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      The Serum High-Sensitive C Reactive Protein and Homocysteine Levels to Evaluate the Prognosis of Acute Ischemic Stroke

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          Abstract

          Ischemic stroke is one of the most common causes of death worldwide and is most often caused by thrombotic processes. We investigated the changes in hsCRP and homocysteine levels, two of these risk factors, during the acute period of ischemic stroke and evaluated the relationship between these levels and the short-term prognosis. HsCRP and homocysteine levels were measured at the 2nd, 5th, and 10th days in forty patients admitted within second of an ischemic stroke. The clinical status of the patients was simultaneously evaluated with the Scandinavian stroke scale. The results were compared with 40 healthy control subjects whose age and sex were matched with the patients. The mean hsCRP levels of the patients were 9.4 ± 7.0 mg/L on the 2nd day, 11.0 ± 7.4 mg/L on the 5th day, and 9.2 ± 7.0 mg/L on the 10th day. The mean hsCRP level of the control subjects was 1.7 ± 2.9 mg/L. The mean hsCRP levels of the patients on the 2nd, 5th, and 10th days were significantly higher than the control subjects ( P < .001). The patients' mean homocysteine levels were 40.6 ± 9.6 μmol/L on the 2nd day, 21.7 ± 11.1 μmol/L on the 5th day, and 20.7 ± 9.2 μmol/L on the 10th day. The mean homocysteine level of the control subjects was 11.2 ± 1.1 μmol/L. The homocysteine levels of the patients were higher than the control subjects at all times ( P < .01). In conclusion, patients with stroke have a higher circulating serum hsCRP and homocysteine levels. Short-term unfavorable prognosis seems to be associated with elevated serum hsCRP levels in patients with stroke. Although serum homocysteine was found to be higher, homocysteine seems not related to prognosis.

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          Direct proinflammatory effect of C-reactive protein on human endothelial cells.

          V Pasceri, J T Willerson, E Yeh (2000)
          The acute-phase reactant C-reactive protein (CRP) is an important risk factor for coronary heart disease. However, the possible effects of CRP on vascular cells are not known. We tested the effects of CRP on expression of adhesion molecules in both human umbilical vein and coronary artery endothelial cells. Expression of vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM-1), and E-selectin was assessed by flow cytometry. Incubation with recombinant human CRP (10 microg/mL) for 24 hours induced an approximately 10-fold increase in expression of ICAM-1 and a significant expression of VCAM-1, whereas a 6-hour incubation induced significant E-selectin expression. Adhesion molecule induction was similar to that observed in endothelial cells activated with interleukin-1beta. In coronary artery endothelial cells, induction of ICAM-1 and VCAM-1 was already present at 5 microg/mL and reached a maximum at 50 microg/mL, at which point a substantial increase in expression of E-selectin was also evident. The CRP effect was dependent on presence of human serum in the culture medium, because no effect was seen in cells cultured with serum-free medium. In contrast, interleukin-1beta was able to induce adhesion molecule expression in the absence of human serum. CRP induces adhesion molecule expression in human endothelial cells in the presence of serum. These findings support the hypothesis that CRP may play a direct role in promoting the inflammatory component of atherosclerosis and present a potential target for the treatment of atherosclerosis.
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            Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism.

            A Furlan, R. Higashida, L. Wechsler … (1999)
            Intravenous tissue-type plasminogen activator can be beneficial to some patients when given within 3 hours of stroke onset, but many patients present later after stroke onset and alternative treatments are needed. To determine the clinical efficacy and safety of intra-arterial (IA) recombinant prourokinase (r-proUK) in patients with acute stroke of less than 6 hours' duration caused by middle cerebral artery (MCA) occlusion. PROACT II (Prolyse in Acute Cerebral Thromboembolism II), a randomized, controlled, multicenter, open-label clinical trial with blinded follow-up conducted between February 1996 and August 1998. Fifty-four centers in the United States and Canada. A total of 180 patients with acute ischemic stroke of less than 6 hours' duration caused by angiographically proven occlusion of the MCA and without hemorrhage or major early infarction signs on computed tomographic scan. Patients were randomized to receive 9 mg of IA r-proUK plus heparin (n = 121) or heparin only (n = 59). The primary outcome, analyzed by intention-to-treat, was based on the proportion of patients with slight or no neurological disability at 90 days as defined by a modified Rankin score of 2 or less. Secondary outcomes included MCA recanalization, the frequency of intracranial hemorrhage with neurological deterioration, and mortality. For the primary analysis, 40% of r-proUK patients and 25% of control patients had a modified Rankin score of 2 or less (P = .04). Mortality was 25% for the r-proUK group and 27% for the control group. The recanalization rate was 66% for the r-proUK group and 18% for the control group (P<.001). Intracranial hemorrhage with neurological deterioration within 24 hours occurred in 10% of r-proUK patients and 2% of control patients (P = .06). Despite an increased frequency of early symptomatic intracranial hemorrhage, treatment with IA r-proUK within 6 hours of the onset of acute ischemic stroke caused by MCA occlusion significantly improved clinical outcome at 90 days.
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              Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study.

              N. S. Rost, P A Wolf, C Kase … (2001)
              The role of C-reactive protein (CRP) as a novel plasma marker of atherothrombotic disease is currently under investigation. Previous studies have mostly related CRP to coronary heart disease, were often restricted to a case-control design, and failed to include pertinent risk factors to evaluate the joint and net effect of CRP on the outcome. We related plasma CRP levels to incidence of first ischemic stroke or transient ischemic attack (TIA) in the Framingham Study original cohort. There were 591 men and 871 women free of stroke/TIA during their 1980 to 1982 clinic examinations, when their mean age was 69.7 years. CRP levels were measured by using an enzyme immunoassay on previously frozen serum samples. Analyses were based on sex-specific CRP quartiles. Risk ratios (RRs) were derived, and series of trend analyses were performed. During 12 to 14 years of follow-up, 196 ischemic strokes and TIAs occurred. Independent of age, men in the highest CRP quartile had 2 times the risk of ischemic stroke/TIA (RR=2.0, P=0.027), and women had almost 3 times the risk (RR=2.7, P=0.0003) compared with those in the lowest quartile. Assessment of the trend in risk across quartiles showed unadjusted risk increase for men (RR=1.347, P=0.0025) and women (RR=1.441, P=0.0001). After adjustment for smoking, total/HDL cholesterol, systolic blood pressure, and diabetes, the increase in risk across CRP quartiles remained statistically significant for both men (P=0.0365) and women (P=0.0084). Independent of other cardiovascular risk factors, elevated plasma CRP levels significantly predict the risk of future ischemic stroke and TIA in the elderly.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0962-9351
                Publication date (Print): 2007
                Publication date (Electronic): 10 April 2007
                Volume: 2007
                Electronic Location Identifier: 15929
                Affiliations
                1Department of Neurology, Medical Faculty, Firat University, 23119 Elazig, Turkey
                2Department of Immunology, Medical Faculty, Firat University, 23119 Elazig, Turkey
                3Department of Cardiology, Erzurum Informary Hospital, 25100 Erzurum, Turkey
                Author notes
                Article
                DOI: 10.1155/2007/15929
                PMC ID: 1892643
                PubMed ID: 17597836
                SO-VID: 82ace49e-4b1c-49a5-8a27-2f691ec89698
                Copyright © Copyright © 2007 Tahir Yoldas et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 14 December 2006
                Date accepted : 8 February 2007
                Categories
                Subject: Clinical Study

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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