Rationale and Objectives
Many patients with systemic lupus erythematosus (SLE) manifest the recurrence of new brain lesions on follow-up magnetic resonance imaging (MRI) scans. We assessed whether the initial MRI findings help to predict the subsequent development of brain lesions in patients with SLE.
Materials and Methods
We enrolled 64 patients with SLE who had undergone initial and follow-up MRI studies. Two radiologists reviewed and categorized the initial MRI findings and divided the patients into those with no lesions on the initial and follow-up MRI scans (group A, n = 18), those with lesions on the initial scans only (group B, n = 32), and those with lesions on the first and new lesions on the follow-up MRI scans (group C, n = 14). We then looked for independent predictors of the subsequent development of brain lesions, such as antiphospholipid syndrome (APS) and findings on the initial MRI studies.
Results
The incidence of lacunar and localized cortical infarcts was significantly greater in group C than group B (50% vs. 0%, P < .001 and 50% vs. 9%, P < .05, respectively). Multivariate logistic regression analysis indicated that lacunar or localized cortical infarcts on the initial MRI scans were independent predictors of the subsequent development of brain lesions (odds ratio [OR]: 5.412, 95% confidence interval [CI]: 1.18–24.85, P = .03), whereas the presence of APS was not (OR: 0.621, 95% CI: 0.18–2.19).
Conclusions
The presence of lacunar and/or localized cortical infarcts on initial MRI scans may predict the development of new brain lesions in patients with SLE.
Systemic lupus erythematosus (SLE) is an autoimmune disease that frequently involves the central nervous system (CNS, . Neuropsychiatric (NP) SLE has been reported in as many as 30%–56% of all patients with SLE , and the quality of life is poorer in patients with NPSLE than without NPSLE . However, the etiology of and basis for NPSLE-associated brain lesions remain uncertain .
The development of NPSLE-associated brain lesions is related to disease activity and severity; one of the most important risk factors for brain lesions is the presence of antiphospholipid syndrome (APS) and/or anticardiolipin antibodies (aPL, . Kaichi et al. showed that abnormal magnetic resonance imaging (MRI) findings were more common in SLE patients with APS than without APS. The recognition of APS is critical for appropriate therapy. Antiplatelet and/or anticoagulation therapy is recommended for NPSLE related to aPL, especially in patients with thrombotic cerebrovascular disease (CVD, . SLE patients without aPL are also potentially at risk for the recurrence of CVD .
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Materials and methods
Patient Selection
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Image Acquisition
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Image Interpretations
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Statistical Analysis
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Results
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Table 1
Demographic and Clinical Characteristics of Patients with SLE
Factor Group A ( N = 18) Group B ( N = 32) Group C ( N = 14)P Value (B/C) Mean age, (year ± SD) 28.8 ± 19.2 32.8 ± 18.8 37.1 ± 16.1 .19 Sex .51 Female [ n (%)] 16 (89) 28 (88) 13 (93) Male [ n (%)] 2 (11) 4 (12) 1 (7) APS positive [ n (%)] 3 (17) 7 (22) 10 (71) <.05 Activity index SLEDAI 13 (10–27) 6 (0–27) 13 (0–28) .28 BILAG Index 20 (15–35) 8.5 (0–21) 7 (4–28) .33 Observation period, (month ± SD) 35.5 ± 35.5 46.9 ± 33.9 26.1 ± 47.9 <.05 Vascular risk factors Hypertension [ n (%)] 11 (61) 1 (3) 3 (21) .08 Hyperlipidemia [ n (%)] 2 (11) 4 (13) 1 (7) .51 Diabetes mellitus [ n (%)] 2 (11) 0 (0) 0 (0) — Smoking [ n (%)] 2 (11) 2 (6) 4 (29) .06 Obesity [ n (%)] 1 (6) 3 (9) 1 (7) .51 Duration of SLE, year: median 5 (1–23) 6 (1–27) 11 (1–23) .24 Treatment Corticosteroids [ n (%)] 18 (100) 30 (94) 14 (100) 0.48 Immunomodulatory drugs [ n (%)] 15 (83) 26 (78) 11 (79) 0.65
APS, antiphospholipid syndrome; BILAG Index, British Isles Lupus Assessment Group Index; SD, standard deviation; SLE, systemic lupus erythematosus; SLEDAI, Systemic Lupus Erythematosus Disease Activity Index; Observational period, time interval between initial and final follow-up magnetic resonance imaging.
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Table 2
Comparison of Initial MRI Findings with Groups B and C
MRI Findings Group B, N = 32; [ n (%)] Group C, N = 14; [ n (%)]P Value White matter hyperintensities 21 (66) 9 (64) .59 Large territorial infarctions 7 (22) 5 (36) .26 Lacunar infarctions 0 (0) 7 (50) <.001 Localized cortical infarctions 3 (9) 7 (50) <.05 Borderzone infarctions 2 (6) 3 (21) .16 Microembolisms 0 (0) 0 (0) — Basal ganglia lesions 2 (6) 1 (7) .67 Hemorrhages 0 (0) 0 (0) — Callosal lesions 0 (0) 0 (0) — Arterial occlusion/stenosis 2 (6) 1 (7) .65
MRI, magnetic resonance imaging.
Table 3
Factors Affecting the Subsequent Development of Brain Lesions: Multivariate Analysis
Factor Odds Ratio 95% Confidence Interval_P_ Value APS positive 0.621 0.18–2.19 .459 Lacunar or localized cortical infarctions 5.412 1.18–24.85 .03
APS, antiphospholipid syndrome.
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Discussion
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