Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From March 1973 to December 1994, 8 patients (2 males and 6 females) aged 34.4 +/- 7.8 years, underwent composite graft replacement (CGR) for aortitis syndrome combined with annuloaortic ectasia (AAE) in our institute. Five patients showed active aortitis syndrome and steroid therapy was administrated to 2 of them. The mean value of the C-reactive protein (CRP) was 1.6 +/- 1.8 before the operation. The maximum diameter of the ascending aorta was 67.1 +/- 10.3 mm (range 53 to 85 mm). Stenosis and/or ectasia of the neck vessels were recognized in 5 cases, as well as the coronary artery in 2 cases. Isolated CGR was performed in 6 cases, and combined with single CABG to LAD in 1 case and with total arch replacement in 1 case. The enlarged ascending aorta was replaced with main graft using the exclusion method and interposed grafts for coronary arteries were sutured with pledgetted mattress sutures all around the coronary ostia. In patients with stenosis of neck vessels, oxygen saturation of the jugular vein was monitored during extracorporeal circulation for surveillance of cerebral ischemia. There was 1 early death due to pulmonary failure. Seven cases survived without any complications during 4-132 months (mean 83.4 months) of the follow-up period. After the operation, 3 cases required steroid therapy during 4-50 months. We concluded that preoperative control of active inflammation, selection of operative procedures, timing for the operation, and the long-term precise management of the intractable disease were essential for successful treatment of aortitis syndrome with AAE.
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PMID:[Surgical results of aortitis syndrome (Takayasu disease) combined with annuloaortic ectasia]. 853 Aug 53

Activation of blood coagulation and fibrinolysis has previously been detected in stroke patients. It is unknown, however, what factors contribute to the acceleration of coagulation reactions, especially in cases where no obvious predisposing factors exist. We therefore postulated and tested the hypothesis that in such patients monocytes may trigger the pathway leading to thrombosis by expressing tissue factor (TF). TF antigen was determined in 48 patients and 40 controls by flow cytometry using an indirect immunofluorescent technique. TF antigen expression was significantly increased on monocytes in young stroke patients in both the acute (p < 0.01) and chronic (p < 0.05) phases of the disease. The TF antigen also possessed functional activity, quantitated by a one-stage clotting assay. TF expression on monocytes was not associated with an elevation in C-reactive protein values. In both acute and chronic phases, blood coagulation activation markers, e.g. the thrombin-antithrombin complex and F1 + 2 fragments, were significantly elevated. However, in the acute phase D-dimer levels were similar to those in controls and were only elevated in the chronic phase of the disease (p < 0.05). In conclusion, in cerebral ischemia TF expression on monocytes suggests enhanced activation of blood coagulation and subsequent fibrinolysis.
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PMID:Monocytes express tissue factor in young patients with cerebral ischemia. 968 64

The study sought to determine whether cerebral ischemia is associated with inflammatory reactions indicated by an increase in levels of selected acute phase proteins (APP), C-reactive protein (CRP), fibrinogen, alpha-1 antitrypsin (AAT) and acidic alpha-1 glycoprotein (AGP). These proteins are thought to be markers of inflammatory reactions. We investigated 30 patients with acute cerebrovascular ischemia, 20 patients with transient ischemic attack, and 20 patients from a control group. Levels of CRP, AAT, AGP, and fibrinogen in blood sera were determined in all patients by kinetic turbidimetry. In the patients with cerebral infarct an increase was found in the levels of APP, which suggests that ischemic necrosis is associated with inflammatory reactions. All patients require active treatment of an inflammatory process that is associated with stroke.
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PMID:Markers of inflammation in cerebral ischemia. 1465 49

The onset of cerebral ischaemia triggers a cascade of proinflammatory molecular and cellular events. Clinical studies suggest that the strength of this acute response is important in early and late clinical outcomes, early clinical worsening, and extent of brain damage. Variables that are predictors of adverse stroke outcome include erythrocyte sedimentation rate, and levels of C-reactive protein (CRP), interleukin-6, tumour necrosis factor-alpha and intercellular adhesion molecule-1. Current data indicate that inflammation serves to fuel atherosclerosis and can act as the link between atherosclerosis and atherothrombosis. Growing evidence indicates that platelets act as prominent players in the inflammatory component of these disease processes. Thus, upon activation, platelets release a series of cytokines and growth factors and express CD40 ligand, which interacts with the CD40 receptor on other major cell types involved in atherosclerosis/atherothrombosis. In healthy volunteers, CD40L expression in platelets is not significantly inhibited by acetylsalicylic acid (ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist clopidogrel or with clopidogrel plus ASA. Of a range of potential inflammatory biomarkers that have been reported in the literature, the best studied is CRP. Such biomarkers may have clinical utility for refined identification of patients at high risk for atherothrombosis in different arterial beds and for monitoring of therapeutic agents in clinical trials.
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PMID:Role of inflammation in stroke and atherothrombosis. 1473 Feb 51

Cerebral ischemia triggers interleukin-6 (IL-6) release into blood. IL-6 is a key mediator of acute phase reaction. Markers of acute phase reaction (C-reactive protein, fibrinogen, fever) have been linked to poor prognosis in stroke patients. Interleukin-6 soluble receptor (sIL-6R) can potentiate IL-6 pro-inflammatory activity. The aim of this study was to investigate the relationship between IL-6 and sIL-6R in stroke patients. Serum cytokine levels were measured in 18 stroke patients and 13 controls using the ELISA method. On the second day of stroke, IL-6 levels were significantly higher in stroke patients than in controls; sIL-6R levels did not differ significantly between groups. Three months after stroke, IL-6 levels did not differ significantly between groups; sIL-6R levels were significantly decreased in stroke patients when compared with that in controls and with levels in acute phase of stroke. Decreased sIL-6R early after stroke might reflect a regulatory mechanism attenuating inflammatory response.
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PMID:Serum interleukin-6 soluble receptor in relation to interleukin-6 in stroke patients. 1545 42

Recent researches focused on the study of the role of the inflammation in the atherothrombotic pathogenesis of the acute cerebral ischemia. The aim of the study was to identify some acute phase proteins with possible role in the pathogenesis of the ischemic stroke. Some acute phase proteins were prospectively investigated by standard methods in sera of 78 patients with ischemic stroke in the first admission day. There were two groups according to neurological deficit one month after the ischemic stroke: good outcome and poor outcome. In the second group mean value of C-reactive protein (CRP) was 0.122 +/- 0.06 g/l (p < 0.01), mean value of C3 was 2.61 +/- 0.36 g/l (p < 0.01), mean value of C4 was 0.73 +/- 0.07 g/l (p < 0.05), mean value of alpha 1-antitrypsin (AAT) was 4.9 +/- 0.46 g/l (p < 0.01), mean value of alpha 1-antichymotrypsin (ACT) was 0.33 +/- 0.04 g/l (p < 0.01), mean value of alpha 1-acid glycoprotein (AGA) was 1.12 +/- 0.15 g/l, (p < 0.05), mean value of fibrinogen was 2.6 +/- 0.22 g/l (p < 0.01), mean value of haptoglobin was 2.8 +/- 0.33 g/l, (p < 0.05), mean value of transferrin was 2.8 +/- 0.26 g/l (p < 0.05), mean value of ferritin was 238 +/- 22.42 microg/l (p < 0.001), mean value of fibronectin was 2.14 +/- 0.17 g/l (p < 0.05), mean value of ceruloplasmin was 1.23 +/- 0.24 g/l (p < 0.01). High significant values of ferritine and significant values of CRP, C3, AAT, ACT and fibrinogen were observed in patients with poor outcome. The presented data suggest that the studied markers are useful to appreciate the role of the inflammatory reaction in the atherothrombotic pathogenesis of the ischemic stroke.
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PMID:Study of some markers of inflammation in atherothrombotic pathogenesis of acute ischemic stroke. 1552 46

Case-control studies and a few prospective studies have indicated that chronic infections may add to the risk of stroke and that acute infections may act as trigger factors for stroke. Such chronic infections include periodontal disease, infection with Chlamydia pneumoniae or Helicobacter pylori, and chronic bronchitis. A causal role of these infectious diseases has not been proved, given conflicting study results, possible residual confounding in observational studies, and the lack of evidence from interventional trials. Therefore, special treatment regimens for stroke prevention based on serologic or genomic evidence of infection are not indicated outside of randomized studies at present. However, the preliminary available evidence suggests that in patients with previous cerebral ischemia, clinically diagnosed chronic infections should be taken seriously and should receive the treatment that is indicated according to current guidelines. This may include appropriate treatment of moderate or severe periodontitis and of chronic bronchitis. Inflammatory parameters (eg, C-reactive protein, leukocyte count, fibrinogen) are independently associated with the risk of first or recurrent stroke. The question of whether these indexes are causally related to stroke or merely represent risk markers is not sufficiently clarified. Their use in monitoring individual risk in daily clinical practice is limited at present by the lack of clearly defined therapeutic strategies to modify these parameters, although statins and other drugs can influence inflammatory markers. Observational studies have shown that influenza vaccination is significantly and independently associated with a reduced risk of stroke and myocardial infarction. Although interventional studies in stroke are lacking, it is recommendable that in accordance with current guidelines patients with previous vascular disease, including stroke, patients with high risk of stroke, and all subjects above age 60, receive an influenza vaccination annually.
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PMID:Role of anti-infective strategies in the prevention of stroke. 1600 50

Ischemic stroke can trigger an acute phase response resulting in a rise of plasma concentration of C-reactive protein (CRP). Clinical data about the relationship between CRP and prognosis suggest that CRP might be involved in the pathogenesis of cerebral ischemia. In the present work, a significant increase of circulating level of CRP was observed in an vivo rat brain ischemia model of middle cerebral artery occlusion. To determine the possible effects of CRP on brain microvessel endothelium, we performed a dose-dependent experiment in mouse brain microvascular endothelial cells (bEnd.3 cells) with emphasis on its relation to cell adhesions molecules. Incubation with CRP (1-75 mg/L) for 24 h significantly increased Lactate dehydrogenase (LDH) leakage from bEnd.3 cells (P<0.01) in a dose-dependent manner, and induced significant up-regulations of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions analyzed by Western blotting (P<0.01). In contrast to earlier report, CRP also induced significant increase in ICAM-1 expression in the absence of serum (P<0.01). In conclusion, the present results suggest that CRP may be involved directly in the development of inflammation in response to cerebral ischemia.
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PMID:C-reactive protein induced expression of adhesion molecules in cultured cerebral microvascular endothelial cells. 1641 76

Hypertension is the most important modifiable risk factor for ischemic stroke, and antihypertensive treatment is of paramount importance to reduce the incidence of stroke mortality and morbidity. The significance and best management of hypertension during the first hours after stroke onset, however, are still matters of debate. Cerebral ischemia results in a complex inflammatory cascade; inflammatory mechanisms are also important participants in the pathophysiology of hypertension. There has been a convergence of evidence that is important to consider in managing systemic blood pressure after stroke to ensure an optimal outcome. The identification of useful markers will allow progress in our ability to treat blood pressure in the acute phase of a stroke. The determination of levels of C-reactive protein, an acute-phase inflammation marker, may help to guide our approach in the management of blood pressure in acute ischemic stroke. Whether this target will be useful in the development of risk prediction strategies or therapies for the treatment of stroke in humans is far from clear.
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PMID:Systemic inflammation, blood pressure, and stroke outcome. 1652 96

Acute cerebral ischemia triggers interleukin-6 (IL-6) release into cerebrospinal fluid and blood. IL-6 induces synthesis of the acute phase proteins (APPs) in the liver. Higher blood IL-6 level in stroke patients is associated with larger infarct size, greater neurological deficit on admission, early neurological worsening, and increased risk of death or poor functional outcome. The level of C-reactive protein (CRP), the major APP in man, rises in blood during acute stroke reaching maximal values between 5 and 7 day after stroke onset. Elevated CRP level in acute ischemic stroke predicts unfavorable outcome and is associated with increased risk of recurrent stroke or other cardiovascular events. Increased level of fibrinogen, another APP, is associated with worse outcome in patients with ischemic stroke. The acute phase reaction accompanies also intracerebral hemorrhage. Serum IL-6 and CRP level increases in the first days after intracerebral hemorrhage. Plasma IL-6 is independently associated with hematoma enlargement and fibrinogen level predicts early neurological deterioration and outcome in patients with intracerebral hemorrhage.
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PMID:Clinical significance of acute phase reaction in stroke patients. 1798 65


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