Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 16 patients treated with intrapulmonary heparin at doses between 10,000 and 20,000 U/week for 1592 patient days, or 4.3 years, only one rethrombosed. This patient has a congenital antithrombin III deficiency. However, the use of intrapulmonary heparin, even in this particular patient, has remarkably decreased her thrombotic events as manifested by studying her history of deep vein thrombosis and pulmonary embolism prior to starting intrapulmonary heparin. This represents a failure rate of 4.2% in the total of 1592 patient days of therapy, or a rethrombosis rate of 1.4% per year. This recurrence rate is far superior to that reported for warfarin-type therapy or for platelet suppressive therapy. From this limited experience, it appears that heparin is an extremely safe and highly effective mode of outpatient prophylaxis for deep vein thrombosis and thromboembolic disease. The ultimate aim of this study is to determine the possibility of calcium heparin being placed into a hand-held aerosol nebulizer that a patient can use at home on a weekly basis. This would provide a highly convenient, safe, and apparently very efficacious mode of therapy for the long-term outpatient prophylaxis of deep vein thrombosis and thromboembolic disease.
 ...
PMID:Clinical use of intrapulmonary heparin. 389 71

The cause of postoperative DVT is considered to be changes in blood coagulation, stasis of blood within the veins, and injury to the vein wall. The coagulation changes have been investigated and documented and involve platelet activation, stimulation of the coagulation cascade, and blunting of endogenous fibrinolytic activity. Stasis has been objectively identified by retention of contrast material in soleal sinuses and marked changes in venous flow velocity in patients in the supine position and in those under general anesthesia. Vein wall injury is more controversial, but has been shown to be directly related to venodilation. Such dilation of veins occurs in response to operative trauma, hence venous endothelial damage most likely plays a part in the milieu responsible for postoperative DVT. The prophylaxis provided by the combination of dihydroergotamine and heparin appears to affect each of the three limbs of Virchow's triad. Heparin achieves its prophylactic benefit by activating antithrombin III. Activated antithrombin III affects numerous sites in the coagulation cascade. It has been shown that 1 micrograms of antithrombin III inhibits the formation of 1 unit of thrombin; however, in the presence of heparin, 1 micrograms of activated antithrombin III inhibits 750 units of thrombin. Dihydroergotamine increases venous smooth muscle tone without affecting arteriolar smooth muscle. Hence, it has the effect of preventing stasis without increasing blood pressure. It also affects the platelet membrane, prostaglandin synthesis, and blood distribution, although these findings need to be elucidated. The combination of dihydroergotamine and heparin seems to have a synergistic prophylactic effect in preventing postoperative DVT. Heparin modifies the coagulation changes, whereas dihydroergotamine minimizes stasis and potentially prevents the endothelial damage caused by excessive operative venodilation. Such a combination of effects can explain the synergistic prophylactic efficacy found when dihydroergotamine and heparin were employed in combination in the multicenter trial [42].
 ...
PMID:Combined dihydroergotamine and heparin prophylaxis of postoperative deep vein thrombosis: proposed mechanism of action. 390 91

Postoperative changes related to coagulation and fibrinolysis and their correlation with the incidence of deep venous thrombosis (DVT) were studied in 30 patients undergoing total hip replacement. Pre- and postoperative measurements of fibrinogen, factor Xa, VIII:C, VIIIR:Ag and its electrophoretic mobility, antifactor Xa activity, antithrombin III (AT III) and its electrophoretic mobility in plasma and serum, fibrin monomers, euglobulin lysis time, fibrinogen degradation products (FDP), alpha 2-antiplasmin and plasmin-antiplasmin complexes were determined. DVT was detected by 125I-fibrinogen leg scanning in 11 patients. There was a significant and progressive increase in fibrinogen, VIII:C, VIIIR:Ag, fibrin monomers, FDP and alpha 2-anti-plasmin levels after operation and likewise a prolongation of euglobulin lysis time. There were changes in electrophoretic mobility of AT III in plasma and serum in 12 patients. The presence of plasmin-antiplasmin complexes was demonstrated in 9 patients. No correlation between the changes in coagulation and fibrinolysis and the incidence of postoperative DVT was found. We conclude that important changes occur in several parameters of coagulation and fibrinolysis after total hip replacement. Such changes are not related to the development of postoperative DVT.
 ...
PMID:Changes in coagulation and fibrinolysis after total hip replacement and their relations with deep vein thrombosis. 393 49

We report on a newly diagnosed family with hereditary antithrombin III deficiency, with thromboembolic complications in the propositus. Both the propositus and his asymptomatic sister had decreased plasma levels of antithrombin III antigen and activity (28-52% of normal with good agreement between functional and immunologic assays). The propositus developed deep venous thrombosis, followed by massive pulmonary emboli despite heparin therapy and was treated with streptokinase and heparin with excellent results. Shortly thereafter, small bowel obstruction required surgical intervention, and antithrombin III concentrate, recently available in the United States as an investigational new drug (I.N.D.), was administered with no postoperative thrombotic complications. He was subsequently asymptomatic while on warfarin prophylaxis but twice developed venous thrombosis when he failed to take warfarin. The addition of danazol therapy led to a sustained rise in the antithrombin III level. Each of these therapeutic approaches is discussed and the literature reviewed with emphasis on the newer agents--streptokinase, antithrombin III concentrate, and danazol.
 ...
PMID:Hereditary antithrombin III deficiency: case report and review of recent therapeutic advances. 394 33

125I-Antithrombin III metabolism studies were performed in 2 patients with ischemic and ulcerative colitis, respectively. Both patients had acquired antithrombin III deficiency and objectively diagnosed deep venous thrombosis. A decreased 125I-antithrombin III plasma disappearance halflife and an increased fractional catabolic rate was found in both patients. The transcapillary flux ratio was elevated in the patient with ischemic colitis. A follow-up study of the first patient during a period when no signs of an ischemic colitis were present and no medication was taken showed completely normal tracer data. The data are consistent with both gastrointestinal loss and intravascular consumption of antithrombin III. The antithrombin III deficiency could not be explained by other causes such as proteinuria, liver dysfunction, or obvious disseminated intravascular coagulation. Reduced antithrombin III plasma levels were considered to have contributed to the development of deep venous thrombosis in both patients.
 ...
PMID:Antithrombin III metabolism in two colitis patients with acquired antithrombin III deficiency. 400 29

An abnormal variant of antithrombin III is reported in a young male with deep vein thrombosis. The heparin cofactor, progressive thrombin inhibition, and factor Xa inactivation are decreased. The abnormality seems to be a mutation which is transmitted in an autosomaldominant way. The half-life and fractional catabolic rate of 125I antithrombin III concentrate is the same in this patient as in patients with the classic type of antithrombin III deficiency and in a control.
 ...
PMID:A Swedish family with abnormal antithrombin III. 401 20

A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache, generalized convulsions and progressive disturbance of consciousness. He developed deep vein thrombosis in his right leg and pulmonary emboli two years earlier when he was placed on heparin and so forth, followed by warfarin sodium. Warfarin was terminated 9 months prior to his recent illness. On neurological examination on admission, he was semicomatous with blurred disc margins, roving eye movements with right abducens nerve palsy, nuchal stiffness and right flaccid hemiplegia. Left carotid angiogram and CT scan revealed extensive superior sagittal sinus thrombosis, complicated with hemorrhagic infarcts in bilateral frontal lobes. When examined for coagulation studies, the patient and his father had decrease in AT III activity and antigen levels. He was treated successfully with antiedematous agents and anticonvulsants during acute phase of illness. He was thereafter placed on warfarin 5-6 mg/day with no further clinical thromboembolic event for 2 years 9 months. There was no neurological abnormality when he was last examined, although he was treated with valproic acid 1,200 mg/day and phenytoin 250 mg/day to control occasional adversive seizures. A coagulation study following infusion of 5,000 units of AT III was carried out. Warfarin was discontinued the day before the study. 0.64 U/kg of AT III administration resulted in a 1% increase in AT III level after the infusion. The biological half life of AT III was 14.4 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Cerebral venous thrombosis with familial antithrombin III deficiency]. 404 Dec 90

Seven members of a family affected by hereditary antithrombin III deficiency were identified. The disorder was associated with recurrent spontaneous episodes of phlebitis, deep venous thrombosis, and pulmonary embolism in middle age. Danazol, a 17-alkyl derivative of ethinyl testosterone, which has been used to treat other antiprotease deficiency states, was assessed in the management of two men with antithrombin deficiency. In a dose of 600 mg a day danazol appeared to correct the antithrombin deficiency. This drug may provide a useful adjunct to anticoagulant treatment, particularly before surgery.
 ...
PMID:Effect of danazol on the biochemical abnormality of inherited antithrombin III deficiency. 406 Jan 4

The effects of peroperative electrical calf muscle stimulation with groups of impulses giving a short lasting tetanus of the calf muscles on postoperative deep venous thrombosis (DVT) and pulmonary embolism (PE) were compared with that of dextran 40 given per and postoperatively. The incidence of DVT and PE during the first 4-6 postoperative days was recorded. The diagnosis of DVT was based on the 125I-fibrinogen uptake test and phlebography and of PE on pre- and postoperative perfusion pulmonary scintigram and chest X-ray examination. Both methods reduced the incidence of PE. Calf muscle stimulation reduced the DVT incidence in patients with malignant disease while the reduction in DVT incidence for the whole group only was significant in the stimulation as well as the dextran 40 group. Mean values for preoperatively determined levels of antithrombin III, beta-thromboglobulin, fibrinopeptide A, plasminogen and ability to release fibrinolytic activity during venous stasis did not differ between those patients who developed or those who did not develop postoperative DVT or PE. However, antithrombin III levels below 80 per cent appeared to predispose to postoperative thromboembolism. The two prophylactic methods have similar effects on the incidence of postoperative thromboembolism. The stimulation method has certain advantages due to its safety and simplicity.
 ...
PMID:Prediction and prophylaxis of postoperative thromboembolism--a comparison between peroperative calf muscle stimulation with groups of impulses and dextran 40. 618 44

A prospective study of antithrombin III, determined by electroimmunochemical assay or an amidolytical method, was carried out with special reference to thromboembolism after total hip replacement. Two hundred and seven patients were randomly allocated to thromboembolic prophylaxis with dextran 70 or low dose heparin combined with dihydroergotamine. Deep vein thrombosis determined by phlebography of the operated leg or pulmonary embolism diagnosed with perfusion/ventilation scintigraphy developed in 51% of the total material and did not differ significantly between the two groups of prophylaxis or between patients with a preoperative At III below normal and those with a normal value. The correlation between the two assay methods for At III was 0.61. An initial, postoperative decrease in At III was noted with a parallel fall in hematocrit and fibrinogen, later followed by an increase of the plasma proteins. It is concluded that the immediate postoperative decrease of At III is mostly due to hemodilution.
 ...
PMID:Pre- and postoperative levels of antithrombin III with special reference to thromboembolism after total hip replacement. 619 14


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>