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)

We studied 23 patients suffering cerebral ischemia who also had laboratory evidence of either a lupus anticoagulant (LA) or an abnormal anticardiolipin antibody (ACA). Four patients had lupus or a lupus-like illness, three had drug-induced lupus, and 16 had no overt evidence of collagen-vascular disease. Cerebral ischemic events were multiple in 71% of the patients; two patients presented with multi-infarct dementia. Recognized cerebrovascular disease risk factors were present in 57% of the patients. The partial thromboplastin time was prolonged in only 35% of the patients. An LA was identified in 15 of 21 patients tested, and an elevated ACA titer was identified in 10 of 12 patients tested. Simultaneous assays for LA and ACA were discordant in eight of 10 patients tested. LA- and ACA-associated brain ischemia is often recurrent, but other risk factors for cerebrovascular disease are often present. The laboratory findings in such patients may display considerable heterogeneity.
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PMID:Lupus anticoagulants, anticardiolipin antibodies, and cerebral ischemia. 249 72

Lupus-like anticoagulants (LLA), lupus anticoagulant and/or anticardiolipin antibody, are increasingly recognized in association with venous and arterial thrombotic events. We recently reviewed our experience with patients undergoing revascularization for lower-limb ischemia who were found to have LLA. Nine patients had LLA based on a prolongation of the partial thromboplastin time or by anticardiolipin assay by an enzyme-linked immunosorbent assay system. The ages of the patients ranged from 23 to 57 years. There were seven (78%) men, six (67%) blacks, two (22%) diabetic patients, and three (33%) hypertensive patients. One patient had systemic lupus erythematosus. All patients except one were cigarette smokers. Four patients had concurrent regulatory protein abnormalities: three protein C deficiencies, one protein S deficiency, and one plasminogen deficiency. The nine patients had 10 lower-extremity arterial reconstructions with two postoperative failures within 30 days. Patients were anticoagulated with heparin or aspirin after all but one operation. Patients at risk were identified on the basis of age (less than 51 years), unexplained early graft thrombosis, or history of venous or arterial thrombotic events. This group of patients is believed to be at risk for early postoperative thrombosis. Postoperative anticoagulation after revascularization for patients with LLA may be beneficial.
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PMID:Lupus-like anticoagulants and lower extremity arterial occlusive disease. 250 7

Antithrombin (AT III), a major circulating anticoagulant, may be influenced by ischemia-induced changes in microvascular integrity and contribute to localized hypercoagulability. In a nonheparinized intact canine hindlimb model we determined AT III activity by chromogenic substrate assay (S-2238); coagulation changes with fibrinogen, activated partial thromboplastin time (aPTT), and prothrombin time (PT); and transvascular exchange by lymph-to-plasma total protein concentration ratio. Femoral venous plasma and lymph samples were assayed during 1 hour of steady state (C), 6 or 8 hours of aortoiliac occlusion (I), and 1 or 3 hours of reperfusion (R). Four groups were studied: GI, sham operated (n = 5); GII, moderate ischemia (n = 7), arterial pressure 30% to 45% C, GIII, 6 hours of severe ischemia (n = 7), arterial pressure 5% to 20% C; and GIV, 8 hours of severe ischemia (n = 5), arterial pressure 5% to 20% C. All parameters varied near baseline in the control group and the group with moderate ischemia. Fibrinogen decreased after 3 hours of ischemia in GIII from 218 +/- 38 to 175 +/- 46 mg/dl (mean +/- SEM) and in GIV from 254 +/- 39 to 201 +/- 44 mg/dl (p less than 0.005) as aPTT and PT increased. All parameters returned to baseline on R in GIII only. Plasma AT III decreased in GIV from 89% +/- 4.6% to 53.6% +/- 16.2% (p less than 0.005) after 3 hours and remained low during late I and R.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activity and transport of antithrombin during acute limb ischemia. 272 60

The aim of our work was to study in a population of high risk patients with hemorrhagic and or thrombotic disease, the preventive or therapeutic effect of a low molecular weight heparin fraction, CY 216 (Choay, France), particularly in surgery. CY 216 was given to 9 patients for the treatment of a thrombosis (pulmonary embolism, acute ischemia, deep venous thrombosis) and to 40 patients in prevention of thrombosis. In this second group, 28 had a high thromboembolic risk such as valvular prosthesis, cardiac arrythmia, coronary artery bypass, etc. For all the patients, CY 216 was injected sub-cutaneously twice or three times a day at the mean dose of 1.5 mg/kg/d, equivalent to 300 U anti-Xa Choay/24 h, and always injected 24 hours before surgery. The biological tests used were: blood cells count, platelet count, prothrombin time, activated partial thromboplastin time, heparinemia levels by two technics: anti-factor-Xa activity and anti-factor IIa activity. None thrombotic complication was observed in the 40 patients prophylactically treated and a constant improvement of thrombosis was noted for the 9 patients with thrombo-embolic disease. In 3 patients, bleeding complications were observed: for 2 patients, all the coagulation tests were normal and anti-Xa activities were less than 0.55 U/ml; in one patient, the bleeding time was prolonged (15 minutes Ivy Incision) and returned to normal when the CY 216 was stopped. Concerning the biology, there was no modification except for anti-Xa activity which mean was 0.30 U/ml (01-07). However, this test is unable to predict either thrombotic or hemorrhagic events.
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PMID:[Prophylactic and therapeutic use of a low molecular weight heparin fraction, CY 216]. 283 83

Increasing evidence has demonstrated the importance of monocyte procoagulant activity (PCA) in the pathogenesis of coagulopathies in a variety of diseases. Because endotoxin precipitated coagulopathies are common sequelae to intestinal ischemia/endotoxemia in the equine species, we investigated the ability of equine peripheral blood monocytes to express PCA. Monocytes isolated from five healthy adult horses were incubated in vitro with Escherichia coli endotoxin (10 micrograms), and the PCA was measured by the ability of cellular lysates to accelerate the clotting times of equine plasma in a modified one-stage recalcification assay. Equine monocyte PCA was identified as thromboplastin based on lack of clot formation in factor VII-deficient plasma. The induction of PCA occurred as early as 2 hr after endotoxin exposure, peaked at 6 hr (396% increase), and then gradually declined. The amount of PCA was proportional to the dose of endotoxin (0.01 to 100 micrograms) and the number of monocytes. Neither platelets nor neutrophils produced PCA, either in the absence or presence of endotoxin (1 microgram). Lymphocytes at a concentration of 4 x 10(6)/ml RPMI did produce a significant amount of PCA, compared to the time-matched controls. Co-incubation of neutrophils or lymphocytes with monocytes did not alter the PCA, whereas coincubation of platelets and monocytes significantly enhanced the expression of PCA. This effect was further augmented by the addition of endotoxin (1 microgram).
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PMID:Endotoxin-induced procoagulant activity in equine peripheral blood monocytes. 320 23

This article reviews late graft patency and the incidence of postoperative complications in 75 infragenicular polytetrafluoroethylene bypass grafts (20 posterior tibial, 26 anterior tibial, and 29 peroneal). All patients received a heparin infusion after operation and were switched to warfarin before discharge to maintain coagulation parameters (prothrombin time and partial thromboplastin time) approximately twice that of control subjects. Primary procedures were done in 14 patients (19%), and the remaining patients had one or more previous procedures. Ninety-seven percent of patients had limb-threatening ischemia. Graft patency was confirmed by interval examinations and Doppler ankle pressure measurements. The mean follow-up was 36 months, and long-term graft patency (4 years) was determined by life-table analysis. The 2-year cumulative patency rate for this group was 45% and the 4-year patency rate was 37%. The latter is significantly better than the patency rates of 12% reported for similar untreated randomized grafts. Anticoagulation was subtherapeutic in 15 patients at the time of graft thrombosis, and if these were excluded, the 2- and 4-year patency rates were 58% and 50%, respectively. Hematomas requiring drainage occurred in 10 patients (13.3%) and six patients (8%) developed wound infections, but graft infection occurred in only two patients. Two patients (2.6%) developed late bleeding complications necessitating cessation of the warfarin. There was one fatal perioperative myocardial infarction (1.3%) and four late deaths, none of which were related to the warfarin therapy. Although the incidence of postoperative hematoma and wound infection was increased, late complications occurred infrequently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved long-term patency of infragenicular polytetrafluoroethylene grafts. 336 34

The optimal approach to management of patients after thrombolytic therapy for acute myocardial infarction (AMI) is unclear. The role of anticoagulation with heparin was evaluated in 75 consecutive patients who received intravenous streptokinase for AMI. Heparin therapy was titrated to keep the partial thromboplastin time (PTT) between 90 and 120 seconds. Seventeen episodes of definite myocardial ischemia (associated with reversible electrocardiographic changes) were observed in 13 patients. When episodes of probable myocardial ischemia are included (typical chest pain relieved by nitroglycerin or associated with more than a 15-mm Hg change in blood pressure but without electrocardiographic changes), 52 episodes occurred in 28 patients. Four episodes of definite and 4 of probable myocardial ischemia occurred within 24 hours of discontinuation of heparin. Analysis of the level of anticoagulation as assessed by PTT at the time of the ischemic events shows that ischemia occurred more often at lower PTTs. Nine hemorrhagic complications occurred, all within 24 hours of streptokinase infusion. In 4 patients bleeding was believed to be major and heparin administration was discontinued; 2 patients with gastrointestinal bleeding required blood transfusions. Our data suggest that after thrombolytic therapy for AMI, the level of anticoagulation is inversely related to the frequency of recurrent ischemic events; that discontinuation of heparin is frequently associated with ischemia; and that administration of heparin is associated with a low incidence of hemorrhagic complications.
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PMID:Role of heparin after intravenous thrombolytic therapy for acute myocardial infarction. 381 72

In most reviews of arterial embolism or thrombosis the source of emboli or the cause of thrombosis can reasonably be established in over 90% of patients. Still about 10% remain without demonstrable cardiac or intraarterial sources. Although hypercoagulability induced by malignancy has been alluded to as a cause of unexplained intravascular thrombosis reports of arterial thromboembolism with such association are rare. Seven patients with unequivocal thromboembolism are presented. Two distinct clinical patterns are observed, one with in situ thrombosis of small arteries and the other with occlusion of large arteries causing limb ischemia or fatal organ infarction. The various pathogenetic mechanisms of arterial thrombosis or embolism in malignancy include sustained spasm of arteries, precipitation of cryoglobulins or other abnormal proteins in small arteries, direct tumor invasion of arteries, fragmentation and embolization of intracardiac or intraarterial metastases and spontaneous arterial thrombosis due to hypercoagulability. The hypercoagulable state can be recognized by the observation of shortened bleeding and clotting times, partial thromboplastin and prothrombin times, elevation of coagulation factors, platelets and yield stress index and resistance to anticoagulation. Patients presenting with arterial thromboembolic events with out demonstrable source should be investigated for malignancy. Conversely patients with malignancy should be searched for evidence of hypercoagulability in an attempt to prevent arterial thromboembolic complications.
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PMID:Arterial thrombosis and embolism in malignancy. 403 Aug 80

Ischemic electrocardiographic changes were recorded within 2 hours of admission using a 12-lead electrocardiographic continuous monitor with a 20-second scanning interval and an alarm mode for asymptomatic events. Blood samples were obtained at admission and at the moment of asymptomatic events (group A). In the other patients who did not develop ischemia, a second blood sample was taken 12 hours later (group B). We determined prothrombin time, activated partial thromboplastin time, clotting factor VIII activity, tissue plasminogen activator activity, tissue plasminogen activator inhibitor-1, cross-linked fibrin degradation product, and thrombin-antithrombin III complexes. There was a statistically significant difference between group A and B patients when the basal samples were analyzed for thrombin-antithrombin III (p = 0.046) and d-Dimer (p = 0.005). Prothrombin fragment 1 + 2 were significantly reduced, and d-Dimer was elevated when basal blood samples were compared with the second sample in patients who developed silent events (p = 0.008 and 0.055, respectively). A plasma concentration of thrombin-antithrombin III complex was also significantly decreased when sample 2 was compared with the basal blood sample (p = 0.039). Five recurrent episodes of angina and 2 nonfatal infarctions occurred, and 4 urgent revascularization procedures were performed in group A. In group B, there was only 1 nonfatal infarction (p = 0.01). The results of the present study suggest that a time-dependent thrombotic process is detectable in the blood stream as a cyclic movement. Further studies are needed to determine if some other factors, such as intensive shear stress in the vessel wall, may activate plaque instability during asymptomatic episodes.
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PMID:Time significance of acute thrombotic reactant markers in patients with and without silent myocardial ischemia and overt unstable angina pectoris. 761 Nov 44

Retinal detachment is a rare complication of preeclampsia, eclampsia and abruptio placentae. We report a case of bilateral retinal detachment in association with severe preeclampsia complicated with abruptio placentae, intrauterine fetal death and disseminated intravascular coagulation. In obstetric complications, placental thromboplastin may release into maternal circulation and activate the extrinsic coagulation system with resultant disseminated intravascular coagulation. This may be responsible for choroidal ischemia and consequent serous retinal detachment.
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PMID:Retinal detachment in association with preeclampsia and abruptio placentae. 763 40


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