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

The use of fibrinolytic agents to control the fibrinolytic enzyme system and lyse pathologic fibrin deposits or thrombus has now assumed a position with anticoagulants and vascular surgery in the physician's therapeutic armamentarium. The principal exogenous activators that are used clinically are streptokinase, urokinase, and tissue plasminogen activator. Acute arterial occlusions are more likely than chronic occlusions to respond to thrombolytic therapy, especially if treatment is instituted within a few hours of onset of symptoms and if the disease is due to embolic material rather than in situ thrombosis. Since the duration of drug infusion necessary to lyse arterial thrombus cannot be predicted, patients in whom tissue viability cannot be determined or in whom ischemia cannot be tolerated during the drug infusion interval are not candidates for intraarterial fibrinolytic drug infusion. In treating patients with venous occlusion, thrombolytic therapy is more effective against proximal clots than in calf thrombosis. No protective effect from pulmonary embolism has been noted in trials comparing heparin with streptokinase. Fifty percent of patients with an initial episode of deep venous thrombosis treated within 72 hours of onset will have complete resolution of thrombus with preservation of valve function.
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PMID:Application of thrombolytic therapy in vascular occlusive disease. A surgical view. 311 28

Careful interpretation of the vascular pathology is important in cases of intestinal ischemia caused by primary mesenteric vein thrombosis because it suggests antithrombin III (AT III) deficiency. This deficiency, an autosomal dominant hereditary disorder, predisposes the patient to venous thrombosis. Similar or acquired deficiencies may also predispose the patient to thrombosis. In hereditary AT III deficiency, 90% of the cases have thrombosis of the leg or iliac veins; 8.3% of the cases, thrombosis of the mesenteric veins. Additionally, some families have a tendency to develop mesenteric vein thrombosis specifically. In this case report, a daughter with probable AT III deficiency had a history of 3 episodes of deep vein thrombosis in the previous 5 years while taking oral contraceptives. Her father, with the same deficiency, died from massive intestinal infarction resulting from portal and mesenteric vein thrombosis. The 19-year old woman developed gradually worsening abdominal pain, signs of peritonitis, and hematemesis. A laparotomy revealed peritonitis that was due to segmental small-bowel infarction; the underlying pathologic condition was mesenteric vein thrombosis. Coagulation study results revealed AT III activity by chromogenic assay, 0.48 u/mL; AT III antigen, 0.5 u/mL; and protein C antigen, 1.15 u/mL. 10 days after discharge, she developed a hemicranial headache with nausea, vomiting, neck tenderness, and photophobia; she was readmitted. A CT scan showed a left posterior parietal cerebral infarct. Repeat AT III activity by chromogenic assay was 0.51 u/mL and AT III antigen level was 0.50 u/mL. Before anticoagulant therapy could be initiated, the patient died 7 days after readmission. The combined lowering of AT III activity and antigen levels to half of normal suggests AT III deficiency. Earlier diagnosis of this deficiency could have been made in light of the patient's own history of thrombosis and the paternal history.
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PMID:Mesenteric venous thrombosis due to antithrombin III deficiency. 333 17

A case of severe vasospasm producing ischemia associated with the administration of dihydroergotamine and heparin for prophylaxis of deep venous thrombosis is presented. We feel that the intensity of the vasospasm was related to the ergot in combination with the use of pressors and the presence of an operative site contiguous to the spastic artery. Based on our experience and a review of the world's literature, we feel that risk of vasospasm in trauma patients outweighs the potential additional benefit of this combination of drugs over heparin prophylaxis alone.
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PMID:Refractory vasospasm occurring in a trauma patient receiving dihydroergotamine and heparin. 340 34

Arterial embolism is usually caused by cardiac disease, and atherosclerotic coronary vascular disease is the primary precursor. Other cardiac states, as well as several uncommon causes, are part of the etiologic spectrum. The earliest signs are pain, paresthesias, pallor, and pulselessness. Severe ischemia is indicated by paralysis, a late feature. Arterial embolism and acute thrombosis can be difficult to distinguish, and deep venous thrombosis may also be suspected in the differential diagnosis. To restore arterial flow, anticoagulation treatment with heparin (Lipo-Hepin, Liquaemin) is given and surgical embolectomy is performed. Heparin infusion is continued until the patient is ambulatory, and then warfarin sodium (Coumadin, Panwarfin) is given over the long term. Fibrinolysis has also been used to treat acute arterial occlusion. Complications of embolism must be carefully guarded against, and additional procedures are sometimes necessary.
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PMID:Management of arterial emboli. Gleanings from 20 years of experience. 357 97

Although heparin has been used extensively to treat Deep Venous Thrombosis (DVT) and arterial ischemia (AI), controversy still exists regarding optimal dosage and the need for monitoring. Different authors have employed various test with variable results. Others, however, persist in giving heparin without laboratory control. This study was made in order to compare, in a prospective, randomized and blind manner, two coagulation tests, namely: Howel Time (HT) and Activated Partial Thromboplastin Time (APTT), in controlling the dose of heparin given by continuous intravenous infusion in DVT and AI. Our results show no significant difference in complications and failures of the therapy with either test, although significantly higher doses of heparin were needed to maintain APTT within therapeutic range than those needed to keep HT within a similar range.
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PMID:Laboratory control of continuous intravenous heparin therapy with Howel time and activated partial thromboplastin time. A prospective, randomized and blind study. 402 44

Homocystinuria, only partially responsive to pyridoxine, was first diagnosed at the age of 14 years in a boy with high myopia, spherophakia and subluxated lenses, when surgical removal of a dislocated lens became necessary. 2 years previously a fracture of the left tibia, treated conservatively, had been followed by ischemia of the leg necessitating amputation. Postoperatively, deep vein thrombosis had developed in the right leg. Plasma homocysteine was lowered to undetectable levels by treatment with betaine in addition to pyridoxine, folic acid and reduction of protein intake. During the two years on treatment no further thromboembolic complications have occurred.
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PMID:[Vascular and ocular complications in a child with homocystinuria]. 661 Sep 36

We report on a woman with an Lp(a) lipoprotein level above the 99th centile of the population distribution of concentrations, who at the age of 43 had had deep vein thrombosis causing a pulmonary embolus and whose brother, who also had a very high level, had suffered a cerebral infarction at the age of 43. She had given birth to three children, all with very low birth weight, one of whom died when 3 months old. The placentas had been small and ischemic. The concurrence of a very high Lp(a) lipoprotein level, familial thromboembolic disease and recurrent placental ischemia with delivery of children with low birth weight suggests the possibility that a very high Lp(a) lipoprotein concentration may predispose to placental insufficiency, presumably arising from pathological changes in maternal uterine vessels in the placental bed. If confirmed, a very high Lp(a) lipoprotein level may be a factor to consider in women who have repeated pregnancies with placental insufficiency and who give birth to children with low birth weight.
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PMID:High Lp(a) lipoprotein level in maternal serum may interfere with placental circulation and cause fetal growth retardation. 798 78

After decades of focus on the effects of cocaine abuse on the central nervous system (CNS), the cardiovascular toxicity of cocaine is just beginning to be appreciated. The most common cardiovascular pathologies associated with cocaine use include: cardiomyopathy, left ventricular dysfunction, myocarditis, arrhythmia, hypertension, myocardial infarction, stroke, arterial thrombosis, deep vein thrombosis, and gastrointestinal, renal, and skeletal muscle ischemia. This article reviews the above pathologies with speculations on the mechanisms by which cocaine produces cardiovascular tissue damage.
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PMID:Cardiovascular and thrombosis pathology associated with cocaine use. 829 12

A case can be made for the participation of polymorphonuclears (PMN) in the initiation and propagation of venous thrombosis. In animal models leukocytes adhered to areas of veins that serve as sites for initiation of thrombi in patients. In addition, PMN are found in white layers of thrombin where they may interact with platelets to attract more of each. This would add bulk and promote coagulation so that red layers are formed. Lidocaine and one of its derivatives inhibited leukocyte adhesion to veins in dogs and lidocaine reduced the incidence of deep venous thrombosis (DVT) in patients after hip replacement, suggesting but not proving that inhibition of PMN adhesion might have contributed. A new approach for preventing PMN contribution to DVT is suggested by recent studies which identified three families of adhesive receptors (integrins, intercellular adhesion molecules and selectins) on endothelium, leukocytes and platelets. Monoclonal antibodies against beta 2-integrins on leukocytes reduced leukocyte adhesion, emigration and PMN-dependent tissue injury in infection, inflammation and ischemia-reperfusion injury in animals. Selectins bind to specific carbohydrate ligands containing sialylated Lewis X, suggesting that relatively small analogues might inhibit PMN adhesion. Both platelets and PMN adhere to polymerizing fibrin through undefined mechanisms. Inhibition of this process might inhibit the buildup of white layers of thrombi.
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PMID:Neutrophils and deep venous thrombosis. 849 64

Acute arterial occlusions of the extremities present with the classical five P's: pain, pallor, pulselessness, paresthesia, paresis. Loss of sensitivity and motility are symptoms of the most severe grade of ischemia. The occlusions are due to embolism in about 70% of subjects and to local thrombosis in 30%. These patients have to be treated immediately with heparin. In the mildest forms, deobliteration is desirable, but in the more severe cases rapid restoration of flow not only saves limbs but also life. Deobliteration may be performed surgically or by means of catheters (local thrombolysis or thrombus aspiration) if available. Deep vein thrombosis, the other kind of emergency situation, requires immediate anticoagulation as soon as pulmonary embolism is suspected. It should be initiated by heparin and followed by oral anticoagulation. In patients presenting without pulmonary embolism but a swollen leg, ruptured Baker cysts or muscle hematomas should be ruled out before anticoagulation is started. Systemic thrombolysis or surgical thrombectomy is reserved for young patients with acute isolated thromboses. Thrombectomy must also be kept in reserve for the most severe form of deep venous thromboses, the phlegmasia cerulea dolens. In thrombophlebitis, no anticoagulation is indicated except in bedridden patients. The others must remain mobile and may be treated by systemic and local antiinflammatory drugs, incision of thrombosed varices, and bandages.
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PMID:[Emergencies in angiology]. 849 73


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