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:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated levels of fibrinopeptide A, a marker of thrombin activity associated with acute myocardial infarction, have been found to decrease after administration of streptokinase when reperfusion occurs. In contrast, in patients without reperfusion and those with reocclusion after streptokinase therapy, fibrinopeptide A remains elevated. In the present study early serial measurements of fibrinopeptide A were used to further characterize this paradoxic increase in thrombin activity after streptokinase and to characterize its response to heparin. In 19 patients with acute myocardial infarction fibrinopeptide A was elevated to 82.3 +/- 43.5 ng/ml (mean +/- SE) before therapy. Thirty minutes after the initiation of streptokinase, fibrinopeptide A increased to 300.1 +/- 117.4 ng/ml (p less than 0.01), consistent with extensive thrombin activity. Fibrinopeptide A remained elevated until 15 minutes after a heparin bolus injection when levels decreased to 15% of the poststreptokinase value (49.2 +/- 13.3 ng/ml) (p less than 0.001). These data document a prompt paradoxic increase in thrombin activity after administration of streptokinase that may be responsible for failure of therapy in some patients.
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PMID:Paradoxic elevation of fibrinopeptide A after streptokinase: evidence for continued thrombosis despite intense fibrinolysis. 362 59

Fibrinopeptide A (FPA), released from the fibrinogen A alpha-chain by thrombin, can be resolved by high-performance liquid chromatography (HPLC) into three forms, the intact peptide (A), a modified peptide phosphorylated at the serine in position 3 (AP), and an N-terminally degraded form (AY). A new method has been developed, using HPLC, that allows direct measurement of the proportions of AP, A, and AY released by thrombin from fibrinogen in plasma samples of 200 ul or less. The method was used to examine variations in the proportions of AP and AY expressed as a % of total FPA in a number of patient and control groups. The mean percentages of AP and AY of plasma fibrinogen were found to be 21.7 and 14.2%, respectively, in normal laboratory controls. In older, apparently normal, individuals these figures were 27.0 and 15.5%, respectively. Cord plasma exhibited very high AP and slightly reduced AY levels (41.6 and 12.4%, respectively) compared with normal adults. Patients with liver failure had low AP levels and high AY levels (11.6 and 21.1%, respectively). Patients recovering from major surgery or acute thrombotic stroke showed an acute-phase rise in fibrinogen level that was accompanied by an increase in AP and variable reduction in AY. Incubation of heparinized whole blood for 8 days in vitro demonstrated a gradual decrease in the proportion of AP and increase in AY of plasma fibrinogen. These results provide some support for the idea that an increased "aging" of fibrinogen in the circulation may result in a decrease in the AP content of fibrinogen accompanied by a more variable increase in AY.
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PMID:Direct analysis of plasma fibrinogen-derived fibrinopeptides by high performance liquid chromatography: investigation of A alpha-chain N-terminal heterogeneity. 364 63

Fibrinopeptide levels were measured in 20 women during transcervical chorionic villus sampling (CVS). Fibrinopeptide A, a sensitive indicator of fibrinogen cleavage by thrombin, significantly increased in five subjects, whereas there was no change in B beta peptide, an indicator of fibrinolysis. The data suggest that modest fibrin formation, uncompensated by fibrinolysis, may be induced in some women by CVS.
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PMID:Fibrinopeptide A increases after chorionic villus sampling. 368 63

The purpose of this investigation was the longitudinal evaluation of the hemostatic system before and after 1, 3, and 6 months of treatment with a triphasic oestrogen-progestogen combination. No changes of circulating platelet aggregates, as an index of in vivo platelet aggregability, and of megathrombocytes, an indirect evaluation of accelerated thrombocytopoiesis, were observed. A very slight, but significant, increase of Fibrinopeptide A (FPA), a reliable index of thrombin formation, was found only after 1 month of treatment; after 3 and 6 months, the increase of FPA was not homogeneous and not significant. Antithrombin III activity (AT III) showed no modifications after the first month; after 3 months AT III increased to a small extent, and after 6 months it was similar to basal values. Our findings indicate that the triphasic combination does not modify platelet functions and induces a low-degree activation of coagulation counteracted by an increased activity of the physiological inhibitors of blood clotting.
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PMID:Platelet and coagulation functions during triphasic oestrogen-progestogen treatment. 395 5

Septic pelvic thrombophlebitis is an uncommon but potentially life-threatening complication of puerperal endometritis. The lack of specific physical findings necessitates a diagnosis based by exclusion on the patient's response to anticoagulation. Fibrinopeptide A (FPA) is the first peptide cleaved from fibrinogen during thrombin-mediated fibrin generation. Because of its short half-life, FPA accurately reflects the level of ongoing fibrin generation. In a preliminary study of 40 puerperal patients, FPA successfully differentiated puerperal fever secondary to endometritis or abscess from fever responsive to a heparin trial. The mean FPA level in patients presumed to have septic pelvic thrombophlebitis was 23.8 ng/ml as opposed to 7 ng/ml in patients with endometritis. No patient with septic pelvic thrombophlebitis as diagnosed by her response to a heparin trial had a level of FPA less than 14 ng/ml. There was no overlap of FPA levels between patients with endometritis or abscess and septic pelvic thrombophlebitis. The data suggest further prospective evaluation of FPA for the diagnosis of septic pelvic thrombophlebitis is warranted.
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PMID:Diagnosis of septic pelvic thrombophlebitis by measurement of fibrinopeptide A. 409 64

Fibrinopeptide A (FPA) concentrations were measured in blood taken by direct cardiac puncture from 31 patients who had died suddenly of ischaemic heart disease (IHD) and from 8 patients who had died suddenly of other causes. Mean FPA concentration in the IHD group was five times higher than that in the non-IHD group. This difference was almost entirely due to the high FPA level in the IHD subjects with a history of the disease. The FPA difference between the IHD and non-IHD groups is unlikely to have been due to differences in methods of resuscitation. A possible interpretation of the findings is that thrombin production causes or aggravates the course of events leading to sudden IHD death, particularly in subjects with a past history of IHD.
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PMID:Fibrinopeptide A and sudden coronary death. 614 43

Pleural fluid from an early, active phase of BCG-induced pleurisy was compared with fluid from late, healing phase, characterized by fibrinous adhesions. Exudates were tested for proteolytic activity on chromogenic peptide substrates designed for plasmin, tissue plasminogen activator, factor Xa, thrombin and plasma kallikrein. Considerable activity of active-phase pleural fluid was found on all of these substrates, and significantly lower values in the healing phase. Most exudates from both stages had very low fibrinogen concentration. Fibrinopeptide A, fibrinolytic products and antiplasmin were found in all exudates. Little or no fibrinolytic effect of pleural fluid was demonstrable on plasminogen free fibrin plates, despite the high activities on the low molecular weight substrates. Occurrence of alpha 2-macroglobulin-enzyme complexes is suggested as an explanation. The experimental results indicate that protease of the fibrinolytic and coagulation systems are active in the chronic inflammation of pleurisy, with higher levels of activity in active pleurisy phase.
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PMID:Fibrinolytic and coagulation mechanisms in stages of inflammation: a study of BCG-induced pleural exudate in guinea pig. 622 6

Through in depth studies, the biochemical pathways of hemostasis-related systems have been elucidated in terms of well-defined molecular mechanisms. The interrelationships of coagulation, fibrinolytic, kallikrein-kinin, platelets, prostaglandins, blood vessel, and complement systems are now well understood. Methods are currently developed to quantitate the molecular markers of each of these systems and define the involvement of each in disease and drug-related aberrations. Molecular markers allow for very early detection of disease states well before clinical manifestations are seen or current coagulation methods are affected. Therefore prophylactic or therapeutic treatment can begin before a disease state causes damage. Platelet factor 4 and beta-thromboglobulin are low molecular weight proteins released from the light (alpha) granules of platelets and provide a reliable index of endogenous activation and consumption of platelets. Serotonin and ADP are released during activation from the beta-granules and can be measured by high-performance liquid chromatography. Fibrinopeptide A is a molecular marker of the activation of the coagulation process and provides a useful index of the action of thrombin on fibrinogen. Elevated levels of this peptide are found in patients with hypercoagulable states or a thrombotic tendency. B beta 15-42 peptides are released at the early stages of fibrinolysis and are a useful collective parameter for the measurement of the activation of fibrinolysis. In both the primary and secondary fibrinolytic disorders this peptide is elevated. Circulating kinins provide information on the activation of the kallikrein system and are useful in monitoring coagulation and shock related disorders. Arachidonic acid metabolites, such as thromboxanes and prostacyclins, are products of platelet and vascular endothelium interactions. Their measurement in peripheral blood provides a useful tool to measure the vascular and platelet-related thrombotic defects. Furthermore, antiplatelet therapy can be monitored using these parameters. Numerous other metabolites of arachidonic acid such as the leukotrienes and PAFs also are generated in various immunopathologic disorders associated with hemostatic activation. Unlike the other coagulant tests, the measurement of molecular markers in native blood or plasma samples provides a true picture of the endogenous physiology. Since no activator or additive is added to influence the test, these markers provide the most relevant information on the pathophysiologic condition. Since most of these markers are proteins or low molecular weight products, isotopic and nonisotopic immunoassays, high performance liquid chromatography and fluorometric methods can be used to analyze their levels. Furthermore, multiple panels can be developed to profile various pathologic states.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Impact of automation on the quantitation of low molecular weight markers of hemostatic defects. 622 30

In a group of healthy women taking oral contraceptives containing 30 micrograms ethinylestradiol combined with two different progestogens (desogestrel and gestoden), Fibrinopeptide A (FPA) plasma levels were evaluated both before and after 3, 6 and 9 months of therapy. FPA levels, which represent an index of thrombin action in vivo, were also determined in untreated subjects during the follicular and the luteal phases of the menstrual cycle. While no modifications of FPA levels were found during the menstrual cycle, a significant increase of this peptide was observed during oral contraceptive treatment. These data suggest that low-dose oral contraceptives, by enhancing the rate of conversion of fibrinogen to fibrin by thrombin, increase the risk of venous thrombosis. Since some mechanisms which compete with the thrombin activity are also increased by oral contraceptives, the significance of this change in the induction of thrombosis cannot be completely clarified.
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PMID:Fibrinopeptide A plasma levels during low-estrogen oral contraceptive treatment. 624 62

Fibrin catabolism was measured during the pregnancy of insulin-dependent diabetic women in both a longitudinal and cross sectional fashion. Samples of maternal peripheral venous blood were obtained in 20 pregnant diabetic women between 26 and 38 weeks' gestational age. Fibrinopeptide A, the first peptide cleaved from fibrinogen during thrombin-mediated catabolism, was measured by radioimmunoassay. Intra-assay and interassay variation for fibrinopeptide A in this laboratory were 2% and 4% respectively. Antithrombin III activity was determined by the method of Odegaard. The patients ranged from 23 to 36 years. Overall blood glucose control was good as reflected in near-normal HbA1 fasting plasma glucose values. The mean HbA1 +/- 1 standard deviation was 7.1% +/- 1.2%. The mean fasting plasma glucose concentration was 101.9 mg% +/- 21.5 mg%. Mean FPA for the diabetic women exceeded control values at each gestational period. Significant differences were found in four of the seven intervals. While the highest FPA was noted in a patient with advanced diabetic vasculopathy, exclusion of this patient did not alter the overall findings. The findings were striking and suggest the need for a prospective study designed to account for White's classification of diabetes and the degree of glucose control. Because complications of the diabetic pregnancy include an increased risk of hypertension in the mother and sudden, unexplained fetal loss, two complications associated with abnormal clotting, the increase in fibrin catabolism in patients in tight metabolic control would suggest that events other than glucose regulation impact upon fibrin catabolism and possibly pregnancy outcome in the diabetic mother.
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PMID:Fibrin generation during the diabetic pregnancy. 651 59


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