Abstract

ABNORMALITIES OF HIPPOCAMPAL SIGNAL INTENSITY PREDICTS HIPPOCAMPAL ATROPHY IN SYSTEMIC LUPUS ERYTHEMATOSUS

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A.T. Lapa, L.F. Silveira, T. Pedro, J. Francischinelli, L.T. Costallat, F. Cendes, S. AppenzellerMedicine Neurology, State University of Campinas, Campinas, BrazilObjectives: To quantify signal abnormalities in the hippocampus (Hsig) of patients with systemic lupus erythematosus (SLE) and to determine if Hsig predicts hippocampal atrophy (HA) in SLE. Methods: We screened consecutive SLE patients followed in a longitudinal cohort in the State University of Campinas. We excluded patients with any clinical factors associated with cerebral atrophy or vasculopathy or illiterate patients. We included all SLE patients with 2 magnetic resonance imaging (MRI) done with a minimum of 1 year interval. Healthy age and sex-matched individuals were selected as controls. All underwent a standardized neuropsychological evaluation. Individual results were converted into standard scores and compared to normative data. Subjects with a total score in any of the 8 domains ≤2 SD below the normative value were considered impaired. SLE patients were additionally assessed for disease activity [SLE Disease Activity Index (SLEDAI)], damage [Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI)] and the presence of antiphospholipid antibodies. MRI was performed on a Helscint 2 Tessla scanner and T1 inversion recovery and T2 coronal images were used for analysis. The software NIH-Image was used for volumetry and signal quantification. Hippocampal volumes (HV) were determined by standardized protocols. Hsig was determined for the head, body and tail of the hippocampus. Values diverging by 2 or more SD from the control mean were considered abnormal. Results: We included 33 SLE patients (29 women; mean age 32.2±11.6 years) and 33 controls (25 women; mean age 34.2±12.9). At study entry, right (mean volume 1981 mm; SD±299.7) and left (mean volume 1910mm; SD±249.6) HV were significantly smaller in SLE patients when compared to right (mean volume 2351mm; SD± 263.6; p<0.05) and left (mean volume 2262mm; SD± 261.5;p<0.05) HV of controls. After a mean follow-up time of 16 months (SD 4.2) we observed significantly smaller right and left HV in SLE patients (p<0.05). No difference in HV was observed in controls. At study entry, HA was identified in the left hippocampus in 4 (12.1%) and in the right hippocampus in 5 (15.1%) patients and in no control. In the second MRI, HA was identified in the right hippocampus in 12 (36.4%) and in the left hippocampus in 13 (39.4%). The presence (r=0.66; p=0.01) and severity (r=0.87; p=0.001) of cognitive impairment correlated directly with HV. Hsig abnormalities were found at study entry in 15 (45.5%) patients. Hsig abnormalities in the body and tail of non-atrophic hippocampi correlated with progression of volume loss during the follow-up period (r=0.8 p<0.001). The presence of Hsig in the head of atrophic hippocampi correlated with progression of hippocampal atrophy (r=0.73 p=0.005) during the same period. No correlation of Hsig and disease activity or prednisone dose was observed. Conclusions: HA is frequently observed in SLE patients and volume loss is progressive in a subgroup of patients. The evaluation of Hsig is an easy tool to determine patients that may have progressive hippocampal volume loss and should be followed more closely with MRI and cognitive evaluation. Disclosure of Interest: A. Lapa: None Declared, L. Silveira: None Declared, T. pedro: None Declared, J. Francischinelli: None Declared, L. Costallat: None Declared, F. Cendes: None Declared, S. Appenzeller Grant/Research support from: Fundação Amparo À Pesquisa Estado São Paulo-Brasil (FAPESP 2008/02917-0 and 2009/06049-6), Conselho Nacional Pesquisa Desenvolvimento-Brasil CNPq (300447/2009-4)Citation: Annals of the Rheumatic Diseases, volume 70, supplement 3, year 2011, page 297Session: SLE, Sjögren's and APS – clinical aspects (other than treatment) (Poster Presentations )

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