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

In order to investigate some aspects of blood coagulation and of platelet function in cerebral ischemia, 18 healthy subjects, 24 patients with previous cerebral infarction and 12 patients with transient ischemic attacks were studied. All patients were in a non-active state of the illness. In all subjects, platelet count, prothrombin time, activated partial thromboplastin time and determination of the fibrinogen concentration were performed as routine. All subjects were tested for platelet adhesiveness, circulating platelet aggregates, factor VIII coagulant (VIII C), factor VIII-related von Willebrand factor (VII RWF), factor VIII-related antigen (VII RAg), antithrombin III (AT III) concentration and activity and euglobulin clot lysis time. No significant difference between patients and controls was found in routine tests, platelet function, AT III concentration or activity. Plasma levels of VIII C, VIII RWF, VIII RAg were significantly increased in both patient groups. The VIII RAg/VIII C ratio was significantly increased only in patients with previous cerebral infarction. Euglobulin clot lysis time was significantly increased in both patient groups.
 ...
PMID:Evaluation of some coagulation parameters in cerebral ischemia. 685 12

The present study evaluates the hematochemical and hemorheologic effects of mesoglycan, a preparation of natural glycosaminoglycans, administered by the intramuscular route to patients with a recent episode of cerebral ischemia. A total of twenty patients (13 males and 7 females), between the ages of 45 and 75, under observation for a cerebral ischemic episode occurring at least 2 months prior to enrollment, were treated with intramuscular mesoglycan (30 mg, twice daily), for 15 days. Blood samples were taken prior to and at the end of treatment to measure the investigated parameters. Following mesoglycan treatment we observed a statistically significant decrease in fibrinogen plasma concentration, total cholesterol and triglycerides, while HDL cholesterol was found to increase. In addition, erythrocytes filterability improved at the end of treatment. No changes were observed in coagulation parameters such as prothrombin time, partial thromboplastin time, or antithrombin III. The results of the present study demonstrate that a 15-days treatment of intramuscular mesoglycan in patients recovering from a cerebral ischemic episode produces significant changes in fibrinogen and lipid plasma levels with no apparent anticoagulant effect.
 ...
PMID:Mesoglycan in treatment of patients with cerebral ischemia: effects on hemorheologic and hematochemical parameters. 816 May 57

We analysed the results of coagulation studies in an unselected series of young adults with acute cerebral ischaemia. Our aims were (a) to determine the prevalence of coagulation disorders among these patients, (b) to investigate the relation between the presence of coagulation abnormalities and large vessel disease or potential sources of cardiac embolism and (c) to evaluate the occurrence of thrombotic events in patients with or without coagulation disorders. One hundred and twenty consecutively admitted patients (53 men, 67 women, median age 38 years, range 15-45) who presented with acute cerebral infarction (n = 89) or a transient ischaemic attack (n = 31) were evaluated. Diagnostic studies consisted of electrocardiography, echocardiography, duplex scanning, and/or angiography. Coagulation studies included activity tests of protein S, protein C, antithrombin, plasminogen, measurement of immunoglobulin G (IgG) anticardiolipin antibodies (ACLA), and a dilute prothrombin assay. Initially, 30 patients had increased ACLA titres and 28 had an abnormal dilute prothrombin assay, suggesting lupus anticoagulant. Decreased protein S, protein C and antithrombin activity were detected in 20, 3 and 3 patients, respectively, excluding patients in whom the abnormalities could be explained by the use of medication, by pregnancy or puerperium. We detected a decreased activity of plasminogen in 5 patients. The disorders could be confirmed by a second assessment in only 2 patients with a protein S deficiency, in none of the patients with a protein C or antithrombin deficiency and in 1 patient with plasminogen deficiency. However, the abnormalities persisted in 19 of 21 patients with increased anticardiolipin IgG titres and in 9 of 20 patients with lupus anticoagulant. A confirmed coagulation disorder was not associated with stroke type or vascular risk factors, but it was more common among patients with large vessel disease (odds ratio: 3.8, 95% confidence interval (CI): 1.1-12.8). Sixteen patients had a recurrent thromboembolic event, but the risk of recurrence was not increased among patients with a confirmed coagulation disorder. Our results suggest that idiopathic coagulation disorders are found in about a quarter of young stroke patients. They are difficult to predict and probably interact with other risk factors.
 ...
PMID:Coagulation disorders in young adults with acute cerebral ischaemia. 945 24

We reported a case of a thrombosis of the retinal and central artery and vein in a 44-year-old patient, with high-grade T-cell lymphoma. Cardiovascular family history and a medical history of cerebral ischemia caused by in situ fibrinolysis, led to perform thorough hematologic and genetic examinations. These disclosed a prothrombin gene G 20210 a variant in a homozygous state. In a heterozygous state, this mutation leads to an increase in plasma prothrombin rate of the order of 30%. Therefore, it is considered to be a major risk factor for venous thrombotic disease. Otherwise, acute leukemia or non-Hodgkin's lymphoma may induce thrombosis of retinal artery and vein by means of an optic nerve infiltration, as well as beta-thalassemia, ocular trauma and retrobulbar anesthesia. Retinal central artery and vein are seldom both involved; whereas occlusions of their branches are more frequent.
 ...
PMID:[Mixed retinal thrombosis in a patient carrying prothrombin gene mutation in a homozygote state]. 1060 75

The presence in the serum of antiphospholipid antibodies (aPL) is associated with venous and arterial thrombosis. This observation has led to the search for these antibodies in young patients with ischemic neurologic syndromes. However, 1% to 5% of healthy people may be found to have circulating aPL without necessarily being at increased risk of thromboembolism. Thus, the finding of APLA in a patient with cerebral ischemia does not necessarily provide an explanation for the etiology of the clinical syndrome. The aim of this study was to determine whether the presence of aPL in young patients with stroke or transient ischemic attacks represents a possible cause of hypercoagulability as defined by ongoing thrombin formation with resultant elevation of prothrombin fragment 1.2 (F1.2) levels. This was a retrospective, case-control study involving 57 subjects. Twenty-seven patients had a recent cerebrovascular ischemic event--either TIA or a stroke. Fifteen were positive for aPL, and 12 were aPL-negative. Thirty subjects, matched for age and sex with no history of cerebrovascular disease, served as controls. Of this group, 20 were aPL-positive and 10 were aPL-negative. Causes of hypercoagulability other than aPL were excluded by laboratory testing. A positive test for aPL was repeated after a 6-week interval and two positive tests were required for a patient to be regarded as being aPL-positive. Levels of F1.2 were measured by an ELISA technique. There was a significant difference (p < 0.05) in the mean F1.2 levels between the aPL-positive group with a history of cerebrovascular disease (mean F1.2 = 2.3733) and each of the other study groups. There was no statistically significant difference between any of the other study groups. Our findings suggest that F1.2 levels are elevated in young patients with cerebrovascular syndromes who have aPL and in whom other causes of hypercoagulability and atherosclerotic vascular disease are absent. Elevated F1.2 in these patients may be a potential marker of the hypercoagulable state associated with aPL.
 ...
PMID:Value of prothrombin fragment 1.2 (F 1.2) in the diagnosis of stroke in young patients with antiphospholipid antibodies. 1077 22

A single mutation in the 3'-untranslated region of the prothrombin gene, resulting in a G to A substitution, was recently reported. This finding added to the growing list of genetic disorders thought to be responsible for familial thrombophilia. Although most studies are in general agreement about the elevated risk of venous thrombosis in individuals carrying this mutation, its role in the first event of venous thromboembolism and recurrent events is unclear. Even less clear is the role that this mutation plays in the formation of arterial thrombosis (including coronary artery disease and cerebral ischemia), as studies show contradicting results. Because of this, it is not recommended as part of the routine screening of patients with venous thromboembolism. However, there are certain subgroups of patients who should undergo testing. The discovery of this prothrombin mutation has important clinical implications because it is the second most common cause of genetic thrombophilia, second only to the factor V Leiden. Moreover, its discovery likely will augment the clinician's ability to systematically risk-stratify an individual's likelihood of developing spontaneous thrombosis.
 ...
PMID:Review and management of patients with the prothrombin G20210A polymorphism. 1103 May 31

Recently, a single mutation in the 3'-untranslated region of the prothrombin gene was reported, resulting in a G-to-A substitution. This finding added to the growing list of genetic disorders thought to be responsible for familial thrombophilia. Although most studies generally agree about the increased risk of venous thrombosis in individuals carrying this mutation, its role in the first event of venous thromboembolism and in recurrent events is unclear. Even less clear is the role this mutation has in the formation of arterial thrombosis (including coronary artery disease and cerebral ischemia) due to contradicting results of studies. This mutation has important clinical implications since it is a common cause of genetic thrombophilia, second only to the factor V Leiden mutation. However, the mutation by itself may not be enough to trigger disease because thromboembolic disease is now generally accepted as a multifactorial disorder. Careful evaluation of this mutation will augment the clinician's ability to stratify systematically an individual's risk of developing spontaneous thrombosis.
 ...
PMID:Prothrombin G20210A polymorphism and thrombophilia. 1085 21

The prevalence of elevated prothrombin (PT) in the absence of the G20210A mutation has not been studied in patients with cerebral ischemia. We carried out a case-control study of PT G20210A and PT activity in 49 adult patients aged 45 years or less, with TIA or ischemic stroke without cardiac embolism or large vessel disease, and 87 controls from a group of blood donors. Five patients were heterozygous for PT 20210A (OR=2.3, 95% CI: 0.6-8.0). Even after exclusion of individuals with the PT gene variant, the PT activity was significantly higher in patients than in controls (1.11 vs. 0.97, P=0.0003). The relative risk of cerebral ischemia in patients within the fourth quartile of PT activity (1.10 U/ml or higher), was 3.2 fold (95% CI: 1.03-9.96), than in patients whose level of PT activity was in the second or third quartile. We conclude that, although PT 20210A may be a weak risk factor for TIA and ischemic stroke in young patients, increased PT activity, which is more frequent than the mutation, appears to be more strongly related to cerebral ischemia.
 ...
PMID:Elevated prothrombin is a risk factor for cerebral arterial ischemia in young adults. 1214 89

Prothrombin, protease-activated receptors (PARs) and the specific thrombin inhibitor protease nexin-1 (PN-1) are expressed in the brain. Recent studies have shown that the serine protease thrombin, depending on its concentration, plays an important role in neuronal degeneration or protection after cerebral ischemia. However, it is still uncertain whether a change in prothrombin or alterations in the expression of specific PAR-subtypes or PN-1 are associated with postischemic thrombin effects. Using semi-quantitative reverse transcription-polymerase chain reaction analysis, we show that prothrombin was up-regulated in the hippocampal formation 24 h after transient global ischemia in rats (two-vessel occlusion with hypotension), whereas the expression of PN-1 and the expression of PAR-subtypes 1-3 did not change significantly. Thus, control of the balance between the expression of prothrombin and PN-1 may reflect an important mechanism that underlies postischemic thrombin effects.
 ...
PMID:Increase of prothrombin-mRNA after global cerebral ischemia in rats, with constant expression of protease nexin-1 and protease-activated receptors. 1216 7

Mutations such as factor V Leiden G1691A (FVL), prothrombin G20210A (FIIM), methylenetetrahydrofolate reductase (MTHFR) C677T, cystathionine beta-synthase (CBS) 844ins68 and endothelial cell protein C receptor (EPCR) 4031ins23 are risk factors for thromboembolism. To assess the role of these mutations in young adults with cerebral ischemia of otherwise undetermined etiology, 93 patients younger than 50 years old with thromboembolic strokes or transient ischemic attacks were studied. One hundred and eighty-six healthy age-matched and sex-matched blood donors served as controls. The FVL mutation was detected in 15/93 patients and 13/186 controls. After adjustment for smoking, arterial hypertension, and hyperlipidemia, the association of the FVL mutation with cerebral ischemia [odds ratio (OR), 3.19; 95% confidence interval (CI), 1.38-7.39] remained significant. One of 93 patients and 6/186 controls were carriers of FIIM (OR, 0.33; 95% CI, 0.04-2.75). We detected the MTHFR TT677 genotype in 9/93 patients and 26/186 controls (OR, 0.66; 95% CI, 0.30-1.47), a CBS 844ins68 mutation in 12/93 patients and 19/186 controls (OR, 1.30; 95% CI, 0.60-2.81), and an EPCR 4031ins23 mutation in 1/93 patients and in no control individual (P = 0.33). In conclusion, in younger adults the FVL mutation is a risk factor for cerebrovascular disease. FIIM, the MTHFR TT677 genotype and the CBS 844ins68 mutation did not contribute to the risk in this group of patients. The EPCR 4031ins23 mutation is very rare, its possible role needs further investigation.
 ...
PMID:Genetic risk factors in young adults with 'cryptogenic' ischemic cerebrovascular disease. 1243 43


1 2 3 Next >>