ABSTRACT
BACKGROUND: Neuropsychiatric systemic lupus erythematosus (NPSLE) is associated with increased morbidity and mortality. METHODS: We used Diffusion Tensor Imaging (DTI) to assess white matter abnormalities in seventeen NPSLE patients, sixteen SLE patients without NPSLE, and twenty age- and gender-matched controls. RESULTS: NPSLE patients differed significantly from SLE and control patients in white matter integrity of the body of the corpus callosum, the left arm of the forceps major and the left anterior corona radiata. CONCLUSIONS: Several possible mechanisms of white matter injury are explored, including vascular injury, medication effects, and platelet or fibrin macro- or microembolism from Libman-Sacks endocarditis.
Subject(s)
Brain/pathology , Lupus Vasculitis, Central Nervous System/pathology , Mental Disorders/pathology , Acute Disease , Adult , Anisotropy , Case-Control Studies , Cohort Studies , Diffusion Tensor Imaging , Female , Humans , Image Processing, Computer-Assisted , Lupus Erythematosus, Systemic/pathology , Male , Nerve Fibers, Myelinated/pathology , Neural Pathways/pathologyABSTRACT
OBJECTIVE: Studies that have examined abnormalities in cerebral blood flow (CBF) in patients with systemic lupus erythematosus (SLE) reported CBF relative to a region assumed to be normal in the brain. We examined the absolute differences in both regional CBF and cerebral blood volume (CBV) between patients with SLE and healthy controls. METHODS: CBF and CBV were measured with dynamic susceptibility contrast (DSC) magnetic resonance imaging (MRI), a technique that provides an alternative to radionuclide perfusion studies and permits quantitative anatomic, CBF, and CBV imaging in a single scanning session. CBF and CBV were measured in lesions and in normal-appearing tissue in the major cerebral and subcortical brain regions. Unlike most perfusion studies in SLE, CBF and CBV values were not normalized to a region of the brain assumed to be healthy. RESULTS: CBF and CBV within MRI-visible lesions were markedly reduced relative to surrounding normal-appearing white matter. CBF and CBV in normal-appearing tissue were both higher in SLE patient groups, with or without lesions, relative to the control group. CONCLUSION: DSC MRI, without normalization to a region presumed to be healthy, revealed that CBF and CBV in normal-appearing tissue in patients with SLE was higher than CBF and CBV in controls. Since this finding was made in subgroups of patients with and without lesions, the higher CBF and CBV appear to precede lesion pathology.
Subject(s)
Brain/anatomy & histology , Cerebrovascular Circulation/physiology , Lupus Erythematosus, Systemic/physiopathology , Magnetic Resonance Imaging/methods , Regional Blood Flow/physiology , Adult , Contrast Media/metabolism , Female , Humans , Middle AgedABSTRACT
OBJECTIVE: Premature carotid and coronary atherosclerosis are common in systemic lupus erythematosus (SLE), but data on aortic atherosclerosis (AA) are limited. Thus, using multiplane transesophageal echocardiography (TEE), we sought to determine the prevalence and clinical correlates of AA in patients with SLE. METHODS: Forty-seven patients with SLE (44 women, age 38 +/- 12 years) and 21 healthy controls (19 women, age 34 +/- 12 years) underwent clinical and laboratory evaluations and TEE to assess AA defined as aortic intima media thickness (IMT) > 0.86 mm or plaques as > 50% focal IMT as compared with surrounding walls. TEE studies were interpreted by an experienced observer unaware of subjects' clinical data. RESULTS: The prevalence of abnormal aortic IMT, plaques, or both lesions was higher in patients as compared to controls (37%, 23%, and 43% vs 14%, 0%, and 14%, respectively, all p = 0.02). In patients, age at diagnosis of SLE was the only positive independent predictor of AA [OR 1.12 per year from diagnosis of SLE, 95% confidence interval (CI) 1.04-1.19, p = 0.001] and cyclophosphamide therapy was the only negative independent predictor of AA (OR 0.186, 95% CI 0.153-0.95, p = 0.04, equivalent to 5.4 times less likely to develop AA). CONCLUSION: AA is common in young patients with SLE and is predicted by a later age at diagnosis of SLE, but is negatively correlated with cyclophosphamide therapy. Thus, early diagnosis and more aggressive immunosuppressive therapy may be required to decrease the development and progression of atherosclerosis in patients with SLE.