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:3.4.21.7 (plasmin)
9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to clarify the effect of hemodialysis (HD) on the fibrinolytic system, fibrinolytic activity was evaluated in 27 patients undergoing regular hemodialysis treatment (RDT) using new parameters including plasma alpha 2-plasmin inhibitor (alpha 2 PI), alpha 2-plasmin inhibitor-plasmin complex (alpha 2 PIC), cross-linked fibrin degradation products (XL-FDP), tissue plasminogen activator (t-PA) activity, t-PA antigen and plasminogen activator inhibitor-1 (PAI-1) antigen. Predialysis baseline levels of plasminogen and alpha 2PI activity in RDT patients were significantly lower and those of alpha 2PIC were significantly higher than normal control values. During a single HD session, alpha 2PIC exhibited a continuous, significant increase reaching about 180% of initial values by the end of HD. alpha 2PI activity was significantly decreased at the end of the HD, though there were no significant changes in plasminogen activity during HD. Predialysis baseline levels of XL-FDP in RDT patients were significantly higher than normal control values. No significant changes in XL-FDP were observed during HD. Both t-PA activity and t-PA antigen significantly increased during HD, and PAI-1 antigen significantly decreased during HD. Von Willebrand factor (vWF) antigen in plasma, which is regarded as reflecting a release reaction by vascular endothelial cells to certain stimuli, also significantly increased during HD. However, neither vWF antigen nor t-PA antigen was increased by heparin administration alone. The changes in alpha 2PI and alpha 2PIC levels suggest that fibrinolytic activity is slightly higher in RDT patients and is even higher during HD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced fibrinolytic activity during the course of hemodialysis. 138 98

We present a 65-year-old female with myelodysplastic syndrome (MDS) who has attended our O.P.D. since 1983. In early December, 1990, dyspnea on effort developed which then progressed to dyspnea at rest at the end of December. She was admitted on January 8 with orthopnea. Chest X-ray films revealed loss of vascular shadows of the right lung. Blood gas analysis showed hypoxemia and hypocapnemia. Abnormalities in the coagulation-fibrinolytic system (increased TAT (thrombin-anti-thrombin III complex) and alpha 2-PIC (plasmin inhibitor complex)), possibly due to MDS, were detected. The diagnosis of pulmonary thromboembolism was made by pulmonary perfusion scintigram and pulmonary arteriography. After commencement of anticoagulation therapy on January 15, the subjective symptoms, blood gas analysis, pulmonary scintigram, and disorders of the coagulation-fibrinolytic system improved. The patient was discharged on March 5, 1991. The present case of myelodysplastic syndrome was associated with abnormalities of the coagulation-fibrinolytic system and was complicated by pulmonary thromboembolism.
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PMID:[Pulmonary thromboembolism associated with myelodysplastic syndrome]. 156 27

Eighteen patients with chronic renal failure due to primary glomerular disease undergoing conservative treatment (CRF patients) were studied to evaluate whether coagulation and fibrinolytic activity in plasma are enhanced in the patients. We measured plasma levels of coagulation-fibrinolysis parameters including thrombin-antithrombin III complex (TAT) (an index of thrombin formation), alpha 2-plasmin inhibitor (alpha 2 PI)-plasmin complex (alpha 2 PIC) (an indicator of plasmin production) and cross-linked fibrin degradation products (XL-FDP) (an index of fibrinolysis secondary to coagulation). There was no correlation between plasma levels of TAT, alpha 2PIC and XL-FDP and serum creatinine levels in CRF patients. Both fibrinogen and TAT were found to be significantly higher in CRF patients than in normal controls. TAT was negatively correlated with serum albumin or total protein. Antithrombin III (ATIII) activity was significantly lower in CRF patients than in normal controls. CRF patients showed significantly but slightly higher alpha 2 PIC and XL-FDP when compared to normal controls. These results suggest that TAT, alpha 2PIC and XL-FDP are good indicators of coagulation-fibrinolysis even in patients with decreased renal function. Coagulation activity is significantly increased in CRF patients but fibrinolysis secondary to coagulation is only slightly enhanced.
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PMID:Coagulation and fibrinolysis in patients with chronic renal failure undergoing conservative treatment. 177 41

In this study, alpha 2 plasmin inhibitor (alpha 2 PI), alpha 2 PI-plasmin complex (alpha 2 PIC), FDP (Fibrinogen/Fibrin Degradation Product) and D.Dimer were analyzed to confirm their clinical usefulness for estimation of symptomatic vasospasm and outcome. That included 34 patients operated on by clipping of aneurysm within 48 hours after onset. The patients were divided into two or three groups for each of the following items: Subarachnoid hemorrhage; Group A1 (Fisher's classification 1 and 2) and Group A2(3) and Group A3(4), Preoperative grade; Group B1 (Hunt and Kosnik I and II) and Group B2 (III and IV), Symptomatic vasospasm; Group C1 (present) and Group C2 (absent), Outcome; Group D1 (good recovery, moderate disability) and Group D2 (severe disability, vegetable). Peripheral venous blood was collected on the day before operation (Day 0) and first, second, 5th, 7th, 10th, 14th, 21st day after operation. Results are following. alpha 2 PI was found to change without significant intergroup or intragroup difference. alpha 2 PIC was significantly higher in A2 group than A1 group at 0 and 2nd day (p less than 0.05), in B2 group than B1 group at 0 day (p less than 0.05) and in C1 group than C2 group at 0 day and 5th day (p less than 0.05). Namely, alpha 2 PIC was already high before operation in patients with severe subarachnoid hemorrhage, poorer grade and/or symptomatic vasospasm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coagulation-fibrinolytic abnormality and symptomatic vasospasm in the acute stage of ruptured cerebral aneurysms--analysis of alpha 2 PI, alpha 2 PIC, FDP and D.dimer]. 183 Jul 49

A Japanese family with congenital abnormal plasminogen is reported. The patient was a 44-year-old male with no past history of thrombosis. Since only the plasminogen (PLG) activity was reduced on laboratory tests before surgery for lumbar disc herniation, coagulation and fibrinolysis studies were performed in the patient and his family. The patient underwent resection of the nucleus pulposus and posteriorlateral fixation of the lumbar spine. The PLG activity was 8% in the patient and his sister, 55% in his father, and 53% and 48% in his nephew brothers. The PLG antigen level was normal in all members of his family examined. IEF of PLG antigen showed abnormal patterns in which all bands were shifted slightly to the cathode side in the patient and his sister, but his father and nephew brothers exhibited duplicated bands showing combinations of normal and abnormal patterns. From these results, the proband and his sister were considered to be homozygotes, and his father and nephew brothers to be heterozygotes for congenital abnormal plasminogen. Acute reactant substances (fibrinogen, CRP, CPK, C1IN, alpha 1AT, etc.) and PIC (plasmin, alpha 2-plasmin inhibitor complex) increased after the operation due to the surgical insult, but the surgery did not trigger thrombosis. This patient is considered not to have developed thrombosis although he was a homozygote for congenital abnormal plasminogen, because the anticoagulation process until thrombogenesis was normal.
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PMID:[A Japanese family with congenital abnormal plasminogen]. 774 38

Twenty-two patients on regular hemodialysis treatment suffering from renal anemia were treated with intravenous recombinant human erythropoietin (rhEPO) for more than 8 weeks. Before and 4 and 8 weeks after the start of rhEPO administration, we measured prothrombin time, activated partial thromboplastin time, fibrinogen (FBG), antithrombin III activity (ATIII), plasminogen activity (PLG), alpha 2-plasmin inhibitor activity (alpha 2 PI), alpha 2-plasmin inhibitor-plasmin complex (alpha 2 PIC), and cross-linked fibrin degradation products (XL-FDP) in citrated plasma to determine whether rhEPO treatment enhances coagulation and fibrinolytic activity. The pretreatment values of FBG, alpha 2 PIC, and XL-FDP were significantly higher than the normal control values. The pretreatment values of ATIII, PLG, and alpha 2 PI were significantly lower than the normal control values. Platelet count and FBG were significantly increased 4 and 8 weeks after treatment with rhE-PO. The prothrombin time was significantly shortened 8 weeks after rhEPO treatment, but the activated partial thromboplastin time did not change. PLG was significantly decreased 4 and 8 weeks after rhEPO treatment, and ATIII and alpha 2 PI were significantly decreased 8 weeks after rhEPO treatment. alpha 2 PIC was significantly increased 8 weeks after rhEPO treatment, and XL-FDP was significantly increased 4 and 8 weeks after rhEPO treatment. These data suggest that in patients on regular hemodialysis treatment coagulation and fibrinolysis are already enhanced before the start of rhEPO treatment and that rhEPO administration further enhances these disorders.
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PMID:Enhanced coagulation and fibrinolysis during treatment with recombinant human erythropoietin in patients undergoing chronic hemodialysis. 804 58

The incidence of early reocclusion is reported to be higher in patients who receive fibrin-specific thrombolytic agents than nonspecific ones. The reason has yet to be clarified. In the present study, we focused on the difference in duration of fibrinolytic activity. The hemostatic parameters of 7 consecutive patients suffering from acute myocardial infarction treated with a fibrin-nonspecific thrombolytic agent (urokinase) were compared with 9 patients who received a fibrin-specific agent (tissue plasminogen activator, t-PA). The plasma concentrations of alpha 2-plasmin inhibitor (alpha 2-PI), plasmin alpha 2-PI complex (PLC), fibrin degradation products E fragment (FDP-E), and D-D dimer (D-dimer) were measured before, soon after, 1, 2, 3, 4, and 6 h and 2, 3, 4, and 7 days after thrombolytic therapy to estimate the hemostatic and fibrinolytic state. A significant decrease in alpha 2-PI (less than the lowest measurable level) with a simultaneous increase in FDP-E and D-dimer was induced soon after the administration of urokinase. FDP-E and D-dimer decreased, with a significant increase in alpha 2-PI, more than 6 h after thrombolytic therapy. In contrast, a less significant decrease in alpha 2-PI with a lesser amount and shorter duration of fibrinolysis were observed in patients who received t-PA. The amount of PIC soon after drug administration was not different between the two groups. Our data suggested that fibrinolytic activities induced by fibrin-nonspecific urokinase persisted longer than expected by its plasma half-life.The fibrinolytic activities might be terminated by the production of alpha 2-PI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolonged activation of fibrinolytic system induced by fibrin nonselective thrombolytic agent can contribute to preventing early reocclusion after coronary thrombolytic therapy. 840 54

The early stage of the state in which coagulation or fibrinolytic pathway is activated has been difficult to be estimated. Recently, it has become possible to detect an early stage of DIC (pre-DIC) due to the development of highly sensitive methods which quantitate so called "molecular markers". Molecular markers can be classified into three groups: 1) activation fragments of coagulation proteins (e.g. F1+2); 2) protease and its inhibitor complex (e.g. TAT, IXa-AT-III, Xa-AT-III and PIC); 3) degradation products (e.g. FPA, FPB beta, SFMC and D-dimer). Among them, F1+2, TAT, FPA and SFMC reflect in vivo thrombin generation, while PIC, FPB beta and D-dimer reflect in vivo plasmin generation. IXa-AT-III and Xa-AT-III may be useful markers to detect hypercoagulable states in an earlier stage of underlying various disorders. Measurement of circulating levels of the zymogens and protease inhibitors is unable to detect small changes caused by low grade DIC or localized thrombotic events. Monitoring plasma levels of molecular markers, however, gives us more specific and accurate information regarding the onset and time course of hypercoagulable states and enable us to diagnose DIC at an early stage and to evaluate the effect of treatment for patients with DIC, specifically.
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PMID:[Diagnosis of predictive state of disseminated intravascular coagulation]. 843 31

Thrombus formation is recognized pathologically in the affected arteries and is supposed to play a major role in the pathogenesis of Takayasu's arteritis; however, hemostatic conditions in this disorder have not been elucidated fully. We determined plasma levels of molecular markers for platelet activity (platelet factor 4; PF4, beta-thromboglobulin; beta TG), thrombotic status (thrombin-antithrombin III complex; TAT, fibrinopeptide A; FPA), fibrinolytic status (plasmin-alpha 2-plasmin inhibitor complex; PIC, D-dimer), and endothelial injury (von Willebrand factor antigen; vWF:Ag, thrombomodulin; TM) in 30 patients with Takayasu's arteritis and 20 age-matched control subjects. Plasma levels of PF4, beta TG, TAT, FPA and D-dimer, but not PIC, in patients with Takayasu's arteritis were substantially higher than those in normal control subjects. The levels of these markers were not different between the active and inactive stages of the disease. Plasma levels of vWF:Ag in patients with Takayasu's arteritis did not differ significantly from those in normal subjects, and plasma levels of TM were significantly lower than those in normal subjects. In patients with Takayasu's arteritis, platelet and coagulation activities are significantly increased, leading to hypercoagulable state and thrombus formation, although there is little, if any, endothelial damage.
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PMID:Hypercoagulable state in patients with Takayasu's arteritis. 872 10

Congenital plasminogen activator inhibitor-1 (PAI-1) deficiency is an extremely rare disorder characterized by a bleeding diathesis that begins in childhood due to hyperfibrinolysis as a result of decreased PAI-1 activity. We now present 4 unrelated pediatric cases of congenital PAI-1 deficiency. All 4 patients had a history of recurrent episodes of subcutaneous bleeding beginning in early childhood. These episodes were characterized by abnormal prolonged bleeding after trauma, tooth extraction, and surgical procedures, as well as by rebleeding following initial hemostasis. The 2 female patients both had symptoms compatible with hypermenorrhea. The family history was positive in 2 of the 4 patients. Hemostatic screening studies in all 4 patients revealed no abnormalities. Testing for factor XIII antigen, von Willebrand factor antigen, ristocetin cofactor activity, alpha(2)-plasmin inhibitor (alpha2PI) activity, and plasminogen activity was normal. The euglobulin lysis times were shortened in all cases as compared with those in normal control subjects. None of the patients had elevated tissue plasminogen activator (tPA) antigen levels, but PAI activity was markedly decreased in all cases. Three of the patients also had reduced levels of PAI-1 antigen. There tended to be a reduction in tPA-PAI-1 complex in all cases. In addition, 2 patients had elevated PIC (plasmin-alpha2PI complex). Tourniquet tests were performed in 2 patients, with no appreciable rise in PAI-1 activity or PAI-1 antigen levels. The administration of tranexamic acid clearly improved hemorrhagic symptoms in these patients. We considered PAI-1 deficiency to be the likely etiology of the congenital bleeding diatheses in these 4 cases.
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PMID:Four cases of bleeding diathesis in children due to congenital plasminogen activator inhibitor-1 deficiency. 1075 81


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