Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 18-year-old woman with primary antiphospholipid syndrome developed a major cerebral infarction leading to brain death despite intensive treatment with steroids, urokinase, glyceol and heparin. Fatal strokes associated with this syndrome are rare. A computed tomographic scan of the brain suggested occlusion of the main trunk of the right middle cerebral artery. The titer of antibodies against cardiolipin/ beta 2-glycoprotein I complex in serum was extremely high.
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PMID:Fatal cerebral infarction in an asymptomatic young patient with primary antiphospholipid syndrome. 750 May 48

Skin ulceration is a cutaneous manifestation of the antiphospholipid syndrome (APS) and is associated with thrombosis of small dermal vessels. Numerous therapeutic agents have been used but are often ineffective. We describe the efficacy of heparin and fibrinolytic agents [urokinase and tissue plasminogen activator (tPA)] in the treatment of longstanding nonhealing cutaneous ulcers. In one patient, heparin plus low dose tPA resulted in healing. In another patient, treatment first with urokinase and heparin, and subsequently with tPA alone, resulted in healing. When the ulcer recurred secondary to severe peripheral edema, tPA plus heparin led to complete resolution of the ulcer. This suggests that fibrinolytic therapy and/or heparin may be useful in other recurrent thrombotic manifestations of the APS as well. However, it must be emphatically stressed that since life threatening adverse reactions can occur secondary to hemorrhage, this treatment should be undertaken only after extensive evaluation and close monitoring of the coagulation status.
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PMID:Systemic therapy with fibrinolytic agents and heparin for recalcitrant nonhealing cutaneous ulcer in the antiphospholipid syndrome. 786 28

We document a 30 y old man with Primary Antiphospholipid Syndrome (PAPS) and thrombosis of the common femoral vein and both the external and common iliac veins, extending to the lower vena cava, which failed to respond to high dose heparin. After three days of fibrinolytic treatment with urokinase there was complete venous recanalization.
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PMID:Fibrinolytic treatment in primary antiphospholipid syndrome. 911 9

Severe renal hypertension due to both unilateral renal arterial occlusion and renal thrombotic microangiopathy developed in a 13-y-old girl as a manifestation of primary antiphospholipid antibody syndrome. The combination of the intravenous high-dose urokinase therapy and oral anticoagulation therapy, comprising aspirin, warfarin and dipyridamole, was significantly effective in improving her renal function and preventing thrombotic events during an 18-month follow-up period.
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PMID:Nephropathy and hypertension as manifestations in a 13-y-old girl with primary antiphospholipid syndrome. 973 41

A 24-year-old Japanese man was admitted because of massive haematemesis and melaena with persistent abdominal pain. Markedly bloody ascites and severely oedematous small intestine were recognized, and angiography then revealed superior mesenteric vein thrombosis. After resection of the necrotic small intestine, continuous intravenous infusion of heparin and urokinase was performed. This patient had no familial or personal history of thrombosis. On the 15th day after operation, an initial search for lupus anticoagulant revealed that the prothrombin time (PT) ratio and dilute activated partial thromboplastin time (aPTT) were positive under heparin treatment, without evidence of rheumatic or connective tissue disease. Thrombocytopenia was observed with a nearly normocellular bone marrow. A follow-up examination 1 year later still revealed an increased aPTT. However, all tests for antiphospholipid antibodies had been negative including dilute aPTT for about 2 years since the 15th day after operation. These findings suggest that, in this patient, superior mesenteric vein thrombosis has not been associated with primary antiphospholipid syndrome but is probably idiopathic. Positive tests for lupus anticoagulant in the initial period may be unreliable due to heparin treatment.
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PMID:Superior mesenteric vein thrombosis presented transient false positivity for lupus anticoagulant under heparin treatment. 1198 2

Acute cerebral ischemia resulting from the occlusion of a large or medium size intracranial artery is a known complication of antiphospholipid antibody syndrome (AAS). Usually these patients are treated by low dose aspirin and anticoagulants to prevent a stroke. We are reporting a case of acute stroke in a patient with AAS in whom combined intravenous and intraarterial thrombolytics were used emergently with an excellent outcome. A 32-year-old woman presented with a left hemispheric stroke of 2.5 hours duration. A computed tomography (CT) study of the brain was normal. The patient was treated with intravenous tissue plasminogen activator but remained aphasic and hemiplegic. Subsequently, the patient had a stable xenon CT cerebral blood flow study demonstrating low flow in the left middle cerebral artery (MCA) territory and an angiogram, which demonstrated occlusion of the left MCA. The patient was then treated with intraarterial urokinase with a rapid and marked improvement in her neurological deficit. The case suggests that stroke patients can be treated safely and effectively with combined thrombolytics.
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PMID:Combined intravenous and intraarterial thrombolytic therapy for treatment of an acute ischemic stroke: a case report. 1789 75

Antiphospholipid syndrome (APS) is an autoimmune disease, and its most critical pathologic process is thrombosis, which may explain most of the clinical features. Acute management of thrombosis involves immediate anticoagulation. Acute proximal venous thrombosis can be managed with thrombolytic therapy to reduce the long-term complications of the postthrombotic syndrome (pain, swelling, skin discoloration, or ulceration) and perform recanalization of occluded vessels. However, thrombolytic therapies are associated with high risks of bleeding. To our knowledge, this is the first report of epidural hematoma mimicking transverse myelitis after catheter-directed thrombolysis in a patient with primary APS. A 42-year-old male was admitted with sudden onset pain and swelling on left lower extremity. Venography demonstrated multiple thrombi on superficial femoral vein, common femoral vein, common iliac vein, and external iliac vein. Laboratory tests indicated the presence of IgM anticardiolipin antibody. He was diagnosed with primary APS with multiple venous thrombi. He was treated with urokinase (200,000/h) as thrombolytic therapy. After 1 day, he complained both leg weakness and urinary dysfunction. T1- and T2-weighted magnetic resonance images of spine showed about 8 cm-sized mass, suggesting hematoma on the posterior epidural space at thoracolumbar area. Despite the successful evacuation of hematoma, neurologic symptoms persisted and he is now receiving aspirin, warfarin, and physical therapy.
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PMID:Epidural hematoma mimicking transverse myelitis in a patient with primary antiphospholipid syndrome. 1807 36

The antiphospholipid syndrome (APS) is characterized by venous and/or arterial thrombosis, or recurrent fetal loss, in the presence of antiphospholipid antibodies (APL). The pathogenesis of APS is multifaceted and involves numerous mechanisms including activation of endothelial cells, monocytes, and/or platelets; inhibition of natural anticoagulant pathways such as protein C, tissue factor inhibitor, and annexin A5; activation of the complement system; and impairment of the fibrinolytic system. Fibrinolysis--the process by which fibrin thrombi are remodeled and degraded--involves the conversion of plasminogen to plasmin by tissue plasminogen activator (tPA) or urokinase-type plasminogen activator, and is tightly regulated. Although the role of altered fibrinolysis in patients with APS is relatively understudied, several reports suggest that deficient fibrinolytic activity may contribute to the pathogenesis of disease in these patients. This article discusses the function of the fibrinolytic system and reviews studies that have reported alterations in fibrinolytic pathways that may contribute to thrombosis in patients with APL. Some of these mechanisms include elevations in plasminogen activator inhibitor-1 levels, inhibitory antibodies against tPA or other components of the fibrinolytic system, antibodies against annexin A2, and finally, antibodies to beta(2)-glycoprotein-I (beta(2)GPI) that block the ability of beta(2)GPI to stimulate tPA-mediated plasminogen activation.
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PMID:Impaired fibrinolysis in the antiphospholipid syndrome. 2042 34