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Exploring the risk factors for ischemic cerebrovascular disease in systemic lupus erythematosus: A single-center
Li Su1, Zhigang Qi2, Shaochen Guan3
1Department of Rheumatology and Allergy, Xuanwu Hospital, Capital Medical University, Beijing, China.
Insights
Cutaneous vasculitis and antiphospholipid antibodies increase ischemic cerebrovascular disease risk in systemic lupus erythematosus (SLE). Hydroxychloroquine (HCQ) therapy offers protection against ICVD in SLE patients.
Area of Science:
- Rheumatology
- Neurology
- Vascular Medicine
Background:
- Ischemic cerebrovascular disease (ICVD) is a severe complication in systemic lupus erythematosus (SLE).
- Identifying risk factors and clinical characteristics of ICVD in SLE is crucial for patient management.
Purpose of the Study:
- To explore risk factors for ICVD in SLE patients.
- To assess the clinical characteristics associated with ICVD in SLE.
- To evaluate the protective role of hydroxychloroquine (HCQ) therapy.
Main Methods:
- Retrospective study of 44 ICVD-SLE patients and 80 non-ICVD-SLE patients (2014-2021).
- Multivariate logistic regression analysis to identify ICVD risk factors.
- Subgroup analysis based on intracranial arterial stenosis (ICAS) gradations.
Main Results:
- Cutaneous vasculitis (OR=7.36), anticardiolipin antibody (aCL) (OR=4.38), and lupus anticoagulant (LA) (OR=7.543) were significant risk factors for ICVD in SLE.
- Hydroxychloroquine (HCQ) therapy showed a protective effect (OR=0.198).
- Moderate ICAS was associated with older age at SLE onset, longer diagnostic delay, and carotid atherosclerotic plaques.
Conclusions:
- Cutaneous vasculitis and antiphospholipid antibodies (aPLs) are key risk factors for ICVD in SLE.
- HCQ therapy demonstrates a protective role against ICVD in SLE.
- ICVD in younger SLE patients involves complement-mediated inflammation, while in older patients, it's linked to moderate ICAS and atherosclerosis.
Objectives:
Ischemic cerebrovascular disease (ICVD) is one of the most common and severe complications in systemic lupus erythematosus (SLE). We aim to explore the risk factors for ICVD in SLE and to assess their associated clinical characteristics.
Methods:
In this study, 44 lupus patients with ICVD (ICVD-SLE) and 80 age- and sex-matched lupus patients without ICVD (non-ICVD-SLE) who were hospitalized in our center between 2014 and 2021 were enrolled. A comprehensive set of clinical and socio-demographic data was recorded. In the ICVD-SLE group, the modified Rankin score (mRS) at 90 days after the occurrence of ICVD, the brain MRI, and arterial ultrasonography findings were collected. Group comparisons were made with continuous variables using an independent t-test or the Mann-Whitney test, and with categorical variables using the chi-square test or Fisher exact test. Multivariate logistic regression analysis was performed to identify the risk factors for ICVD in SLE. Patients with ICVD-SLE were divided into three subgroups according to the gradations of intracranial arterial stenosis (ICAS). The subgroup comparisons were performed by one-way ANOVA test or Kruskal-Wallis test.
Results:
Of the 44 patients with ICVD, 45% had a large-vessel ischemic stroke, 50% had a symptomatic lacunar stroke, and 9% had a transient ischemic attack. 2 (4.5%) had both large-vessel ischemic stroke and symptomatic lacunar stroke. Multivariate logistic regression analysis showed that cutaneous vasculitis (OR=7.36, 95% CI=2.11-25.65), anticardiolipin antibody (aCL) (OR=4.38, 95% CI=1.435-13.350), and lupus anticoagulant (LA) (OR=7.543,95% CI=1.789-31.808) were the risk factors, and hydroxychloroquine (HCQ) therapy (OR=0.198, 95% CI=0.078-0.502) was the protective factor, after controlling for confounders. During the analysis of the subgroups, no significant difference was observed between the patients in the group without internal carotid arterial occlusion (ICAS) and those with severe ICAS except for diagnostic delay. However, patients in the moderate ICAS group were older when SLE occurred (P<0.01), had a longer diagnostic delay (P<0.01), a lower percentage of hypocomplementemia (P=0.05) and steroids and HCQ therapy (P=0.01, P=0.05, respectively), a trend toward lower mRS score, but a higher incidence of carotid atherosclerotic plaque (P<0.01), when compared with the other two subgroups.
Conclusion:
Cutaneous vasculitis and antiphospholipid antibodies (aPLs) are associated with an increased risk of ICVD, while HCQ therapy may provide protection against ICVD in SLE. The ICVD in younger lupus patients is associated with complement-mediated inflammation and poorer outcome, and require immunosuppressive therapy, whereas the ICVD in elderly patients are characterized by moderate ICAS and carotid atherosclerotic plaques.
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