THU0014 Twenty-Year Follow-Up of Brain MRI in A Series of Patients with Systemic Lupus Erythematosus

Abstract

Background Conventional MRI (cMRI) is a first level investigation in the diagnostic work-up of Systemic Lupus Erythematosus (SLE) patients with neuropsychiatric (NP) manifestations. Objectives To evaluate the long-term evolution of cerebral abnormalities by (cMRI) in patients with SLE. Methods Thirty patients (29F, age 53.5±11.3 yrs, disease duration 24.9±6.7 yrs) with SLE were prospectively observed and brain MRI studies (T1, T2, GRET*2 and FLAIR sequences) were obtained at baseline (MR-1 - 0.5 Tesla) and repeated after 19.4±3.7 yrs of follow-up (1.5 Tesla – MR-2). An experienced neuroradiologist analyzed the MRI comparing the following outcomes: 1) number of focal subcortical white matter hyperintensity (WMHI) lesions, 2) presence of parenchymal defects secondary to large-vessel ischemic lesions, 3) cerebral atrophy visually assessed and quantified using the Evans' index. Cumulative MRI brain damage was calculated according to a modified scoring system proposed by Petri et al (1). Each patient was assessed for the presence of NP manifestations SLE-related (NP-SLE) or unrelated (NP-nonSLE), according to criteria proposed by the Italian Study Group on NP-SLE (2). Demographic, clinical and serological data were also recorded in order to identify risk factors associated with worsening of brain MRI abnormalities. Multiple stepwise regression analysis were applied. P-values <0.05 were considered significant Results Twenty patients (66.6%) had an increased number of focal WMHI lesions whilst 8 patients (26.7%) showed a significant increase of Evans' index, defined as an increase greater than the sample mean + standard deviation. Modified Petri's score worsened in 23 patients (76.7%) and when the entire cohort was considered the difference between baseline and follow-up resulted statistically significant (MR-1: 1.3±1.5 vs. MR-2: 2.9±2.1; p<0.0001). Brain MRI showed parenchymal defects secondary to large-vessel ischemic lesions in 6 patients (20%) 4 of which were not present at baseline. Previous WMHI lesions on MRI (p=0.016; OR 231.4 and 95%CI: 2-1980) resulted as the only independent risk factor for the development of new WMHI lesions, whilst treatment with antimalarials (p=0.004; OR 0.01 and 95%CI: 0.0-0.25) was independently associated with a reduced risk. Hyperlipidemia (p=0.044; OR 10.1 and 95%CI 1.1-97.0), resulted independently associated with an increased risk to develop cortical atrophy. Finally, a cumulative steroids dose higher than 50 grams (p=0.026; OR 8.8 and 95%CI 1.2 – 61.0) was the only independent risk factor for increase in cumulative brain MRI damage. Twenty-one patients reported at least one NP event (7pts had >1 event). Fourteen patients were classified as NP-SLE and 7 as NP-nonSLE. The only independent risk factor for new NP-SLE manifestation was a previous NPSLE event (p=0.015; OR 10.2 95%CI 1.5 – 67.2) whilst higher modified Petri's score was an independent risk factor for the development of NP manifestations of any nature. Conclusions Worsening of MRI brain damage in SLE patients is r...