Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with systemic lupus erythematosus may develop premature atherosclerosis, notably coronary artery disease. A group of 10 patients with peripheral vascular disease presenting with intermittent claudication or gangrene were studied from a group of 563 patients followed prospectively at the Wellesley Hospital Lupus Clinic. These 10 patients were compared with the next lupus clinic patient matched for age and sex, with respect to demographic characteristics and risk factors. The patients and controls did not differ significantly in lupus activity criteria count, partial thromboplastin time, the number with antibody to cardiolipin, number receiving steroids or mean steroid dose, family history of atherosclerosis, hyperlipidaemia, smoking, hypertension or use of oral contraceptives. The risk factors for developing peripheral vascular disease were a longer duration of systemic lupus erythematosus and a longer duration of use of steroids. Eight of the 10 patients had coexistent coronary artery disease or transient ischaemic attack.
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PMID:Peripheral vascular disease in patients with systemic lupus erythematosus. 154 39

A lupus inhibitor paradoxically prolongs phospholipid-dependent coagulation assays, but may increase risk of thromboembolism. We studied seven patients with cerebral infarcts and one with TIA who had lupus inhibitor. The average age at onset of cerebral ischemia was 41 years. Three patients had multiple cerebral ischemic events. The activated partial thromboplastin time was longer than that of controls, but usually within normal limits. Other abnormalities included biologic false-positive VDRL, antinuclear antibodies, thrombocytopenia (three patients each), and deep vein thrombosis (two patients).
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PMID:Cerebral infarct, TIA, and lupus inhibitor. 309 32

Intravenous heparin therapy is often used in patients presenting with transient ischemic attack (TIA) or stroke as either bridging therapy for anticoagulation with warfarin, or as primary therapy in suspected intracranial arterial dissection, crescendo TIAs, or suspected hypercoagulable states. We examined the use of a bolus of intravenous heparin at the start of anticoagulation during hospital admission for patients with TIA or stroke. A subgroup analysis of a prospective, single-blinded, randomized clinical trial was undertaken to examine the effect of providing an intravenous bolus of heparin prior to continuous intravenous maintenance heparin therapy. Pre-treatment clinical factors were comparable between subgroups. Thirty-three patients received a bolus at initiation of therapy and 173 patients did not. Patients receiving a bolus had a significantly higher first activated partial thromboplastin time at 6 h after initiation of therapy than patients without bolus (87.6 +/- 36.3 versus 61.0 +/- 8.1 s). Patients receiving bolus achieved an initial activated partial thromboplastin time greater than the minimum threshold for the therapeutic range of anticoagulation (> 60 s) sooner than patients without bolus (9.6 +/- 7.3 versus 14.5 +/- 10.8 h), but did not have a significantly greater chance of achieving therapeutic range (60-90 s). The fraction of time during which anticoagulation was therapeutic was similar between patients receiving bolus or not. There was no significant difference between the number of supratherapeutic coagulation results, total dosage of intravenous heparin received, complications due to anticoagulation, nor the times required for discontinuation of heparin and discharge from hospital between subgroups. The use of an intravenous heparin bolus during initiation of anticoagulation for TIA or stroke does not appear to be associated with greater risks and can achieve a minimum therapeutic range faster than therapy without heparin bolus.
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PMID:The use of a bolus of intravenous heparin while initiating heparin therapy in anticoagulation following transient ischemic attack or stroke does not lead to increased morbidity or mortality. 1285 32

Transient ischemic attack is no longer considered a benign event but, rather, a critical harbinger of impending stroke. Failure to quickly recognize and evaluate this warning sign could mean missing an opportunity to prevent permanent disability or death. The 90-day risk of stroke after a transient ischemic attack has been estimated to be approximately 10 percent, with one half of strokes occurring within the first two days of the attack. The 90-day stroke risk is even higher when a transient ischemic attack results from internal carotid artery stenosis. Most patients reporting symptoms of transient ischemic attack should be sent to an emergency department. Patients who arrive at the emergency department within 180 minutes of symptom onset should undergo an expedited history and physical examination, as well as selected laboratory tests, to determine if they are candidates for thrombolytic therapy. Initial testing should include complete blood count with platelet count, prothrombin time, International Normalized Ratio, partial thromboplastin time, and electrolyte and glucose levels. Computed tomographic scanning of the head should be performed immediately to ensure that there is no evidence of brain hemorrhage or mass. A transient ischemic attack can be misdiagnosed as migraine, seizure, peripheral neuropathy, or anxiety.
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PMID:Transient ischemic attacks: Part I. Diagnosis and evaluation. 1610 Aug 51

An 85-year-old woman receiving anticoagulant therapy for transient ischemic attack suddenly developed bilateral femoral nerve palsy and severe pain in the bilateral groin and thighs. Her platelet count, prothrombin time and activated partial thromboplastin time were within the therapeutic range. Hematomas in the bilateral iliopsoas muscles were clearly detectable on CT scan. The right hematoma was larger than the left one and caused more severe femoral neuropathy, but improved gradually without surgical decompression. This case is reported here because bilateralism is exceptional, and iliopsoas hematoma should be suspected when a patient receiving anticoagulant therapy presents with pain in the groin or thigh.
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PMID:Bilateral iliopsoas hematomas complicating anticoagulant therapy. 1602 Aug 97

High levels of factor XI have been implicated as a risk factor for deep venous thrombosis and possibly cardiovascular disease; however, the relationship between elevated factor XI activity and stroke has yet to be established. We retrospectively evaluated factor XI activity, factor XI antigen, and high-sensitivity C-reactive protein (hs-CRP) values in samples from 65 patients with stroke, 13 with transient ischemic attack (TIA), and 17 with venous thrombosis, younger than 55 years with normal prothrombin and partial thromboplastin times who underwent evaluation for a hypercoagulable state. Factor XI activity levels were more than normal in 22% of patients with stroke or TIA and 18% of patients with venous thrombosis, producing odds ratios of 5.3 and 4.1 for stroke or TIA and venous thrombosis, respectively. Factor XI activity levels correlate with factor XI antigen levels by Deming regression analysis (slope, 1.3; R = 0.667) and a lack of correlation of both with hs-CRP suggests that factor XI is not an acute phase reactant. Our findings suggest an association between elevated factor XI activity and stroke.
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PMID:Elevated factor XI activity levels are associated with an increased odds ratio for cerebrovascular events. 1688 Jan 42

Early initiation of heparin therapy for treatment of stroke is not only associated with an improved outcome, but also with the risk of hemorrhagic transformation. We compared the efficacy of three unfractionated heparin bolus regimens (0 U/kg, 30 U/kg, or 80 U/kg) in achieving a therapeutic activated partial thromboplastin time over the first 6-hour period in a cohort of 54 patients admitted with transient ischemic attack or stroke. Patients treated with the low bolus dose (30 U/kg) were more often within the therapeutic range for activated partial thromboplastin time at two hours after the initial bolus than patients treated with the other regimens. The percentage of therapeutic activated partial thromboplastin time results within the first six hours of treatment was greater in the group treated with the low bolus dose. Using the low bolus dose may reduce complication rates and improve clinical outcomes in the future clinical trials.
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PMID:Optimal dosing of intravenous unfractionated heparin bolus in transient ischemic attack or stroke. 1911 59

Aspirin is widely used for the prevention of recurrent stroke in patients with transient ischaemic attack (TIA) and ischaemic stroke of arterial origin, because it is effective and inexpensive. Clopidogrel and the combination of aspirin and extended-release dipyridamole are more effective than aspirin, but are also much more expensive. No other antithrombotic regimens provide significant advantages over aspirin, although cilostazol and the novel platelet protease activated receptor-1 antagonist, SCH 530348, are currently being evaluated. For patients with TIA and ischaemic stroke of cardiac origin due to atrial fibrillation, vitamin K antagonists (VKAs) are highly effective in preventing recurrent ischaemic stroke but have important limitations and are thus underused. Antiplatelet therapy is much less effective than VKAs. The direct thrombin inhibitor, dabigatran etexilate, has shown efficacy over warfarin in a recent trial. Other new anticoagulants, including the oral factor Xa inhibitors, rivaroxaban, apixaban, and edoxaban, the parenteral factor Xa inhibitor, idrabiotaparinux, and the novel VKA, tecarfarin, are currently being assessed.
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PMID:Antithrombotic drugs for patients with ischaemic stroke and transient ischaemic attack to prevent recurrent major vascular events. 2017 Aug 41

Patients with a transient ischemic attack (TIA) or ischemic stroke are at high risk for a recurrent stroke. Platelet inhibitors can reduce this risk in patients with non-cardioembolic stroke or TIA. Aspirin is used for secondary prevention in patients with a low risk of recurrent stroke while the combination of aspirin and dipyridamole or clopidogrel is recommended in patients with a higher risk. Patients with atrial fibrillation have a five-fold increased risk of stroke. In comparison to placebo oral anticoagulation reduces the risk of stroke by 60-70% in primary and secondary stroke prevention. Aspirin can still reduce the relative stroke risk by 22% in patients with atrial fibrillation who have contraindications against anticoagulation. Given the limitations of oral anticoagulation with vitamin K antagonists a new generation of anticoagulants is currently being investigated which include factor Xa inhibitors and direct thrombin antagonists. Dabigatran has been shown to be as efficacious as warfarin given at a lower dose and significantly more efficacious when administered at a higher dosage. Both cerebral and intracranial hemorrhages were reduced by 60-80% in patients treated with dabigatran when compared to warfarin.
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PMID:[Antithrombotic and anticoagulation therapy after stroke and transient ischemic attacks]. 2118 35

New oral anticoagulant drugs are emerging as alternatives to warfarin for the prevention of stroke in patients with non-valvular atrial fibrillation. Two agents are direct factor Xa inhibitors (rivaroxaban and apixaban), and the third is a direct thrombin inhibitor (dabigatran). They have been separately compared to warfarin in large randomised trials. Our objective was to indirectly compare the three agents to each other for major efficacy and safety outcomes. Studies were assessed for comparability and the odds ratios of selected outcomes for each anticoagulant versus one another were estimated indirectly. The three cohorts differed significantly in terms of CHADS(2) score and the number of individuals with a past history of stroke, transient ischemic attack or systemic embolism. The estimated odds ratio of stroke or systemic embolism was 1.35 for rivaroxaban vs dabigatran 150 mg (p=0.04), 0.97 for rivaroxaban versus dabigatran 110 mg (p=0.81), 1.22 for apixaban versus dabigatran 150 mg (p=0.18), 0.88 for apixaban versus dabigatran 110 mg (p=0.34) and 0.90 for apixaban versus rivaroxaban (p=0.43). The estimated odds ratio of major bleeding was 1.10 for rivaroxaban versus dabigatran 150 mg (p=0.36), 1.28 for rivaroxaban versus dabigatran 110 mg (p=0.02), 0.74 for apixaban versus dabigatran 150 mg (p=0.004), 0.87 for apixaban versus dabigatran 110 mg (p=0.17) and 0.68 for apixaban versus rivaroxaban (p<0.001). In conclusion, the available data indicate no significant difference in efficacy between dabigatran 150 mg and apixaban for the prevention of stroke or systemic embolism in patients with non-valvular atrial fibrillation. It appears however that apixaban is associated with less major bleeding than dabigatran 150 mg or rivaroxaban and that rivaroxaban is less effective than dabigatran 150 mg in preventing stroke or systemic embolism. Such an indirect comparison should be used only to generate hypotheses which need to be tested in a dedicated randomised trial comparing the three drugs directly.
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PMID:An indirect comparison of dabigatran, rivaroxaban and apixaban for atrial fibrillation. 2283 27


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