Cell adhesion molecular markers in ischaemic stroke patients: correlation with clinical outcome and comparison with primary autoimmune disease

Introduction: Several studies have found increased concentration of proinflammatory, post-ischaemic markers during acute stroke, such as sICAM-1 and sICAM-1, that may modulate the patients' prognosis. We have therefore evaluated the molecular profiles of sICAM-1 and sICAM-1 in ischaemic stroke patients, to correlate them with neurological deficits and to compare them with the molecular levels obtained from patients with primary autoimmune disease. Material and methods: Thirty-six first-ever ischaemic stroke patients (SG) as well as 32 healthy volunteers (CG) and 31 multiple sclerosis patients (MS), both as controls, were included in the prospective study. sICAM-1 and sVCAM-1 were determined at the 1(st), 5(th) and 14(th) day after stroke in SG, comparing with a single sample level in CG and MS. Evaluation of the neurological deficit at the 1(st) and the 14(th) day after stroke was based on Rankin scale, functional independence measure (FIM), Orgogozo score and NIHS scales. Results: In SG, sICAM-1 level was significantly lower at the 5th day vs. the initial serum level (p < 0.05). A non-significant linear increase of SG sVCAM-1 level was observed between the sampling days. All SG sICAM-1 levels were significantly higher vs. CG and lower vs. MS levels (p < 0.05). At the 14(th) day, SG sVCAM-1 level was significantly higher vs. CG levels (p < 0.05), but there were no significant differences between SG levels and MS levels. A significant correlation between sVCAM-1 levels at the 1(st) and 14(th) day and clinical outcome scales was assessed. Conclusions: The observed sICAM-1 decrease at the 5(th) day after stroke may be associated with an anti-inflammatory effect in ischaemic penumbra. The sVCAM-1 profile indicates a chronic inflammatory state in stroke, and its determination seems to be a good molecular marker of the patients' neurological state at the beginning and two weeks after the ischaemic episode. The systemic inflammatory response by cell adhesion molecules that accompanies acute stroke is less intensive than that observed during the autoimmune response in primary autoimmune disease such as MS.