Association between homocysteine and endothelial dysfunction markers in stroke disease.
BACKGROUND
Evidence shows that there is an increase in concentrations of markers of endothelial dysfunction immediately following acute ischaemic stroke. Several studies suggest that endothelial dysfunction may be partly caused by oxidation related to the effects of raised total plasma homocysteine.


OBJECTIVE
The aim of this study was to measure changes in total plasma homocysteine and markers of endothelial dysfunction in stroke disease within a known period of time post infarct.


METHODS
We studied 40 acute ischaemic stroke patients (mean age +/- SD, 50.2 +/- 9.5 years) and 42 hospitalised non-stroke patients (mean age, 44.3 +/- 14.9 years). Fasting venous blood was obtained within 24 h, 3 days and 7 days after the stroke onset and hospitalisation for non-stroke patients for measurements of total plasma homocysteine, markers of endothelial dysfunction including intracellular adhesion molecule (i-CAM), vascular cell adhesion molecule-1 (v-CAM) and leukocyte adhesion molecule-1 (E-selectin) and C-reactive proteins (CRPs).


RESULTS
We found no significant differences in baseline total plasma homocysteine, E-selectin, v-CAM, vitamin B(12), and folate concentrations between ischaemic stroke patients and non-stroke controls. i-CAM concentrations were significantly higher and CRPs non-significantly lower at baseline in stroke patients compared with controls. Although all endothelial dysfunction markers increased significantly during the study period, the rise in E-selectin levels was less than that seen in i-CAM, and v-CAM. Total plasma homocysteine concentrations showed positive correlations with creatinine (r = 0.537; P < 0.02), and inverse correlations with both vitamin B(12) (r = -0.560; P < 0.001) and folate (r = -0.469; P < 0.002); however, there were no significant correlations between total plasma homocysteine or B-vitamins and markers of endothelial dysfunction in ischaemic stroke patients or controls.


CONCLUSIONS
We found evidence of an increase in markers of endothelial dysfunction following acute ischaemic stroke but this had no relationship with total plasma homocysteine concentrations.
Abdulle
Abdishakur M
AM
Department of Internal Medicine, Faculty of Medicine and Health Sciences, United Arab Emirates (UAE) University, Al-Ain, United Arab Emirates.
Pathan
Javed Y
JY
Moussa
Nagi
N
Gariballa
Salah
S
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D002545:Brain Ischemia / Q000097:blood* / Q000150:complications; D002097:C-Reactive Protein / Q000032:analysis; D003404:Creatinine / Q000097:blood; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular; D005260:Female; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D020521:Stroke / Q000097:blood* / Q000150:complications; D013997:Time Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014652:Vascular Diseases / Q000097:blood* / Q000209:etiology; D014803:Vitamin B Complex / Q000097:blood
D015415:Biomarkers; D001786:Blood Glucose; D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D006710:Homocysteine; D014803:Vitamin B Complex; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D003404:Creatinine