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)

To assess the risk of deep vein thrombosis in haemophiliacs with long-term central venous catheters, we studied haemophiliacs followed at our centre with implantable venous access devices (ports) in place for > 6 months. Medical records were reviewed for a history of catheter-related complications. Each patient was examined for physical stigmata of thrombosis. Patency of the vessels was evaluated by contrast venography. Of 21 males with ports, 19 had factor VIII deficiency and two factor IX deficiency. Nineteen ports were evaluable (i.e. were in place for > 6 months). Seventeen patients have their original ports in place; two ports were replaced for mechanical dysfunction (1) and recurrent infection (1). Difficulty withdrawing or infusing occurred with three ports, two of which were cleared with urokinase. Physical examination was normal on all 19 patients. Venograms were performed in 13 of 19 patients. Parents of the remaining six patients refused venography because of the need for peripheral venipuncture. One patient had a small nonocclusive thrombus on the same side as his functioning catheter, and another had minimal narrowing of the subclavian vein at the site of a prior catheter. The overall prevalence of clinically relevant upper venous system thrombosis identifiable by contrast venography was zero (95% CI, 0-23%). We conclude that haemophiliacs do not have as high a risk of thrombosis as other populations of patients with central venous catheters. The theoretical risk of thrombosis should not preclude use of central venous catheters in patients with haemophilia.
 ...
PMID:Contrast venography in young haemophiliacs with implantable central venous access devices. 987 59

A number of recent data suggest that mast cells (MC) and their products are involved in the pathophysiology of thrombosis. In the current study, we have evaluated the number, distribution, and phenotype of MC in patients with deep vein thrombosis of the lower limb (DVT) (n = 15). Contralateral nonthrombosed limb veins served as control (CO). MC were examined by Giemsa staining and by immunohistochemistry using antibodies against tryptase, chymase, tissue-type plasminogen activator (tPA), urokinase (uPA), urokinase receptor (uPAR), and plasminogen activator inhibitors (PAI-1, PAI-2). We found an increase in the number of tryptase-positive MC in DVT compared with CO (DVT: 9.1+/-1.0 v CO: 4.7+/-0.6 MC/mm2, P < .05). Most of these MC appeared to accumulate in the adventitia of the thrombosed veins, in vicinity of the vasa vasorum. In both DVT and CO, MC reacted with monoclonal antibodies to c-kit, tryptase, and chymase. MC also stained positive for tPA and urokinase receptor, but did not express detectable PAI-1 or PAI-2. As compared with CO, a decreased proportion of MC in DVT was found to stain positive for chymase and tPA. Together, our results show that MC increase in number in DVT and express a profibrinolytic phenotype. We hypothesize that MC and MC-derived profibrinolytic molecules play a role in the pathophysiology of DVT.
 ...
PMID:Mast cells are augmented in deep vein thrombosis and express a profibrinolytic phenotype. 1002 47

A 49-year-old kidney transplant recipient was admitted with the diagnosis of acute iliofemoral deep venous thrombosis (DVT) extending into the external iliac vein in close proximity to the renal vein anastomosis. Thrombolytic therapy with urokinase was used and complete lysis of the thrombus was achieved within 36 hr. We feel that this method of therapy, rather than standard anticoagulation, represents the treatment of choice for acute DVT in the presence of a renal graft. Using this method we were able to salvage the kidney and avoid the complications of postphlebitic syndrome and pulmonary embolus.
 ...
PMID:Thrombolytic therapy: the treatment of choice for iliac vein thrombosis in the presence of kidney transplant. 1039 41

Although an increasing incidence of upper extremity venous thrombosis (U/E-DVT) has been reported, a relative paucity of information regarding the etiologic categories, precipitating causes, and proper management for this disorder is available. To settle on a strategy for the management of U/E-DVT, retrospective analyses were performed using records from the authors' hospital. In 12 patients (seven men, five women), 61 (mean) years of age, diagnosed as having symptomatic venography-proved U/E-DVT and followed up for 41 (mean) months, etiologic factors, precipitating causes, treatments, and outcomes were retrospectively analyzed. As etiologic factors, five of the patients had neoplastic disease, one had hemodialysis, and two had transvenous pacemaker implantations. Among various precipitating causes of U/E-DVT, hypoproteinemia was most frequently noted (67%). Various types of therapeutic management were selected: from thrombolysis with urokinase in six, balloon angioplasty in two, thrombectomy in two, and venous bypass surgery in one patient. Pulmonary embolism did not occur in any of the patients and only three of them complained of mild intermittent arm swelling during the follow-up period. Four patients died of neoplastic disease or heart failure (three within the first 6 months). This study, though limited, suggests that the rate of mortality depends on multiple underlying medical problems in U/E-DVT patients. Low incidences of late postthrombotic sequelae and pulmonary embolism were noted in this series. Symptomatic U/E-DVT patients could be managed conservatively with a revised supplementary therapy for their precipitating causes of U/E-DVT.
 ...
PMID:Upper extremity vein thrombosis: etiologic categories, precipitating causes, and management. 1043 94

Plasminogen activator inhibitor (PAI-1), a member of the serine protein family, is the most active in vivo inhibitor of fibrinolysis induced by plasminogen, tissue plasminogen activator (tPA), and urokinase type plasminogen activator (uPA). While the association between elevated PAI-1 and thrombogenesis has been well studied for several disease processes, including coronary disease, postoperative deep vein thrombosis (DVT), myocardial infarction, malignancy, and diabetes, few studies have concentrated on the correlation between elevated PAI-1 levels and thrombogenesis in patients with myeloproliferative disorders. Essential thrombocythemia (ET), a chronic myeloproliferative disorder, characterized by the overproduction of poorly functioning platelets, is associated with both thrombotic and hemorrhagic life-threatening complications. Although the events resulting in thrombogenesis in such patients may be multifactorial in nature, an association between elevated PAI-1 levels and thrombus formation has been proposed. Herein we present a patient diagnosed with ET complicated by multiple episodes of arterial thrombosis. Elevations in PAI-1 levels were documented repeatedly. The role of elevated PAI-1 when associated with other disease processes is also discussed.
 ...
PMID:Clinical implications of elevated PAI-1 revisited: multiple arterial thrombosis in a patient with essential thrombocythemia and elevated plasminogen activator inhibitor-1 (PAI-1) levels: a case report and review of the literature. 1043 40

A healthy, middle-aged Japanese man with no family history of thrombotic disorders presented with acute abdominal pain due to ischemic colitis. Two months later, he developed left leg pain and swelling. A venogram of the lower limbs, computed tomography, and a scintigram of pulmonary blood flow revealed deep vein thrombosis of the left lower limb extending to the inferior vena cava and emboli of both pulmonary arteries with bilateral pleural effusions. The responsible coagulation disorder was not detected in this case. Since these thrombi were refractory to the thrombolytic therapy with urokinase and anticoagulant therapy with warfarin, prednisolone was chosen for the suppression of accompanying thrombophlebitis. Two months following the initiation of prednisolone (20 mg/day), the venous thrombosis, abnormal pulmonary shadows, and pleural effusions had completely resolved. This case demonstrates the successful treatment of idiopathic venous and pulmonary thrombosis with glucocorticoids.
 ...
PMID:A case of idiopathic deep vein thrombosis improved with glucocorticoid therapy. 1043 71

Thrombolytic drugs, streptokinase and urokinase, were initially used in pulmonary embolism. More recently, new drugs like alteplase, reteplase, lanoteplase and saruplase have been a breakthrough in the treatment of acute myocardial infarction. Their efficacy has been demonstrated when treatment is initiated before the 6th hour of infarction onset. A 50% reduction of death rate is expected, if treatment starts within the 1st hour. Alteplase and reteplase are the most efficient thrombolytics despite a higher risk of cerebral bleeding. In pulmonary embolism with clinical signs of severity, thrombolysis is clearly indicated. In deep vein thrombosis of the lower limbs, therapeutic thrombolysis is still controversial. Some acute ischemic strokes (before the 3rd hour) could be treated with alteplase if there is no absolute or relative contraindication for thrombolysis. In prosthetic heart valve thrombosis, thrombolysis may be used if surgical treatment is contraindicated but the risk of bleeding and embolism should be taken into account.
 ...
PMID:[Indications for thrombolytics]. 1058 97

The goals of treatment of acute iliofemoral DVT should be prevention of fatal PE, reduction of pain and swelling of the involved leg, trying to stop the development of phlegmasia cerulea dolens and venous gangrene, prevention of disabling PTS by early removal of the blood clot, avoiding proximal venous obstruction, preserving normal, functioning valves in the leg veins, and preventing reflux. The authors recommend an aggressive approach with rapid removal of the occluding thrombus in the leg veins extending up into the iliac veins in active patients with a short history of symptomatic DVT, usually less than 7 days. This approach is not justified in chronically ill, bedridden, high-risk, or aged patients, or those with serious intercurrent disease or limited life expectancy. In these patients, such interventions can only be indicated for limb salvage in phlegmasia cerulea dolens when conservative treatment does not prevent the development of an acute compartment syndrome with venous gangrene. The preferred means of accomplishing early and quick removal of the thrombus is CDITT. Most of the authors' positive experience with thrombolysis is based on the use of urokinase. The Food and Drug Administration (FDA) has put this drug on temporary hold for almost 1 year. The alternative drugs (e.g., tissue plasminogen activator [tPA]) have not been tested for CDITT of DVT, and tPA is not FDA-approved for this indication. When there are contraindications or failure of thrombolysis, TE with a temporary AVF is a valid alternative.
 ...
PMID:Indications for surgical treatment of iliofemoral vein thrombosis. 1080 68

Heparin-induced thrombocytopenia (HIT) is a rare complication of anticoagulative heparin therapy. The more severe HIT type II is defined by peripheral thrombocytopenia combined with thrombotic and thromboembolic events. We report the case of a 24 year old male patient who was admitted to our ICU with thromboembolic obstruction of the right central pulmonary artery, and deep venous thrombosis (DVT) of the right superficial femoral vein. Systemic thrombolytic therapy with urokinase for seven days resulted in nearly complete resolution of the thromboembolic material in the pulmonary arteries. Antithrombotic therapy with intravenous heparin and overlapping oral phenoprocoumon was continued on the regular ward. Six days later, the patient had to be readmitted to the ICU with evidence of hemodynamic compromise due to massive bilateral pulmonary thromboembolism that could be confirmed by CT scan--DVT had extended to the right iliacal vein. Additionally, peripheral thrombocyte counts had markedly declined from 112.000 to 35.000/microliter within 3 days, indicating the presence of a Hit type II. This was verified by positive ELISA testing for antibodies against platelet factor 4 (PF4)-heparin-complex. A filter device was temporarily implanted into the inferior vena cava. The patients condition stabilized upon reinitiated systemic thrombolysis and replacement of heparin therapy against recombinant hirudin. Pulmonary artery pressures normalized. Peripheral thrombocytopenia diminished within three days. HIT type II is a severe complication of anticoagulative therapy with heparin. Here we report a case, and discuss diagnostic procedures as well as differential diagnosis to HIT type I.
 ...
PMID:[Heparin-induced type II thrombocytopenia as the etiology of severe recurrent pulmonary embolism]. 1123 57

An 80-year-old woman was admitted to the Traumatologic Hospital of Florence because of bilateral post-traumatic humeral fractures. Subcutaneous calcium heparin was immediately administered to prevent deep venous thrombosis. Nine days later, the patient was referred to the Internal Medicine Unit because of severe immune-mediated heparin-induced thrombocytopenia and bilateral deep venous thrombosis. Heparin therapy was immediately discontinued, and the patient was switched to warfarin therapy. Diagnosis of heparin-induced thrombocytopenia was confirmed by positivity of anti-heparin-PF4 antibodies. On the second day of warfarin therapy, bilateral limb venous gangrene with a high risk of limb amputation appeared. To reduce thrombin generation, i.e., the mechanism by which heparin-induced thrombocytopenia induces thrombotic events, intravenous treatment with dermatan sulphate and low-dose urokinase was initiated. After 10 days of treatment, the limb venous gangrene disappeared, and low-dose warfarin therapy was again introduced. The patient was discharged 40 days after admission, and a Doppler ultrasound study showed only minimal signs of deep vein thrombosis in the right popliteal veins. Although in Italy the use of dermatan sulphate has been limited to the prevention of deep vein thrombosis, this case shows that it should be considered a useful agent for the treatment of thrombotic complications secondary to heparin-induced thrombocytopenia. Patients with acute immune-mediated heparin-induced thrombocytopenia should not be treated with warfarin alone. Frequent platelet count monitoring from day 5 of heparin treatment remains the best means of early detection of immune-mediated heparin-induced thrombocytopenia.
 ...
PMID:[Calcium heparin-induced immunologic thrombocytopenia complicated with venous gangrene of the legs. Report of a clinical case]. 1169 2


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