Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.69 (APC)
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The influence of two different methods of autologous transfusion, preoperative donor plasmapheresis (Abbott Autotrans) and postoperative autotransfusion (intraoperative blood salvage, Dideco Autotrans), on the intravascular hemostatic system was investigated. Forty-two patients undergoing total hip surgery and preoperative donor plasmapheresis were prospectively randomized into three groups. For substitution of blood loss, patients in group 1 (control group, n = 12) received in addition to cristalloids and colloids only homologous blood, group 2 (n = 14) autologous blood, and group 3 (n = 16) additionally intra- and postoperative autologous fresh frozen plasma (FFP). The investigation included blood parameters (hemoglobin, hematocrit, thrombocytes), clotting status (prothrombin time, plasma thromboplastin time, thrombin time, fibrinogen, plasminogen, and antithrombin III), and immunological methods such as fibrinopeptide A (FPA), thrombin-antithrombin III (TAT), and protein C. No significant difference was found with respect to total amount of infusion, intraoperative blood loss, autologous transfusion, and blood parameters. Excellent quality of the autologous FFP was demonstrated by investigation of the specimens before administration. The autologous packed red cells showed high levels of TAT and FPA as an indicator of thrombin generation. Their administration caused a significant increase in TAT and FPA levels in groups 2 and 3 compared to group 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Measures for reducing the use of homologous blood. Effects on blood coagulation during total endoprosthesis]. 144 16

Mesenteric venous thrombosis is a rare insidious event that is difficult to diagnose. Approximately half the cases in the past were deemed "primary" or "idiopathic." These cases were also frequently associated with a previous history of thromboembolism and a family history positive for thromboembolism. Inherited hypercoagulable disorders, such as deficiency of protein C, protein S, or antithrombin III, will probably explain many "primary" cases. Prompt diagnosis, especially with modern imaging techniques, and prompt anticoagulant therapy decrease mortality.
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PMID:Evolution of our understanding of the pathophysiology of primary mesenteric venous thrombosis. 153 72

Hypercoagulable states are disorders of blood coagulation, which include deficiencies of natural anticoagulants, disorders of the fibrinolytic system, presence of antiphospholipid antibody and abnormalities of platelet function. These disorders are well known causes of venous thromboembolic disease and are being recognized in association with arterial thromboembolic occurrences with increasing frequency. The performance of standard prosthetic vascular reconstructions may result in disastrous outcomes in patients with unrecognized and untreated hypercoagulable states. From 1986 to 1990, we identified 12 patients with hypercoagulable states, six of whom presented with evidence of arterial thromboembolism. All of the patients were men who smoked and were somewhat younger than the usual patient with atherosclerosis. Their ages ranged from 41 to 62 years. Four patients presented with ischemic rest pain, one patient with blue toe syndrome and one with rapidly progressive claudication. Four patients had undergone prior vascular reconstruction and two had previous pulmonary emboli. Evaluation of these patients to identify hypercoagulability included determinations of prothrombin time (PT) and partial thromboplastin time (PTT), platelet count, antithrombin III, protein C, free protein S and total protein S levels, along with platelet aggregometry. Two patients had protein S deficiency, one had protein C deficiency, one patient had protein C and S deficiency and two patients had hyperaggregable platelets. Four patients had prosthetic reconstructions and two had autogenous reconstructions. Three of the four patients undergoing prosthetic reconstructions had subsequent loss of limb and one patient died. Only one patient with prosthetic reconstruction had a patent graft on long term anticoagulation. Both patients undergoing autogenous procedures had successful revascularization with limb salvage.
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PMID:Hypercoagulable states in arterial thromboembolism. 154 37

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.
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PMID:Biological risk factors for sudden death in patients with coronary artery disease and without heart failure. 156 56

The molecular defect responsible for a dramatic prolongation of all standard clotting tests discovered in a 15-yr-old boy has been identified. Initial investigations revealed the presence of an activated Factor X (Factor Xa) and thrombin inhibitor which copurified with alpha 1-antitrypsin (alpha 1-AT), thereby suggesting the occurrence of an alpha 1-AT variant similar to alpha 1-AT Pittsburgh. This was confirmed by dot-blot analysis and direct sequencing after amplification by the polymerase chain reaction. A G to T transition at nucleotide 10038 results in the substitution of Met to an Arg, converting alpha 1-AT into an Arg-Ser protease inhibitor (serpin) that inhibited thrombin and Factor Xa more effectively than antithrombin III. Surprisingly, there was no bleeding history in the proband. The common mutation Z, which may explain a reduced expression of the allele bearing the Arg 358 Met mutation, was not observed in the propositus' DNA. To exclude the presence of another mutation, the coding regions and intron/exon junctions were sequenced. No other mutation was found. Recently, the patient experienced his first hemorrhagic episode at the age of 17. The level of the abnormal inhibitor had increased twofold 2 mo before. The large decrease in protein C concentration may account for the mild bleeding tendency in this case, despite the presence of the alpha 1-AT Pittsburgh mutation. An abnormal protein C pattern was observed in patient's plasma, suggesting that the circulating deficiency might be due to a deleterious effect of the abnormal inhibitor on both intracellular processing and catabolism of protein C.
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PMID:Met 358 to Arg mutation of alpha 1-antitrypsin associated with protein C deficiency in a patient with mild bleeding tendency. 156 92

We retrospectively evaluated the hemostatic system of 13 patients during implantation (2 to 35 days) of the Jarvik 7-70 total artificial heart (TAH). Although all patients were clinically manageable while on the TAH, 5 had excessive generalized bleeding. After the heart transplant procedure, 2 patients had neurological events and 1 patient, thrombosis of the leg. While the patients were supported by the TAH, the routine coagulation assays (prothrombin time, activated partial thromboplastin time, fibrinogen, factor assays, and platelet count) showed slight abnormalities but no correlation to hemorrhagic or thrombotic events. In contrast, plasma and cellular activation markers, which are highly sensitive and specific for hypercoagulability, fibrinolysis, or platelet activation, revealed activation in all patients. Most striking was the marked activation of the fibrinolytic system (p less than 0.05 to 0.001). Correlations of individual patient data compared with the average TAH group response could be made between excessive enhancement of fibrinolysis (increased D-dimer and tissue plasminogen activator and decreased plasminogen activator inhibitor) and bleeding. A hypercoagulable state (increased fibrinogen and thrombin-antithrombin complex and decreased antithrombin III and protein C), decreased fibrinolysis (decreased tissue plasminogen activator and D-dimer), activated platelets (increased thromboxane B2), or combinations of these were associated with thrombosis. The hemostatic activation returned to normal 1 day after removal of the TAH. These data suggest that the patient with a TAH requires more sophisticated laboratory monitoring and individualized treatment for excessive fibrinolysis, hypercoagulable state, or platelet activation to avoid thrombotic and hemorrhagic complications.
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PMID:Hemostatic abnormalities in total artificial heart patients as detected by specific blood markers. 157 Sep 81

The prospective study reported here evaluated the relationship between coagulopathy, catecholamines, and outcome in severe head trauma. Thirty-six trauma patients (10 with penetrating injuries, 26 with blunt injuries, 50% overall mortality) were evaluated. These patients had severe head trauma (Glasgow Coma Scale score less than 9). Blood was analyzed for platelet count, prothrombin time (PT), partial thromboplastin time (PTT), and fibrinogen, D-dimer, antithrombin III, protein C, and protein S levels. A 24-hour urine sample was collected for vanillylmandelic acid (VMA), normetanephrine, and metanephrine determinations. A control group of five patients undergoing elective neurosurgery was also studied. Statistically significant differences between head injury survivors and nonsurvivors were present for platelet count, PT, and fibrinogen activity. There were no differences in the results of the other coagulation tests or in urinary catecholamine levels. The trauma patients differed from the elective neurosurgery patients with regard to D-dimer levels, PT, PTT, protein C levels, and urinary normetanephrine concentrations. Head trauma patients have a coagulopathy that is absent in patients following elective neurosurgical procedures. The coagulopathy may correlate with poor survival in head trauma and may be related to a catecholamine surge.
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PMID:Coagulopathy and catecholamines in severe head injury. 158 49

Protein C together with its plasmatic cofactor protein S and antithrombin III probably represent the most important plasmatic inhibitor in coagulation. Protein C deficiency constitutes a high risk factor for venous thrombosis. Cerebral venous thrombosis is a manifestation which is scarcely referred to in protein C deficiency. The case of a 32 year old patient with protein C deficiency is presented. The patient was admitted for an endocraneal hypertension syndrome. CT and MR demonstrated multiple hemorrhagic cerebral infarctions. Arteriography confirmed vertebral venous thrombosis. Only six cases sufficiently documenting cerebral venous thrombosis due to protein C deficiency were found in the literature. In most cases coadjuvant factors exist predisposing thromboembolic disease. The present clinical case demonstrates the importance of considering protein C deficiency in the diagnosis of cerebral venous thrombosis in young adults.
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PMID:[Cerebral venous thrombosis and hereditary protein C deficiency]. 159 2

The effect of subcutaneous administration of recombinant human erythropoietin (rHuEPO) on plasma natural coagulation inhibitors (protein C, protein S, and antithrombin III) was evaluated in 10 uremic patients on continuous ambulatory peritoneal dialysis (CAPD). These patients were commenced on a 16 week-course of twice weekly rHuEPO by the subcutaneous route. The hemoglobin increased significantly from 6.9 +/- 1.3 g/dl to 9.6 +/- 1.9 g/dl after subcutaneous rHuEPO treatment (p less than 0.01) at an average dose of 84 +/- 9 U/kg body wt/week. With rHuEPO therapy, a significant increase in platelet counts was observed, albeit within the normal range. A significant increase in the prothrombin time was demonstrated at 6 weeks after treatment and increased activated partial thromboplastin time was observed at 6 weeks and 16 weeks after rHuEPO administration although these measurements still remained in normal range. CAPD patients have comparable or even higher plasma levels of natural coagulation inhibitors compared with healthy controls supporting our previous findings that patients on CAPD have normal plasma levels due to an effective compensatory production despite peritoneal losses of these proteins with CAPD. No change in either the immunological or the functional activity of these natural coagulation inhibitors was demonstrated with rHuEPO therapy and clinical thrombosis was not observed during and after rHuEPO therapy. We conclude that there is no laboratory evidence of increased risk of thrombogenesis due to reduction of natural coagulation inhibitors with rHuEPO therapy.
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PMID:Effect of subcutaneous administration of recombinant human erythropoietin on plasma protein C, protein S, and antithrombin III levels in patients on continuous ambulatory peritoneal dialysis. 160 9

This study analyzed the coagulation changes in twenty patients after orthotopic liver transplantation. The procoagulant, anticoagulant, and fibrinolytic systems were studied during the first two postoperative weeks. Within the first postoperative day all extrinsic and intrinsic pathway factors became normal except factors IX, VII, and X, which recovered within the next 24 hr. Of interest are the changes in factor VIII, which reached a high concentration with an increase in its antigenic fraction during the study. However, coagulation inhibitors showed a different pattern. In fact, antithrombin III (AT-III) and protein C (PC) needed from 7 to 14 days to reach normal values. Total protein S (TPS) and free protein S (FPS) did not recover until day 7, whereas heparin cofactor II (HC-II) remained at subnormal levels throughout the study. Thrombin-antithrombin III complex (TAT) values were strikingly elevated in the immediate postoperative period. Fibrinolysis parameters showed plasminogen (PL) levels in the normal range until day 4. Antiplasmin (AP) followed a curve parallel to that of plasminogen but its levels were higher during this observation period. Similarly the initial elevation in plasminogen activator inhibitor 1 endothelial type (PAI-1) levels remained high until days 4 and 7. In summary, it can be concluded that during the postoperative phase after OLT a hypercoagulable state is developed as a result of diminished anticoagulant and fibrinolytic activity. This coagulation might be a nontechnical factor contributing to the thrombotic vascular complications of some liver recipients.
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PMID:Diminished anticoagulant and fibrinolytic activity following liver transplantation. 160 81


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