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: UNIPROT:P00750 (PLA)
16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

New assays for thrombin-antithrombin III complex, plasmin-alpha 2-plasmin inhibitor complex, FDP-D-dimer, t-PA/PAI-1 complex and prothrombin fragment F1+2 are reviewed as molecular markers for disseminated intravascular coagulation (DIC). These are sensitive to early stage indication of DIC. Fluctuation of their levels was also relative to the state of DIC. It is therefore believed that they will play an important role in the diagnosis of DIC, as solid members of its parameter. On the other hand, t-PA/PAI-1 complex is suggested to be the complication marker of DIC, such as multiple organ failure (MOF), as its level was thought to reflect endothelial cell stimulation during DIC.
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PMID:[New useful parameters or makers in diagnosis and condition. Analysis of disseminated intravascular coagulation--mainly molecular markers]. 843 26

Ancrod is a purified coagulant venom which renders blood incoagulable by cleaving fibrinopeptide A (FPA) from fibrinogen, but the mechanism involved in the clearance of fibrin from the circulation is unknown. To investigate the fibrinolytic response to ancrod, and to increase understanding of clearance mechanisms, six patients with peripheral vascular disease causing claudication were infused with ancrod at 2 u/kg over 6 h followed by 2 u/kg at 12 h intervals for 38 h. Venous blood samples were taken at time 0, 3, 6, 25 and 49 h for assay of fibrinogen (Fbg), fibrinopeptide A (FPA), total fibrin(ogen) degradation products (TDP), fibrin degradation products (FbDP), fibrinogen degradation products (FgDP), cross-linked fibrin degradation products (XL-FDP), tissue plasminogen activator (tPA), urinary type plasminogen activator (u-PA), plasminogen, alpha 2 antiplasmin (alpha 2 AP) and plasminogen activator inhibitor-1 (PAI-1). Fibrinogen (median and range) was 2.3 (1.4-3.90) g/l at time 0 and thereafter was undetectable. FPA rose from 2.5 (1.8-3.6) to 600 and 188 pmol/l at 3 h and 6 h and remained elevated. TDP, FbDP and FgDP increased greatly following ancrod while there was no evidence of XL-FDP. The surprising increase in FgDP during defibrination suggests either that fibrinogen is digested following its incorporation into circulating fibrin protofibrils or that some of the fibrin subunits in the photofibril retain one of the two fibrinopeptide A's. tPA and uPA remained unchanged. Plasminogen fell from 125 (100-155)% to 79 (40-118)% at 49 h and alpha 2 AP fell from 91 (75-107)% to 24 (10-35)% at 49 h. The level of PAI-1 was depressed during defibrination, with the exception of the 6 h data. The results demonstrate that ancrod removes FPA from fibrinogen to produce non-cross-linked (soluble) fibrin. This is cleared from the circulation without evidence of an increase in the circulating activities of the plasminogen activators, tPA or UK, but with evidence of plasminogen activation and consumption.
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PMID:The fibrinolytic response to ancrod therapy: characterization of fibrinogen and fibrin degradation products. 845 76

In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 +/- 14.3 v 3.2 +/- 1.7 micrograms/ml:P < 0.01), t-PA (19.4 +/- 14.9 v 11.3 +/- 0.8 ng/ml:P < 0.01), and functional PAI-1 activity (11.6 +/- 6.3 v 4.2 +/- 4.1:P < 0.01) with lower platelet counts (347 +/- 110 v 563 +/- 230 x 10(9)/1:P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.
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PMID:Acute-phase response and the hypercoagulable state in pulmonary tuberculosis. 870 31

We studied the influence of age on mortality and severity of clotting abnormalities in 79 children (median age: 3.1 years) with meningococcal sepsis. Parameters of coagulation and fibrinolysis and plasma levels of cytokines were prospectively measured on admission. The mortality rate was 27%. The age of survivors was significantly different from that of non-survivors (p = 0.013). With the exception of FVII, vWF and t-PA, parameters of coagulation and fibrinolysis, as well as plasma cytokine levels were related to outcome. Patients were divided in two groups: younger and older than median age. The mortality in children < or = 3.1 years was 40% versus 13% in children > 3.1 years (p = 0.006). In contrast to cytokine levels, which were not different between the two age groups, fibrinogen, prothrombin, factors V, VII, VIII, vWF, protein C, antithrombin, FDP, and the ratio PA1-1/t-PA were related to age, indicating a more severe coagulopathy in children < or = 3.1 years despite a similar degree of inflammatory response. A relative deficiency of coagulation factors due to an immature state of the clotting system, as well as an inadequate fibrinolytic response, both related to age may have caused this more severe coagulative response in younger children, and may have contributed to the higher mortality rate.
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PMID:Age-related differences in outcome and severity of DIC in children with septic shock and purpura. 897 13

We examined various hemostatic abnormalities in 395 patients with disseminated intravascular coagulation (DIC), in 177 patients in a Pre-DIC stage, and in 99 patients who did not exhibit DIC. Pre-DIC was defined as the condition at least one week before the onset of DIC. The differences in activated partial thromboplastin time (APTT), FDP, prothrombin time (PT) ratio, fibrinogen, and platelet count between DIC and Non-DIC patients were significant, but there were no significant differences in these parameters between Pre-DIC and Non-DIC patients. Plasma levels of fibrin-D-dimer, thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex (PPIC), soluble fibrin monomer (sFM), prothrombin activated peptide F1 + 2 (F1 + 2), thrombomodulin (TM), tissue type plasminogen activator (t-PA), and PA inhibitor (PAI-I) in DIC patients were significantly higher than levels in Non-DIC patients. However, only TAT, sFM and PAI-I values in the Pre-DIC patients were significantly higher than the values in the Non-DIC patients. Almost all the hemostatic molecular markers examined had high sensitivity for DIC, but only TAT and PPIC had high sensitivity for Pre-DIC. Specificity for DIC was also high with TAT, sFM, and F1 + 2. Early diagnosis and early treatment are important in DIC; we believe that it is possible to predict Pre-DIC by assessing values for the combination of hemostatic molecular markers.
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PMID:Diagnosis of pre-disseminated intravascular coagulation stage with hemostatic molecular markers. The Mie DIC Study Group. 911 56

The aim of study was the evaluation of tissue plasminogen activator (t-PA) and its inhibitor (PAI-1) in the II type diabetes on the base of the common fibrinolytic system tests as euglobulin lysis time (ELT) and the concentration of fibrin/fibrinogen products (FDP). The studies were performed in 21 outpatients suffering of II type diabetes aged 38-65 (median 56.0) years treated with diet and sulphonylcarbamide derivates. The control group contained 18 healthy persons aged 33-65 (median 42.0) years. In the blood the following determinations were performed: antigen of t-PA and PAI-1, ELT and FDP. In the blood of patients with II type diabetes increased. t-PA Ag and PAI-1 Ag concentrations were observed.
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PMID:[Plasminogen tissue activator and plasminogen tissue inhibitor in type II diabetes]. 929 93

Green pit viper (Trimeresurus albolabris and Trimeresurus macrops) venom was found to have a thrombin-like effect in vitro but cause a defibrination syndrome in vivo. The effects of venom on fibrinolytic system have not been well characterized. This knowledge can help to define the roles of antifibrinolytic therapy, give insights in fibrinolytic system regulation and potentially lead to identification of a new profibrinolytic agent from this venom. Forty-six cases of green pit viper bites were studied for various coagulation and fibrinolytic parameters and correlated with serum venom levels measured by ELISA. Fibrinolytic system activation is very common as indicated by low plasminogen (50%), low antiplasmin (56.5%) and elevated fibrin-fibrinogen degradation products (FDPs, 97.4%) levels. FDP test is very sensitive and a normal level is useful for exclusion of systemic envenomation. In contrast to some other models of defibrination syndrome, such as Russell viper (Daboia russelli siamensis), elevation of plasminogen activator activity (PA) was found indicating a hyperfibrinolytic state. Definite increase in tissue-type plasminogen activator (t-PA) antigen (p = 0.00075) with a modest elevation of its inhibitor plasminogen activator inhibitor-1 (PAI-1) (p = 0.27) probably contributes to this effect. This supports the idea that the balance between plasminogen activators and inhibitors can determine fibrinolytic responses in pathologic states. Fibrinopeptide A levels were markedly elevated (68.43 +/- 51.57 ng/ml in cases and 2.83 +/- 3.80 ng/ml in control, p < 0.0001) and correlated well with clinical severity suggesting that the fibrin deposition from the thrombin-like effect is the main mechanism of fibrinolysis. Therefore, antifibrinolytic agents probably have no role in treatment. However, the components of green pit viper venom that have these profibrinolytic effects in human are interesting and should be further identified.
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PMID:The effects of green pit viper (Trimeresurus albolabris and Trimeresurus macrops) venom on the fibrinolytic system in human. 1021 86

Colonic ischaemia may complicate aortic graft surgery with high mortality from associated colonic necrosis. Loss of the mucosal barrier function due to ischaemia may promote translocation of endotoxins with secondary systemic disseminated coagulation leading to multiple organ failure. Short-chain fatty acids (SCFAs) stimulate the microcirculation in the human rectum. The aim of this study was to investigate whether SCFA enemas influence systemic endotoxinaemia and fibrinolytic activity during and after elective aortic graft surgery for arteriosclerosis. Thirty-two patients were randomized to SCFA or placebo enemas twice daily from the day before surgery to 7 days after. Blood samples for endotoxin, plasminogen activator inhibitor-1 (PAI-1) activity, tissue-type plasminogen activator (t-PA) antigen, and cross-linked fibrin degradation products (XL-FDP) were drawn before, during, and 7 days after surgery. Four patients, two in each treatment group, developed postoperative endotoxinaemia. PAI-1 was significantly higher on days 2 and 4 in SCFA-treated patients, whereas t-PA was comparable Petween the groups. During the postoperative course, a progressive and near-identical XL-FDP increase was found in the two groups. In elective aortic graft surgery for arteriosclerosis, SCFA enemas likely stimulate systemic PAI-1 activity by promoting colonic tissue reperfusion following aortic unclamping. Endotoxinaemia and fibrinolytic shutdown are uncommon findings.
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PMID:Short-chain fatty acid enemas stimulate plasminogen activator inhibitor-1 after abdominal aortic graft surgery: a double-blinded, placebo-controlled study. 1082 75

The effects of progestogens on hemostatic function seems to be minimal, however, in this longterm surveillance study of the effects of Norplant among 100 healthy, nonsmoking, nonalcohol drinking, and nonlactating Singaporean women indicates the possibility of an increased predisposition of thrombosis. Clinical assessment and blood sampling were taken prior to insertion and at 6, 12, 24, 36, and 48 months. Laboratory tests included prothrombin time (PT), activated partial thromboplastic time (APTT), hematocrit and platelet count as hemostatic measures. Also measured were fibrinogen, coagulation factor II, a 1-stage assay for factors V and VII, factor VII, factor X, antithrombin III, plasminogen activator activity on the fibrin plate and FDP, platelet aggregation, factor VIIIR. 20 normal controls not on any medication were used and international standards were applied in most cases. The coefficients of variation of the various tests with reference control plasma or sera are summarized. The paired t test was used to assess statistical differences. Skewed results were analyzed with the Wilcoxon signed rank test. % changes between pre- and postinsertion levels were also utilized. The results were that the hemoglobin concentration increased from 12.1 gm/dl to 13.4 gm/dl in the 1st year, and then decreased to preinsertion levels within 3 years, and increased to 13.3 gm/dl in the 4th year. The 4th year also reflected no menstrual disorder. PT and APTT appeared significantly shortened in year 1. PT continued to shorten in 3 more years, while APTT increased to the preinsertion mean. Vitamin K dependent factors II and VII decreased significantly in year 1, while factors V and X increased significantly. Factor II increased minimally within 2 more years, but decreased again in year 4. Factor VII continued to decrease over the 4 years. The concentration of factors II and VII were significantly lower after 4 years. Factor V increased 14.4% in year 1, but decreased below preinsertion levels in the next 3 years, and then decreased to preinsertion levels in year 4. No significant changes in fibrinolytic activity occurred in 4 years. Major changes occurred in mean platelet count, which rose significantly in year 1 and increased concentration in year 4. In 4 years, platelet aggregation using ADP or equine collagen rose significantly. Serious thought must be given to the risk of thrombosis and potential for hypercoagulation.
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PMID:Haemostatic function changes in Singapore women using Norplant implants: a four year review. 1228 17

We measured the plasma level of fibrinogen in 560 patients with disseminated intravascular coagulation (DIC) and evaluated its relationship with outcome and with other hemostatic markers. Forty-seven percent of patients had >200 mg/dL of plasma fibrinogen and 24% had <100 mg/dl of plasma fibrinogen, suggesting that plasma fibrinogen level is not a sensitive marker for DIC. In our analysis of outcome and plasma fibrinogen levels, the rate of death was high in leukemia/lymphoma patients with high fibrinogen concentration, but no significant difference in outcome was observed in relation to plasma fibrinogen concentration in non-leukemia/lymphoma patients with DIC. Among patients with leukemia/lymphoma, the frequency of organ failure was markedly high in patients with high plasma levels of fibrinogen. Among patients without leukemia/lymphoma, the frequency of organ failure increased concomitantly with the increase in plasma fibrinogen levels. The international normalized ratio was significantly increased in leukemia/lymphoma patients with low fibrinogen. FDP levels were slightly increased in patients with low fibrinogen. Platelet count was significantly low in patients without leukemia/lymphoma with high fibrinogen. DIC score increased concomitantly with the reduction in plasma fibrinogen levels. Plasma levels of thrombomodulin and tissue factor were significantly high in patients with high fibrinogen levels. Plasma levels of antiplasmin and plasminogen were significantly decreased in patients with low fibrinogen. Plasma levels of plasmin plasmin-inhibitor complex and tissue type plasminogen activator/plasminogen activator inhibitor-1 complex (PAI-I) were significantly higher in patients with low fibrinogen than in those with high fibrinogen. Plasma levels of PAI-I and IL-6 were significantly higher in patients with high fibrinogen than in those with low fibrinogen. Patients with high fibrinogen levels showed less activation of secondary fibrinolysis, which might explain the occurrence of organ failure and poor outcome.
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PMID:High plasma fibrinogen level is associated with poor clinical outcome in DIC patients. 1250 60


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