Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma samples from patients with alcoholic cirrhosis were analysed for plasminogen activators and for inhibitors of the fibrinolytic system. Plasminogen activator activity was considerably increased in patients' plasma compared with normal. Immunochemical characterisation of these plasminogen activators showed that they included both tissue type and urokinase type plasminogen activator. The major inhibitor of plasmin, alpha 2-antiplasmin, was decreased in the patients, but no evidence for the generation of plasmin was found.
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PMID:Plasminogen activators in alcoholic cirrhosis: demonstration of increased tissue type and urokinase type activator. 623 48

The present study was performed to analyze the relationship between portal hypertension and alterations of the endothelium-derived proteins thrombomodulin, plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1), which were determined in plasma samples of 28 alcoholic cirrhotic patients and 46 controls. Although cirrhotics showed lower levels of PAI-1, but higher thrombomodulin and t-PA levels than controls, no relationship was observed between thrombomodulin, t-PA or PAI-1 and portal pressure. Therefore, the hypothesis that splachnic endothelial damage secondary to portal hypertension leads to altered thrombomodulin, t-PA and PAI-1 levels in alcoholic cirrhosis is not supported by the results of this study.
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PMID:Lack of relationship between plasma thrombomodulin and portal hypertension in alcoholic liver disease. 1071

A 49-year-old male with alcoholic cirrhosis suffered several spontaneous, life-threatening, deep muscle bleeding episodes. Laboratory evaluation indicated excessive fibrinolysis with low plasminogen, low alpha2-antiplasmin, undetectable plasminogen activator inhibitor type 1 (PAI-1) activity, high tissue plasminogen activator (t-PA) activity and high t-PA antigen. Treatment with oral anti-fibrinolytic agents prevented further bleeding episodes. Decompensated cirrhosis eventually necessitated orthotopic liver transplantation. Post-operatively, the patient did not require oral anti-fibrinolytic agents, and there were no significant bleeding events. Circulating PAI-1 activity, t-PA activity and antigen normalized by 3 months post transplant. In short, the profound bleeding diathesis, as well as the imbalance in t-PA and PAI-1 levels, corrected after liver transplantation. Recognition of such patients is important, because the bleeding diathesis is an indication rather than a contraindication for orthotopic liver transplantation.
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PMID:Profound imbalance of pro-fibrinolytic and anti-fibrinolytic factors (tissue plasminogen activator and plasminogen activator inhibitor type 1) and severe bleeding diathesis in a patient with cirrhosis: correction by liver transplantation. 1461 53