Abstract

Objective Inflammatory endothelial activation mediated by intercellular adhesion molecule-1 (ICAM-1) plays a role in the pathogenesis of large- and small-vessel disease. We explored the association between soluble ICAM-1 (sICAM-1) and white matter lesion (WML) as a manifestation of cerebral small-vessel disease. Methods One hundred and seventy-five elderly individuals aged ≥ 60 without neurological deficits were studied. Subcortical deep white matter hyperintensity (SDWMH) and periventricular hyperintensity (PVH) were rated separately. Lesions in each category were then divided into three groups (grade 0-I, grade II, grade III) according to the Fazekas scale. Results Plasma sICAM-1 levels were positively associated with grades of WML (for SDWMH: 297.4 ± 135.6 ng/mL in grade 0-I, 391.3 ± 145.5 ng/mL in grade II, and 450.2 ± 232.9 ng/mL in grade III, p < 0.001; for PVH: 282.5 ± 116.5 ng/mL in grade 0-I, 402.3 ± 160.4 ng/mL in grade II, and 428.1 ± 227.7 ng/mL in grade III, p < 0.001). Multivariate analysis showed higher sICAM-1 levels, age and hypertension were the independent risk factors associated with the presence and severity of WML. More than 4-fold increased risk of WML was observed in patients with the highest quartile of sICAM-1 (all WML OR = 4.694, 95% CI: 1.805–12.204; moderate WML OR = 4.618, 95% CI: 1.543–13.825; severe WML OR = 4.893, 95% CI: 1.236–19.368). Conclusion Increased plasma sICAM-1 suggests inflammatory process may be involved in the pathogenesis of WML.

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