The possible prognostic role of vcam-1 in stroke patients

الملخص EN

Hypothesis: The vascular endothelium promotes inflammation through the up-regulation of inflammatory leukocyte-endothelial cell adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selecting.

These molecules bind to circulating leucocytes and facilitate their migration into the Central Nervous system CNS.

In the CNS, these cells produce a number of cytotoxic molecules that may facilitate cell death and increase the infarct volume.

Objective : to define the extent of expression of VCAM-1 in correlation to the clinical disability and outcome in stroke patients.

Methods : complete lipid profile, fibrinogen assay, lipoprotein (a) and FIM were determined in 25 recent stroke patients at the time of admission and compared with 15 matched apparently healthy control subjects.

Results : the difference between the mean total cholesterol (TC) level of patients and controls was not significant.

However, high density lipoprotein (HDL) was significantly lower in patients as compared to controls but low density lipoprotein LDL was significantly higher.

The concentration of Lp (a) and fibrinogen level, were significantly higher in the patients’ group than controls.

The concentration of VCAM-1 was significantly higher in stroke patients as compared to controls.

Multiple regression analysis was performed to assign the predictors for functional independence measures (FIM) as a clinical outcome for the functional disability.

The independent parameters were the duration of stroke as well as the laboratory tests (lipid profile, Lp (a), fibrinogen and VCAM-1).

The duration of stroke and VCAM-1 level negatively correlated with FIM, meaning that patients with high VCAM-1 level demonstrated more functional disability as manifested by low FIM score.

Conclusion : the most sensitive parameters that can predict FIM were the duration of stroke and VCAM-1 level.

Further research on the role of inflammatory CAMs in the pathogenesis of ischemic cerebrovascular disorders should lead to new diagnostic and therapeutic strategies in an attempt to reduce leukocyte-induced damage in stroke.