Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.68 (tissue plasminogen activator)
 11,311 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the fibrinolytic system in patients with chronic low back pain using a venous occlusion test to stimulate fibrinolysis, and we subsequently determined the levels of tissue plasminogen activator (TPA) and fast-acting inhibitor of TPA (PAI). There were 20 patients with a mean age of 50 years. Two thirds had radiographically spinal stenosis. Scar tissue around the spinal nerves was seen in 11 cases. Thirteen patients had undergone back surgery, whereas 21 healthy subjects served as controls. In the basal samples, TPA activity was decreased in the patients while TPA antigen level was increased compared with the controls. No clear explanation for this defective function of TPA in the patients was obtained, because no difference was seen in PAI level in basal samples. After the venous occlusion, no difference was observed in TPA activity between the two groups excluding the constitutionally defective fibrinolytic system in the patients. However, our results confirm low basal fibrinolytic activity in patients with chronic low back pain with manifest spinal pathology.
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PMID:Fibrinolytic defect in chronic back pain. A controlled study of plasminogen activator activity in 20 patients. 153 90

It has been reported that plasma fibrinolytic activity is abnormal in some patients with chronic low back pain. In an attempt to confirm this finding we studied 22 patients with chronic mechanical low back pain and compared them with 18 healthy controls who denied symptoms of back pain. Factors known to interfere with plasma fibrinolysis such as age, weight, seasonal and diurnal variation, exercise, smoking and drugs were controlled as far as possible. Plasma fibrinogen was significantly higher (2.8 versus 2.3 g/l, P < 0.005) in patients than in controls, but there were no significant differences in the median plasma concentrations of euglobulin clot lysis time, fibrin plate lysis area, plasminogen, alpha-2-antiplasmin, tissue plasminogen activator activity, and antigen, tissue plasminogen activator inhibition and plasminogen activator inhibitor-1 antigen level. The results fail to confirm abnormalities of plasma fibrinolytic activity in a group of unselected cases of chronic low back pain.
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PMID:Lack of evidence for abnormal fibrinolysis in chronic low back pain. 836 4

A 53-year-old man developed a deep venous thrombus (DVT) and pulmonary embolism (PE) shortly after an open Roux-en-Y gastric bypass was performed. He later suffered a life-threatening gastrointestinal bleed while on anticoagulation for the DVT. Thus, anticoagulation was held and an inferior vena cava (IVC) filter (G2, Bard Inc., Tempe, AZ, USA) was placed for PE prophylaxis. About 10 days after filter placement, he presented with severe low back pain and syncope. He also presented with hypotension and anuria unresponsive to intravenous fluids. A STAT non-contrast CT scan of the abdomen revealed that his IVC filter had migrated from an infrarenal to a suprarenal position. Given the high clinical suspicion for renal vein thrombosis, an attempt at IVC filter retrieval was made. The filter could not be retrieved because it was embedded in a large IVC thrombus that extended from the hepatic veins down to the common iliac veins. The patient received nearly 4 days of tPA that was administered at the site of the thrombus with a long thrombolytic catheter (UNIFUSE, Angiodynamics, Queensbury, NY, USA). While his creatinine peaked at 7.6 on hospital Day 4, he eventually began to produce urine and his creatinine had declined to his baseline of 1.0 on follow-up 1 month later. About 18 months after admission, his creatinine had further declined to 0.8. We report the first published case of acute renal failure due to bilateral renal vein thrombosis in the setting of IVC filter migration and thrombosis. This report highlights an important, but rare complication of IVC filter placement as well as the non-operative management of acute bilateral renal vein thrombosis.
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PMID:Bilateral renal vein thrombosis and subsequent acute renal failure due to IVC filter migration and thrombosis. 2042 Aug 4