Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lupus anticoagulant (LAC) is an acquired circulating serum immunoglobulin that prolongs all phospholipid-dependent coagulation tests. It has been recently associated with focal cerebral ischemia. We present here a case of LAC associated multiple cerebral ischemic events in a young adult and discuss laboratory criteria for a reliable diagnosis. In order to detect the presence of LAC, both the activated partial thromboplastin time (PTT), the kaolin clotting time (Exner assay) and the tissue thromboplastin inhibition assay (Schleider assay) should be evaluated. We conclude that LAC should be looked for in all young stroke patients with otherwise unexplained cerebral infarctions.
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PMID:[Lupus anticoagulant antibody (LAC) and juvenile cerebral ischemic attack: a clinical case]. 251 6

Serial determinations of beta-thromboglobulin (BTG), platelet factor 4 (PF4), fibrinopeptide A (FPA), antithrombin III (ATIII), protein C (PC), fibrin (ogen) degradation product (FDP), FDP D-dimer, activated partial thromboplastin time (APTT), prothrombin time (PT), and euglobulin lysis time (ELT) were performed in 18 patients with non-progressing stroke and 14 patients with progressing stroke in order to predict the development of progressing stroke. Increasing levels of BTG, PF4 and FDP with frequent fluctuation were noted in both kinds of stroke. Fluctuation of FPA levels was also noted but was less pronounced. PC levels were found to be slightly decreased with fluctuation but the mean was still in the lower normal limit. BTG, PF4 and PC all elevated at the time of deterioration of physical condition in patients with progressing stroke, whereas FPA had no definite change at that time. From our study, we conclude that both platelet activation and coagulation process do occur in both kinds of stroke. But the latter plays a minor role in the formation of thrombosis. The hemostasis change, especially concerning the thrombosis formation, probably plays a role in the development of progressing stroke, but we cannot predict their development even by the detections of the newly known molecular substances appearing in various steps of the hemostatic mechanism. Development of new tests for understanding the whole dynamic change of the thrombosis process is necessary for accurate prediction of the progressing stroke in the future.
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PMID:The serial hemostasis-related changes in patients with cerebral infarction: comparison between progressing and non-progressing stroke. 253 1

To characterize the clinical features of patients with acute cerebral infarction who sustained intracerebral hemorrhage related to heparin anticoagulation, we describe 10 patients and review reports of 16 cases. Cardiac-source embolism was identified in seven (70%) of the 10 patients and consisted of atrial fibrillation in six of the seven. The middle cerebral artery territory was affected in nine patients (90%), with moderate-sized or large infarcts by clinical and computed tomographic criteria. The interval between stroke onset and intracerebral hemorrhage was less than 72 hours in 80% of the patients. Intracerebral hemorrhage occurred less than or equal to 24 hours after the time heparin was started in 80% of the patients. The activated partial thromboplastin time closest to the time of intracerebral hemorrhage was greater than 2 x control in seven patients. Our findings in the 10 patients are similar to those of the 16 cases previously reported and suggest that heparin-related intracerebral hemorrhage occurs early after stroke onset, usually with moderate-sized or large infarcts, and with excessive anticoagulation in some patients.
Stroke 1989 Nov
PMID:Intracerebral hemorrhage in stroke patients anticoagulated with heparin. 268 44

We retrospectively and prospectively reviewed the incidence of stroke in 105 patients with systemic lupus erythematosus (SLE). Stroke occurred in 14 (15%) of 91 consecutive patients with documented SLE; nine (64%) of the 14 had multiple cerebral infarcts. Factors associated with stroke and the frequency of stroke were systemic thrombosis (30%), elevated partial thromboplastin time (36%), spontaneous abortion (50%), age over 60 years (57%), transient ischemic attacks (57%), previous stroke (64%), and cardiac valvular disease (86%). The major period of risk for the first stroke was during the first 5 years of SLE. The most frequent etiology was a cardiogenic embolus or an antibody-mediated hypercoagulable state, with cerebral vasculitis occurring only in association with infection. Because of the decreased fibrinolysis seen in patients with SLE, anticoagulant therapy may be the most effective preventive treatment currently available. Anticoagulant therapy seemed to prevent recurrent focal cerebral ischemia in our patients and was associated with relatively few and minor complications. Patients with a history of transient ischemic attacks or cardiac valvular lesions are at high (57% and 87%, respectively) risk of stroke. Patients who have had a stroke are at high (64%) risk for a recurrent stroke. Anticoagulant therapy is recommended for all of these patients.
Stroke 1989 May
PMID:Frequency, etiology, and prevention of stroke in patients with systemic lupus erythematosus. 230 Sep 86

Lupus anticoagulants are circulating autoantibodies, primarily directed against phospholipids, that prolong the partial thromboplastin time. They have been previously associated with systemic arterial and venous thrombosis and arterial stroke, but not with cerebral venous thrombosis. We describe 2 young patients with cerebral venous thrombosis documented by intravenous digital subtraction angiography in whom a lupus anticoagulant was demonstrated. Both patients improved with corticosteroid and anticoagulant therapy.
Stroke
PMID:Cerebral venous thrombosis with lupus anticoagulants. Report of two cases. 311 Oct 17

Polymeric drug delivery systems that allow the application of substances to a localized region for specified periods of time have been developed. A model for intravascular thrombosis in the rat common carotid artery was established using a combination of balloon catheter endothelial injury with 1-hour occlusion of the vessel. After endothelial injury in 11 Sprague-Dawley rats, the adventitial surface of the carotid artery was exposed to the polymer polyvinyl alcohol (PVA) containing heparin and was compared with exposure to PVA alone in the contralateral (control) vessel. Subsequent determinations of the coagulation parameters systemic prothrombin and partial thromboplastin times showed no systemic effect of heparin. All 11 control vessels demonstrated complete or partial thrombosis, whereas only one of 11 heparin/PVA-treated vessels showed a small thrombus. Morphometric analysis of the cross-sectional thrombus: lumen ratio in 10 rats showed a significant reduction (p less than 0.005) in thrombus size for treated vessels (4.1 +/- 9.6%) compared with control vessels (60.2 +/- 25.8%). Scanning electron microscopy verified the absence of thrombus in the treated vessels despite complete endothelial desquamation. In a second group of eight rats, endothelial injury without occlusion did not cause thrombosis in treated or control arteries. The coagulation parameters for this group of eight unoccluded rats were similarly unaffected by heparin/PVA treatment. Our observations suggest that a localized antithrombotic effect of heparin can be achieved without systemic anticoagulation using a polymeric drug delivery system. This technique may be applied to a variety of surgical and nonsurgical clinical conditions.
Stroke 1988 Dec
PMID:Local anticoagulation without systemic effect using a polymer heparin delivery system. 320 3

Six alcoholic patients developed extensive cerebral hemispheric hemorrhages with both intraventricular and subarachnoid blood. All patients had evidence of liver damage, low platelet counts, and abnormal prothrombin and partial thromboplastin times. Four patients presented with seizures; in two of the four, these seizures were initially diagnosed as alcohol withdrawal seizures. Four patients were comatose with lateralizing neurologic deficit; two patients were comatose without lateralizing neurologic deficit, suggesting a metabolic encephalopathy. In one patient there was delayed neurologic deterioration. In all six patients, computed tomography showed large diffuse cerebral hemispheric hemorrhages, prominent intraventricular blood, and breakthrough into the subarachnoid spaces, which was confirmed by necropsy findings. There was marked mass effect but minimal surrounding edema. All six patients died. In three, autopsy showed no evidence of aneurysm, vascular malformation, neoplasm, or amyloid angiopathy and no arteriolar hypertensive changes.
Stroke 1988 Dec
PMID:Alcoholic intracerebral hemorrhage. 320 17

98 post-menopausal women were randomly allocated to either Org OD 14 [(7 alpha, 17 alpha)-17-hydroxy-7-methyl-19-norpregn-5(10)-en-20-yn-3-one] 2.5 mg/day or placebo. Treatment was continued for up to 6 yr. Any thromboembolic episode that occurred was recorded. Prothrombin time (PT), partial thromboplastin time (PTT), factor VII level and factor X level were measured prior to treatment and at yearly intervals. Antithrombin III level was measured in the last two yr of the study. There was one cerebrovascular accident after 3 months of placebo therapy but no other thromboembolic episodes. No significant difference was found between the effects of Org OD 14 and placebo with regard to any clotting factors at any time interval, although factor VII and factor X levels were consistently lower in the OD 14 group than in the placebo group. Antithrombin III levels measured after 5 and 6 yr were significantly higher (P less than 0.01) in the OD 14 group, suggesting a reduced risk of thrombosis in the treatment group.
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PMID:Effects of long-term Org OD 14 administration on blood coagulation in climacteric women. 329 4

Embolic stroke was induced in rabbits using autologous blood clot. One hour after stroke, animals received heparin anticoagulation (AC) for five hours (acute AC) or five days (chronic AC). Animals received excessive AC (partial thromboplastin time greater than 3.0 times control), adequate AC (partial thromboplastin time, 1.2 to 2.5 times control), or saline. After the animals were killed, the brains were examined for macroscopic evidence of intracerebral hemorrhage. There was no significant increase over control in the incidence or severity of hemorrhage in any of the four treatment groups. The data suggest that heparin AC does not promote intracerebral hemorrhage after experimental embolic stroke.
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PMID:Intracerebral hemorrhage after experimental embolic infarction. Anticoagulation. 363 95

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67


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