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)

Any diffuse lesion of the liver induces permanent hypercoagulation with subsequent permanent lysis and possible consumption or DIVC/Hemostasis depends on two distinct mechanisms: the platelets, whose functional activity is more important than numbers, and the coagulolytic equilibrium of the plasma. Apart from the activating and inhibiting enzymes of coagulation and lysis, the lungs and liver play an important role. The lungs filter and then determine lysis of the corpuscular agglomerates. The liver produces epuration of the activated factors and prothrombinase, as well as the plasminogen activator. Except in extremely severe cases, however, these functions are rarely involved. Investigations must be complete and include a test of platelet aggregation, a TEG on total blood to analyze whole coagulation, and tests for consumption and lysis. Coagulation and bleeding time tests are of great value during severe hemorrhagic attacks. Pathological examination should evaluate the condition of the vascular state and, more particularly, the presence of fibrin thrombi with the appropriate methods.
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PMID:[Introduction to the study of hemostasis in cirrhotic patients (author's transl)]. 625 23

In the control group, a significant decrease in platelet aggregability could be demonstrated after reperfusion. This was paralleled by a decrease in platelet counts. When PGE1 was infused during OLT, the post-reperfusional decreases in platelet aggregability and platelet counts in the control group could be prevented. Furthermore, our investigation demonstrated that PGE1 infusion led to higher t-PA activity during the anhepatic phase. This was paralleled and followed by lower alpha 2AP levels at the end of the anhepatic phase and after reperfusion. The higher t-PA levels in the PG group did not result in clinical signs of hyperfibrinolysis during OLT. The aprotinin administration in both groups is most certainly responsible for the absence of hyperfibrinolytic signs in the TEG and the low overall requirement for transfusions, explaining the comparable transfusion rate in the two groups (Fig. 5). Further investigations involving more patients are required to evaluate the clinical effect of PGE1 therapy.
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PMID:Influence of prostaglandin E1 infusion on hemostasis in orthotopic liver transplantation. 768 52

We reported two cases of massive bleeding due to critical hyperfibrinolysis during living-related liver transplantation (LRLT) for end stage liver cirrhosis. The total volume of bleeding amounted to 57930 ml with the case 1, and amounted to 55980 ml with the case 2. TEG was useful for diagnosis of the hyperfibrinolysis. We administrated large amounts of FFPs, MAPs, PLTs, and gabexate mesilate. By rapid transfusion, we could manage to finish the procedures without hypotension, and complications were not observed at the early postoperative stage. We thought that the cause of the hyperfibrinolysis is the increasing blood tissue plasminogen activator (t-PA) due to long-anhepatic stage and small graft size. During anesthesia, since the functional start of a transplant liver is indispensable to it, in order to support a transplant liver for an improvement of hyperfibrinolysis, it is important to keep the homeostasis, such as body temperature, blood pressure.
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PMID:[Massive bleeding due to hyperfibrinolysis during living-related liver transplantation for terminal liver cirrhosis; report of two cases]. 1466 65