statistical assessment consisted of a discriminant analysis performed with SAS-package with MRI data as dependent variables and, as independent variables, age, sex, arterial hypertension, diabetes mellitus, cardiopathy, migraine, neurological symptoms, antiphospholipid antibodies, SLE, steroid treatment.
  
  
  RESULTS
  The prevalence of cerebral atrophy was increased in both SLE and PAPS groups relative to controls. PVH and WMH scores were significantly higher in SLE and PAPS than in controls. Focal infarct did not differ in the SLE group when compared with PAPS. PVH and WMH scores were significantly higher in patients with neurological symptoms. Using a correlation test we found a weak significant correlation between cerebral atrophy and lupus anticoagulant. The multivariate analysis found only three independent variables related to PVH and WMH: age, the diagnosis of SLE and cerebral atrophy.
  
  
  CONCLUSIONS
  Age, presence of SLE and presence of neurological symptoms were independently related with WMH and PVH, but not antiphospholipid antibodies.
authors.affiliation: Department of Internal Medicine, University of Lille, France.
authors.forename: E
authors.initials: E
authors.lastname: Hachulla
authors.forename: U
authors.initials: U
authors.lastname: Michon-Pasturel
authors.forename: D
authors.initials: D
authors.lastname: Leys
authors.forename: J P
authors.initials: JP
authors.lastname: Pruvo
authors.forename: V
authors.initials: V
authors.lastname: Queyrel
authors.forename: E
authors.initials: E
authors.lastname: Masy
authors.forename: J
authors.initials: J
authors.lastname: Arvieux
authors.forename: C
authors.initials: C
authors.lastname: Caron
authors.forename: F
authors.initials: F
authors.lastname: Brevet-Coupé
authors.forename: P Y
authors.initials: PY
authors.lastname: Hatron
authors.forename: B
authors.initials: B
authors.lastname: Devulder
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000032:analysis; D017152:Antibodies, Antiphospholipid / Q000276:immunology*; D016736:Antiphospholipid Syndrome / Q000175:diagnosis / Q000276:immunology; D001284:Atrophy; D001323:Autoantibodies / Q000032:analysis / Q000276:immunology; D001921:Brain / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D002544:Cerebral Infarction / Q000473:pathology; D005260:Female; D006023:Glycoproteins / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis / Q000276:immunology; D007075:Immunoglobulin M / Q000032:analysis / Q000276:immunology; D016015:Logistic Models; D016682:Lupus Coagulation Inhibitor / Q000032:analysis; D008180:Lupus Erythematosus, Systemic / Q000175:diagnosis / Q000276:immunology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012307:Risk Factors; D012720:Severity of Illness Index; D013927:Thrombosis / Q000175:diagnosis; D053482:beta 2-Glycoprotein I
chemical_list: D017153:Antibodies, Anticardiolipin; D017152:Antibodies, Antiphospholipid; D001323:Autoantibodies; D006023:Glycoproteins; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D016682:Lupus Coagulation Inhibitor; D053482:beta 2-Glycoprotein I