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Volume 111, Issue 10, Pages 847-851 (December 2009)


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Plasma level of sICAM-1 is associated with the extent of white matter lesion among asymptomatic elderly subjects

Jing Hao Hanac, Ka Sing Wonga, Yan Yan Wangb, Jian Hui Fuc, Ding Dingc, Zhen HongcCorresponding Author Informationemail address

Received 5 February 2009; received in revised form 14 August 2009; accepted 17 August 2009.

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±135.6ng/mL in grade 0-I, 391.3±145.5ng/mL in grade II, and 450.2±232.9ng/mL in grade III, p<0.001; for PVH: 282.5±116.5ng/mL in grade 0-I, 402.3±160.4ng/mL in grade II, and 428.1±227.7ng/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.

a Department of Medicine & Therapeutics, Chinese University of Hong Kong, Hong Kong

b Department of Geriatrics, Huashan Hospital, Fudan University, Shanghai, China

c Department of Neurology, 12 Wulumuqi Zhong Rd, Huashan Hospital, Fudan University, Shanghai, 200040, China

Corresponding Author InformationCorresponding author. Tel.: +86 021 5288 8158; fax: +86 021 6248 1930.

PII: S0303-8467(09)00232-7

doi:10.1016/j.clineuro.2009.08.018


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