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      About Neurodegenerative Diseases: 3.0 Impact Factor I 4.3 CiteScore I 0.695 Scimago Journal & Country Rank (SJR)

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      Assessment of Relations between Clinical Outcome of Ischemic Stroke and Activity of Inflammatory Processes in the Acute Phase Based on Examination of Selected Parameters

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          Abstract

          Background and Purposes: Inflammatory factors play an important role in the pathogenesis of ischemic stroke. They may influence circulation during the acute phase of stroke and enhance the ischemic region. Materials and Methods: We examined 51 patients – 36 patients in the early stage of stroke, i.e. the first 24 h after onset. Of these, 15 patients had infection and 21 had no infection during the week preceding stroke. There were 15 patients with noninflammatory diseases in the control group. We analyzed parameters of inflammation such as: activity of serum chitotriosidase by fluorimetric assay, C-reactive proteins (CRP), number of white body cells (WBCs), IgG and fibrinogen. We also assessed the neurological stage according to the Scandinavian Stroke Scale (SSS). Results: In our study, we observed a statistically significant difference (p < 0.05) in the activity of most parameters of inflammation. This difference could be seen in the levels of CRP, number of WBCs and the activity of chitotriosidase, apart from IgG and fibrinogen, between the control group and groups with versus without infection. A significantly increased level of CRP (p < 0.0005) and fibrinogen (p > 0.01) was found on the first day in the stroke group as compared to the control group. The neurological stage on day 4 after stroke, assessed according to the SSS, was significantly worse in the group of patients with infection before stroke than in stroke patients without infection (p < 0.008). Conclusion: These results suggest the importance of active inflammatory processes in the pathogenesis of stroke. We observed increased activity of chitotioridase, a parameter of the inflammatory process, in stroke. This study is one more proof that inflammatory processes caused by infection may influence the occurrence of stroke and worsen its outcome. It could be another step towards understanding immunological processes during the acute phase of stroke. The study may also help establish new diagnostic and therapeutic strategies and could be a useful tool for prophylaxis.

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          Marked elevation of plasma chitotriosidase activity. A novel hallmark of Gaucher disease.

          C. E. Hollak, S van Weely, M van Oers … (1994)
          Gaucher disease (GD; glucosylceramidosis) is caused by a deficient activity of the enzyme glucocerebrosidase (GC). Clinical manifestations are highly variable and cannot be predicted accurately on the basis of the properties of mutant GC. Analysis of secondary abnormalities, such as elevated plasma levels of some hydrolases, may help to increase insight into the complicated pathophysiology of the disease and could also provide useful disease markers. The recent availability of enzyme supplementation therapy for GD increases the need for markers as early predictors of the efficacy of treatment. We report the finding of a very marked increase in chitotrisidase activity in plasma of 30 of 32 symptomatic type 1 GD patients studied: the median activity being > 600 times the median value in plasma of healthy volunteers. In three GC-deficient individuals without clinical symptoms, only slight increases were noted. Chitotriosidase activity was absent in plasma of three control subjects and two patients. During enzyme supplementation therapy, chitotriosidase activity declined dramatically. We conclude that plasma chitotriosidase levels can serve as a new diagnostic hallmark of GD and should prove to be useful in assessing whether clinical manifestations of GD are present and for monitoring the efficacy of therapeutic intervention.
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            Inflammation, hemostatic markers, and antithrombotic agents in relation to long-term risk of new cardiovascular events in first-ever ischemic stroke patients.

            Mario Di Napoli, Elaine F. Papa, (2002)
            The measurement of markers of inflammation or thrombosis has been proposed as a method to improve the prediction of risk in patients with vascular disease. We evaluated the usefulness of these markers as predictors of cardiovascular events in ischemic stroke patients. We analyzed levels of C-reactive protein (CRP), fibrinogen, and D-dimer within the first 24 hours after stroke onset in 473 first-ever ischemic stroke patients and determined the cumulative survival curves free of cardiovascular events in relation to the level of each of these markers according to the Kaplan-Meier method. We adjusted for possible confounding variables using a multivariate Cox proportional-hazards model. Patients in the highest tertiles of D-dimer, fibrinogen, and CRP were associated with an excess risk of new cardiovascular events of 36% (P=0.0134), 63% (P<0.0001), and 72% (P<0.0001), respectively, compared with patients in the lowest tertile. The patients in the highest tertile of CRP had 4 times the risk (hazard ratio, 4.04; P<0.0001) of a new cardiovascular event. Smoking, age, sex, and body mass index did not modify risk, and risk was independent of other confounding variables and of D-dimer and fibrinogen levels. The use of ticlopidine was associated with a significant risk reduction among patients with lower (86%, P=0.0159) and middle (69%, P<0.0001) levels of CRP, whereas a nonsignificant excess risk (27%, P=0.3896) was evident among those with the highest levels. Elevated levels of CRP, more than of D-dimer and fibrinogen, are related to the risk of new cardiovascular events after ischemic stroke. The efficacy of antiplatelet therapy in secondary prevention appears to be directly related to level of inflammatory and thrombotic markers.
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              Progression in Lacunar Stroke Is Related to Elevated Acute Phase Parameters

              Heinrich J. Audebert, Tina Pellkofer, Martin Wimmer … (2004)
              Background and Purpose: Despite the small size of lacunar infarcts, progression of neurological deficits is a common problem in this stroke subtype. This investigation studied the frequency and the course of neurological deterioration as well as predictors and possible underlying pathomechanisms of early progression in lacunar stroke. Methods: Fourty-six consecutive patients with acute lacunar stroke were prospectively evaluated by daily clinical neurological examination including the National Institutes of Health Stroke Scale (NIHSS) and follow-up using the Barthel Index after 3 months. Progressive neurological deficit was defined as worsening by ≧1 point in the NIHSS for motor function. Progressive and stable patients were compared regarding clinical profile, inflammatory parameters (leukocytes, body temperature, C-reactive protein), coagulation parameters (fibrinogen, D-dimer, vWF, PTT), and glutamate plasma concentration, as well as blood glucose and blood pressure. Results: Eleven patients (23.9%) showed progression of stroke symptoms, 9 of these within the first 24 h after admission. The score on the NIHSS on admission was similar in patients with progressive stroke and stable patients, but significantly higher in the progressive stroke group on days 2 (p = 0.01), 3 (p = 0.001) and at discharge (p = 0.003). Deterioration was significantly associated with a higher leukocyte count (p = 0.012), higher body temperature (p = 0.031) and a higher fibrinogen concentration (p = 0.046) on admission. Barthel Index at discharge (p = 0.001) and after 90 days (p < 0.001) was significantly worse in the progressive stroke group. Conclusions: Progression in lacunar stroke usually occurs within 24 h and may be related to an acute-phase response. The long-term prognosis of progressive stroke patients is persistently worse compared with patients with nonprogressive stroke.
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                Author and article information

                Journal
                Journal ID (publisher-id): ENE
                Journal ID (nlm-ta): Eur Neurol
                Journal ID (doi): 10.1159/issn.0014-3022
                Title: European Neurology
                Publisher: S. Karger AG
                ISSN (Print): 0014-3022
                ISSN (Electronic): 1421-9913
                Publication date Subscription-year: 2005
                Publication date (Print): July 2005
                Publication date (Electronic): 29 July 2005
                Volume: 53
                Issue: 4
                Pages: 188-193
                Affiliations
                Departments of aNeurology and Epileptology, Center for Medical Postgraduate Education, and bNeuropathology and cGenetics, Institute of Psychiatry and Neurology, Warsaw, Poland
                Article
                Publisher ID: 86355 Other ID: Eur Neurol 2005;53:188–193
                DOI: 10.1159/000086355
                PubMed ID: 15956787
                SO-VID: f4ba3f2b-d83c-4ab6-9d99-5bd2357f18ae
                Copyright © © 2005 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 02 September 2004
                Date accepted : 04 April 2005
                Page count
                Tables: 2, References: 27, Pages: 6
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Keywords: Inflammation,Chitotriosidase,Ischemic stroke
                Data availability:
                ScienceOpen disciplines: Geriatric medicine, Neurology, Cardiovascular Medicine, Neurosciences, Clinical Psychology & Psychiatry, Public health
                Keywords: Inflammation, Chitotriosidase, Ischemic stroke

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