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:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of experimental meningococcal septicemia and the efficacy of heparin sodium therapy were evaluated by inoculating rabbits intraperitoneally with type B meningococci in mucin. Half the rabbits died, and the respiratory distress and circulatory failure that occurred during the terminal phase of the disease were associated with diffuse pulmonary capillary and venular thrombosis and with renal glomerular fibrin deposition. Platelet and leukocyte counts and plasma fibrinogen levels decreased in all rabbits, and prothrombin and partial thromboplastin times were prolonged. Pretreatment with heparin sodium diminished intravascular fibrin deposition but failed to prevent the pulmonary microthrombi and did not either reduce the mortality or improve the survival time. We conclude that death in meningococcal septicemia is due to widespread thrombosis of the pulmonary microcirculation. The disease is complicated by diffuse intravascular coagulation, which can be controlled with heparin sodium but which is not immediately life-threatening.
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PMID:Experimental meningococcal septicemia. Effect of heparin therapy. 94 60

This report reviews the manifestations in fifteen children of proved adenoviral pneumonia. Patients' ages ranged from 43 days to 4 years and 1 month. Twelve cases were younger than 2 years old. Adenoviral infections were proved by positive viral cultures or a four-fold increase of the complement fixation titer. Prolonged fever and cough were found in all cases. In 13 patients, respiratory distress occurred; 5 needed mechanical ventilation. Injected throats, conjunctivae and ear drums were common. Other clinical pictures included abdominal discomfort, hepatomegaly, skin rash, convulsion and bleeding tendency. Abnormal laboratory findings were mild anemia, leukopenia, thrombocytopenia, elevated erythrocyte sedimentation rate and C-reactive protein, impaired liver function test, and prolonged prothrombin time and partial thromboplastin time. Anemia (11 cases), leukopenia (7 cases) and elevated transaminases levels (7 cases) were more common than previously reported. All patients had para-hilar peribronchial infiltrates in chest roentgenography. Segmental atelectasis and compensated hyper-expansion were found frequently. Pleural effusion were noted in six of our cases. Air leak syndrome occurred in three patients who had received mechanical ventilation. Three of the 15 patients expired: one had a preceding measles infection, all had disseminated intravascular coagulopathy. For patients with antibiotic-resistant pneumonia, adenoviral studies should be done. Extrapulmonary manifestations, and some abnormal laboratory findings, i.e., mild anemia, leukopenia, impaired liver function are clues to adenoviral infections, while bleeding tendency can be regarded as a poor prognostic sign for children with adenoviral pneumonia.
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PMID:Adenoviral pneumonia in children. 132 94

High-dose interleukin-2 (IL-2) immunotherapy can cause hypotension, respiratory distress, interstitial edema, and thrombocytopenia, similar to endotoxic shock. We have observed that IL-2 has no direct effect on coagulation factors in vitro, but it has been observed to alter the coagulant properties of vascular endothelium. Accordingly, we investigated the possibility that IL-2 infusions initiate plasma fibrinolysis and disseminated intravascular coagulation (DIC). We studied the clinical course, platelet count, and coagulation profile in response to IL-2 infusion in seven patients, two with metastatic melanoma and five with metastatic renal cell carcinoma. Every patient experienced hemodynamic instability and thrombocytopenia, and one patient suffered an unusual complication, mesenteric thrombosis. No patient had appreciable changes in the prothrombin time or the partial thromboplastin time, nor did factors V or VIII decline in the two patients observed. In four patients examined, we found decreased titers of Hageman factor (factor XII), high molecular weight kininogen, prekallikrein, and plasma thromboplastin antecedent, as if these had been consumed by reactions of the intrinsic pathway of thrombin formation. Circulating D-dimer fragments were found in the plasma of every patient at some point during each infusion cycle, and we observed decreased titers of plasminogen in the four patients just mentioned, suggesting that IL-2 infusions initiated fibrinolysis. Taken together, the clotting factor derangements and related toxicity phenomena cannot be ascribed firmly to DIC. Activation of the intrinsic (contact) system of coagulation, however, may provide one link between the vascular endothelial surface alterations caused by IL-2 infusions and the development of the systemic toxicity that resembles septic shock.
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PMID:Fibrinolysis, thrombocytopenia, and coagulation abnormalities complicating high-dose interleukin-2 immunotherapy. 198 12

In 46 newborn calves with and without respiratory distress syndrome which had been delivered prematurely by caesarean section a blood coagulation profile was established. These animals were compared with 26 healthy, 5- to 8-day-old calves. Prematurely delivered calves showed a lower average plasma fibrinogen concentration than animals delivered in due time. Calves which developed a respiratory distress syndrome had a slightly prolonged prothrombin time and partial thromboplastin time as well as a lower antithrombin III activity already immediately postnatum compared with healthy prematures and some-day-old calves. It has to be assumed that in calves with respiratory distress syndrome--in analogy to pulmonary immaturity--the blood clotting mechanism is not yet fully developed. In healthy prematures and surviving asphyctic calves hemostasis remains largely stable during the first day of life, whereas plasma fibrinogen concentration increases. In the calves not surviving the examination period prothrombin time and partial thromboplastin time postnatum became significantly longer. Only in these severely asphyctic calves the presence of a consumption coagulopathy seems likely. A secondary reactive fibrinolysis was not observed.
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PMID:[Changes in the blood coagulation potential of premature calves with and without respiratory distress syndrome]. 271 60

Central venous plasma concentrations of thromboxane B2 (TXB2) the stable metabolite of the vasoconstrictor platelet aggregator thromboxane A2, were measured in 12 patients with septic shock. In 8 patients dying with septic shock the concentration of plasma TXB2 (912 +/- 250 pg/ml) was ten times higher than that in 4 survivors of septic shock (92 +/- 25 pg/ml) and 6 controls (91 +/- 18 pg/ml). Prothrombin time and partial thromboplastin time were significantly prolonged in nonsurvivors compared with survivors. Similarly, the alveolar-arterial oxygen gradient was significantly raised in nonsurvivors (233 +/- 39 mm Hg) compared with survivors (112 +/- 47 mm Hg). This study demonstrates that the metabolism of arachidonic acid to thromboxanes is increased in patients dying of septic shock and this raises the possibility that thromboxanes may be involved in the disseminated intravascular coagulation and respiratory distress syndrome associated with severe sepsis.
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PMID:Plasma thromboxane concentrations are raised in patients dying with septic shock. 612 85

Sensitized and control calves were challenged with an intravenous dose of 0.2 mL/kg horse serum. Changes in the blood pressure, blood cellular components, plasma kaolin activated p-tosyl-1-arginine methyl ester esterase activity, plasma antithrombin III levels and activated partial thromboplastin time were monitored. Anaphylaxis induced a severe drop in carotid arterial pressure and respiratory distress. There was a decrease in the total white blood cell count from a mean of 10,000 to a low of 1,900 per microL, a decrease in the percentage neutrophils and an increase in the percentage of lymphocytes from 57.4% to 94.8%. A drop was observed in the mean platelet count from 463 x 10(3)/microL. The time required for kaolin to produce maximum p-tosyl-1-arginine methyl ester esterase activation increased from two minutes in the controls to three minutes in calves undergoing anaphylaxis and was observed three to 90 minutes after the administration of horse serum. Antithrombin III levels in the plasma appeared to drop during anaphylaxis but were not significantly depressed (p greater than or equal to 0.5). A statistically significant (p < 0.5) drop in the rate of blood coagulation was observed by the activated partial thromboplastin time assay at 15 to 30 minutes after horse serum injection.
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PMID:A study of the effect of acute systemic anaphylaxis on blood coagulation and TAME esterase activity in calves. 699 96

Factor VII deficiency is an autosomal recessive hereditary disorder characterized by a normal partial thromboplastin time and a prolonged prothrombin time. Definite diagnosis of this condition requires a specific Factor VII assay. Its quite uncommon occurrence in the newborn was first described by Alexander and associates in 1951. A one-day-old male, full-term newborn was presented here with skin pallor, respiratory distress and bitemporal bulging masses noted immediately after birth. Computed tomography scan of the brain revealed a subgaleal hematoma and subarachnoid hemorrhage. Laboratory studies revealed prolonged prothrombin time and a Factor VII level less than 1%. Literature on the clinical manifestation and management of Factor VII deficiency is reviewed briefly.
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PMID:Factor VII deficiency with intracranial hemorrhage: a case report. 825 61

In preterm infants the activity of antithrombin III (AT-III), the main inhibitor of thrombin, is reduced depending on gestational age and complications such as sepsis or respiratory distress syndrome. Babies with low levels of AT-III have been shown to have a higher mortality and an increased incidence of intracranial hemorrhage. In our study we tried to show the effect of early AT-III substitution on coagulation parameters and the incidence of intraventricular hemorrhage (IVH). One hundred three preterm infants at a gestational age of 25-32 weeks (mean 28.9 weeks; birth weight 600-2,170 g, mean 1,285 g) received AT-III concentrate at a single dosage of 50-200 IU/kg on the day of birth and subsequently only in case of a new decrease below an AT-III activity of 50%. We measured AT-III activity, Quick's prothrombin time (PT), partial thromboplastin time (PTT) and platelet count on the day of birth, and after 1 and 5-9 days in 25 patients. AT-III activity before substitution was lower than described for term infants (20-72%, mean 40%). Within the first week of life Quick's PT and PTT reached almost term values. No significant differences of the platelet count were found within the first week of life. The incidence of IVH was lower than in current epidemiologic studies: in only 13% of the study patients. Six percent of the infants had IVH grade I, 3% grade II, 4% grade III and none grade IV. Therefore, in preterm infants AT-III substitution may reduce the incidence and progression of intracranial hemorrhage.
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PMID:Antithrombin-III substitution in preterm infants--effect on intracranial hemorrhage and coagulation parameters. 926 73

Although heparin has been used clinically for prophylaxis and treatment of thrombosis, it has suffered from problems such as short duration within compartments in vivo that require long term anticoagulation. A covalent antithrombin-heparin complex has been produced with high anticoagulant activity and a long half-life relative to heparin. The product had high anti-factor Xa and antithrombin activities compared with noncovalent mixtures of antithrombin and heparin (861 and 753 units/mg versus 209 and 198 units/mg, respectively). Reaction with thrombin was rapid with bimolecular and second order rate constants of 1.3 x 10(9) M-1 s-1 and 3.1 x 10(9) M-1 s-1, respectively. The intravenous half-life of the complex in rabbits was 2.6 h as compared with 0.32 h for similar loads of heparin. Subcutaneous injection of antithrombin-heparin resulted in plasma levels (peaking at 24-30 h) that were still detectable 96 h post-injection. Given the increased lifetime in these vascular and intravascular spaces, use of the covalent complex in the lung was investigated. Activity of antithrombin-heparin instilled into rabbit lungs remained for 48 h with no detection of any complex systemically. Thus, this highly active agent has features required for pulmonary sequestration as a possible treatment for thrombotic diseases such as respiratory distress syndrome.
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PMID:Covalent antithrombin-heparin complexes with high anticoagulant activity. Intravenous, subcutaneous, and intratracheal administration. 926 54

Recently, we developed a covalent antithrombin-heparin complex (ATH) as a possible treatment for respiratory distress syndrome. ATH reacted rapidly with thrombin and efficiently catalyzed the inhibition of either thrombin or factor Xa by exogenous antithrombin. In order to investigate mechanisms for the conjugate's unusual anticoagulant properties, changes in fluorescence due to covalent linkage or addition of exogenous antithrombin were studied in relation to reaction with thrombin derivatives or factor Xa. The emission spectrum of ATH was similar to that of antithrombin plus heparin mixtures. ATH quickly inhibited thrombin or factor Xa activities, as measured by a fluorogenic substrate. Fluorescein-labeled heparin was displaced from either thrombin or active site blocked thrombin by ATH, indicating that thrombin must bind to the conjugate's heparin moiety. Interaction of thrombin with ATH's heparin component was confirmed by a slow reaction rate of conjugate with a thrombin mutant that has weak heparin binding. Total intrinsic fluorescence increased when exogenous antithrombin was added to ATH, indicating that the catalytic mechanism may occur through a second inhibitor binding site. Thus, ATH reacts directly with thrombin through a bridge mechanism and probably catalyzes the reaction of thrombin with antithrombin by a second binding sequence on its heparin chain.
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PMID:Investigation of the anticoagulant mechanisms of a covalent antithrombin-heparin complex. 985 96


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