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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An inadequate efficiency of the fibrinolytic system was revealed in 50-60% of subjects suffering young age from venous thrombosis or myocardial infarction. In a group of 27 patients with the history of deep venous thrombosis of the idiopathic type the authors revealed a significant relationship between the elevated body weight and inadequate fibrinolysis manifested by a reduced fibrinolytic capacity and excess inhibitor of plasminogen activator and its inadequate decline after desmopressin infusion (DDAVP). In a group of 29 patients, who had suffered a myocardial infarction when young, the authors revealed a significant association between reduced fibrinolytic capacity and elevated body weight, hypertriglyceridaemia and increased immunoreactive insulin secretion after a glucose load. In half the investigated subjects it proved possible to improve the reduced fibrinolytic capacity by a low energy diet.
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PMID:[Disorders of fibrinolysis and thrombophilic states, risk factors and possibilities of dietary effects]. 205 93

4 kinds of progestin only oral contraceptives (OCs) and numerous combined OCs containing ethinyl estradiol (EE) or occasionally mestranol and either norgestrel or norethindrone are currently available in Australia. All progestins except norgestrel are effective in vivo after metabolism to norethindrone. Mestranol is effective in the human after demethylation to EE. The main side effects of OCs, including menstrual disturbances and changes in weight and mood, are primarily of nuisance value. Menstrual blood loss with OCs is almost invariably less than during spontaneous menses, but breakthrough bleeding and midcycle spotting may cause concern in patients. Amenorrhea and weight gain are rare with low dose pills. Approximately 6 in 1000 women remain anovulatory for 12 months or more after discontinuing OCs, but it is not yet know whether the amenorrhea is related to pill use and it is usually corrected by induction of ovulation. Cardiovascular side effects including venous thrombosis and pulmonary embolism are seen less frequently with new lower dose pills. The effects of OCs on the cardiovascular system are complex and depend on the interaction of estrogen and progestin. Amounts of estrogen and progestin should be the lowest possible to prevent ovulation, and routine monitoring should be provided for all women using pills. Older high dose formulations altered lipid metabolism in the direction of greater risk of coronary heart disease. Although research suggests the lowest dose triphasic pills have no significant effect, not enough large studies have been done with matched controls. Any effects on carbohydrate metabolism of the low dose pills are apparently minor and of little clinical significance. Insulin dependent diabetics with adequate supervision may safely use low dose pills. Combined OCs reduce the incidence of endometrial and ovarian malignancy. No relationship between OCs and the risk of breast cancer has been demonstrated except possibly in women under 35 when the cancer developed. The risk of intraepithelial neoplasia may be increased in women taking OCs for more than 8 years. Data on drug interactions are inconclusive, but women on rifampicin should use some other method. Absolute contraindications to OCs include breast cancer, history of deep venous thrombosis or pulmonary embolism, active liver disease, use of rifampicin, familial hyperlipidemia, previous arterial thrombosis, and pregnancy, while relative contraindications include smoking, age over 35, hypertension, breastfeeding, and irregular spontaneous menstruation. Progestin only OCs have a higher rate of failure and irregular bleeding than combined pills and their main use is for breastfeeding women and those with contraindications to estrogen. The pill of 1st choice should be a triphasic low-dose formulation.
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PMID:Oral contraceptives. 650 52

The amino-terminal domain of fibronectin has a fibrin binding site and a site for covalent cross-linking to fibrin. This fibrin binding domain was isolated from human recombinant fibronectin and labeled with In-111; the final molecular weight was 12 kD. It was applied to a pilot study of 62 patients; 30 who were thought to have deep vein thrombosis and 32 controls. All 30 patients had either impedance plethysmography, duplex ultrasound, contrast venography, or various combinations of the three. Eight disagreements in the 30 patients suspected of having deep vein thrombosis were registered between fibrin binding domain imaging and the other examinations. Three of the patients with negative scan results had clots that were 1 week old or older, and this may be a limitation of the technique. In three other patients who had negative scan results, but positive alternative studies, there was a history of previous episodes of deep vein thrombosis and this could be a cause of false-positive results in the other modalities. There was one documented false-negative scan in a fresh clot. Normal scans were obtained in the lower extremities of the control patients, except in two who demonstrated uptake at the sites of insulin injections. The initial results of this feasibility study are encouraging and warrant further investigation.
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PMID:A new thrombus imaging agent. Human recombinant fibrin binding domain labeled with In-111. 762 40

Plasminogen activator inhibitor-1 plays a major role in the fibrinolytic system as the main physiological inhibitor of both tissue-type and urinary-type plasminogen activators. The inhibitor is present in plasma in small amounts and derives mainly from endothelial cells. Positive correlations have been reported between plasma levels and different parameters, such as serum triglycerides, insulin plasma levels and body mass index. Moreover, high plasma inhibitor concentrations have been observed in different disease states, but it must be stressed that plasminogen activator inhibitor-1 behaves as an acute-phase reactant and measurement of plasma levels is not significant in the acute phase of the disease. A possible predictive value of inhibitor levels for thrombotic events such as deep vein thrombosis and ischemic heart disease has been studied. On the basis of available studies, the predictive value is not clear for venous thrombosis, whereas plasminogen activator inhibitor-1 levels can predict some coronary events, at least in subgroups of young patients with a first myocardial infarction. It remains to be established if treatments able to reduce plasma inhibitor levels lead to a decrease in the risk of thromboembolic events.
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PMID:Predictive value for thrombotic disease of plasminogen activator inhibitor-1 plasma levels. 851 17

Observational studies suggest that hormone replacement therapy (HRT) reduces the risk of coronary artery disease by approximately 50%. This review focuses on possible mechanisms for this reduction in disease risk. HRT reverses many of the lipid and lipoprotein change associated with menopause, and the route of hormone delivery influences these changes. Oral HRT improves serum markers of clotting, although it may increase the risk of deep vein thrombosis. Endothelial function, particularly endothelium-dependent vasodilation, improves with estrogen. Central body fat appears to be reduced with oral HRT, possibly reducing the risk of coronary artery disease. Insulin sensitivity, which worsens after menopause, may be improved with HRT. Global systolic function, as measured by ejection fraction, may improve with oral HRT. Understanding how HRT regimens influence cardiovascular risk may allow physicians to make intelligent choices about HRT for particular patients.
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PMID:Hormone replacement therapy: cardiovascular benefits for aging women. 989 22

(1) The precise cardiovascular risk of oral contraceptives is poorly known because of a lack of reliable clinical studies and the numerous potential biases in epidemiological studies. (2) The absolute risk of coronary events is very low in women under 35 who are non smokers, have no history of coronary heart disease and have normal blood pressure. In women over 35, smoking over 10 cigarettes a day and arterial hypertension substantially increase the risk of coronary heart disease. (3) The absolute risk of stroke is low in young women who are not hypertensive and do not smoke. It is higher in the case of arterial hypertension. (4) The absolute risk of deep vein thrombosis is increased but remains moderate. Obesity, a family history of deep vein thrombosis, and hereditary clotting disorders are risk factors. (5) The cardiovascular risks linked to oral contraception seem to disappear after cessation. (6) The use of oral contraceptives with very low doses of oestrogen (less than 50 mug ethinylestradiol) reduces the associated risk of stroke. The risk of deep vein thrombosis is probably higher with combined contraceptives containing a third-generation progestagen (desogestrel or gestoden). (7) The coronary and cerebrovascular risks of progestagen-only contraceptives are poorly documented. Low-dose progestagen-only oral contraceptives have little effect on clotting factors or on carbohydrate and lipid metabolism. There may be a risk of deep vein thrombosis, however, with this type of contraceptive. (8) History, physical examination and simple laboratory tests before prescribing or renewing oral contraceptives are sufficient to detect the main contraindications, i.e. arterial hypertension, a history of coronary or cerebrovascular conditions, deep vein thrombosis, hypercholesterolaemia exceeding 3 g/l, hypertriglyceridaemia exceeding 3 g/l, unusually severe headache on a combined oral contraceptive and prolonged immobilisation. However, a combined oral contraceptive can be considered for some women with cardiovascular risk factors such as moderate hypercholesterolaemia or hypertriglyceridaemia, well-controlled insulin-dependent diabetes, uncomplicated cardiac valve disease, migraine not worsened by a combined oral contraceptive, varicose veins or a family history of deep vein thrombosis. (9) Pharmacists should be aware of these risk factors so that they can advise patients to see a doctor if new health problems arise between visits.
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PMID:Cardiovascular risk of oral contraceptives. Low, and mainly in women at risk. 1034 51

In the final step of the clotting cascade coagulation factor XIII (FXIII) is activated by thrombin. The activated enzyme (FXIIIa) has an important role in the final stage of blood coagulation in cross-linking soluble fibrin to a stable insoluble clot. The role of FXIII in cardio- and cerebrovascular diseases has been investigated recently. The widespread Val34Leu polymorphism in the gene coding for the FXIII subunit A (FXIII Val34Leu) has been shown to protect against myocardial infarction and ischemic stroke, but is also associated with an increased risk for hemorrhagic stroke. Additionally, FXIII Val34Leu is supposed to be protective against pulmonary embolism and deep vein thrombosis. As possible mechanisms for the antithrombotic effect, premature depletion of the mutant protein from circulation and altered fibrin structures of clots cross-linked by the mutant FXIIIa are under discussion. The connection between FXIII and the insulin resistance syndrome also attracts attention, i.e. the interaction between a component of the coagulation cascade and thus a thrombotic risk factor and classical atheromatous risk factors. Therefore, FXIII must be considered as another coagulation factor contributing to complex interactions between genes and environment important for the pathogenesis of cardio- and cerebrovascular and thromboembolic diseases.
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PMID:[Role of coagulation factor XIII in cardio- and cerebrovascular diseases]. 1219 86

An abrupt onset of a neurological deficit is a rare occurrence in patients with cystic fibrosis (CF). As many CF patients have indwelling intravenous catheters, one of the complications may be deep venous thrombosis. Cerebral thromboembolism through an intracardiac shunt should be considered in CF patients who develop unexplained acute neurological deficits. We report on the case of a 19-year-old CF patient with insulin-dependent diabetes mellitus who was on oral contraceptives and had a Port-A-Cath(R) in place. The patient developed an acute neurological deficit after pulmonary function testing. Radiologic investigations of her head and neck were unremarkable, except for bilateral maxillary and ethmoid sinusitis. An electroencephalogram showed epileptiform discharges primarily from the right hemisphere. A transthoracic echocardiogram (TTE) revealed a small thrombus in the right atrium. A transesophageal echocardiogram (TEE) demonstrated a left-to-right shunt through a patent foramen ovale (PFO) that was not found by TTE. Extensive investigation to rule out congenital and acquired thrombophilia was negative. Treatment consisted of aspirin and discontinuation of oral contraceptives and vitamin K supplementation. Spontaneous complete recovery of the neurological deficits occurred within 24 hr after onset of symptoms.We conclude that paradoxical embolism should be in the differential diagnoses of CF patients who have indwelling intravenous catheters and who develop an unexplained stroke. An extensive investigation to rule out intracardiac abnormalities and thrombophilia should be considered. The risks and benefits of PFO closure vs. prophylactic anticoagulant and antiplatelet aggregation treatment in this group of patients should be carefully weighed.
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PMID:Acute neurological deficits in a young adult with cystic fibrosis. 1252 78

Sepsis and septic shock are the leading causes of death in non-cardiological intensive care units in developed countries despite recent advances in critical care medicine. Sepsis is the systemic inflammatory response to infection, often associated with hypoperfusion followed by tissue injury and organ failure. Activation of monocytes/macrophages and neutrophils with consecutive release of proinflammatory mediators and activation of the coagulation cascade, seem to play a key role in the pathogenesis of sepsis. Elimination of the septic focus,antimicrobial therapy and supportive treatment are the cornerstones of sepsis therapy. Adequate and rapid volume replacement and if necessary application of catecholamines are of highest priority to optimize tissue perfusion. Norepinephrine is the vasopressor of choice and dobutamine the preferred inotropic agent. Most experts recommend hemoglobin levels of 8-10 g/dl in severe sepsis. In addition,lung protective ventilatory strategies as well as enteral and parenteral nutrition are part of the clinical management of septic patients. In mechanically ventilated patients intensive insulin therapy to maintain blood glucose at a level between 80 and 110 mg/dl has significantly reduced mortality.Furthermore,prophylaxis of deep vein thrombosis and of stress ulcer bleeding are individually applied to septic patients. Treatment of septic patients with anti-mediator strategies or high dose AT III were not successful so far. In contrast,now two new promising treatment options may be emerging: application of small doses hydrocortisone and activated protein C [drotrecogin alfa (activated)]. Large and in part multicentric studies especially in the last 2 years now allow the practicing clinician to perform a partially evidence-based management of patients with sepsis. In addition, for the first time two options for specific therapy of sepsis,application of small doses hydrocortisone and activated protein C [drotrecogin alfa (activated)],are available which may further improve prognosis for septic patients.
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PMID:[Clinical management of patients with sepsis]. 1257 61

The pharmacotherapy of burn care has evolved from the first topical antibiotics instituted > 30 years ago. These have helped greatly to reduce the incidence of burn wound sepsis, but a better understanding of the principles of burn care has resulted in earlier burn wound excision and complete coverage with autograft, cadaver skin, synthetic dressings, and amnion. This has markedly reduced septic complications and ameliorated the hypermetabolic response to burn injury. The hypermetabolic response, which is mediated by hugely increased levels of circulating catecholamines, prostaglandins, glucagon and cortisol, causes profound skeletal muscle catabolism, immune deficiency, peripheral lipolysis, reduced bone mineralisation, reduced linear growth, and increased energy expenditure. Supportive therapy and pharmacological manipulation, acutely and during rehabilitation, with growth hormone, insulin and related proteins, oxandrolone and propranolol can ameliorate the hypermetabolic response, improving survival and long-term outcome. Despite judicious use of topical and systemic antibiotics, opportunistic nosocomial bacterial resistance threatens to annul the improved survival of patients with severe burns. Patterns of emerging resistance encountered in burn units need to be considered, in light of a decreasing antibiotic armamentarium. A holistic approach to pharmacotherapy of severely burned patients including current practice in antimicrobial control, analgesia, sedation, and anxiety management is required. Current therapy of frequently encountered problems, such as post-burn pruritus, prophylaxis of deep venous thrombosis and peptic ulceration, and pharmacological manipulation of inhalation injury in the burned patient is described. Current pharmacotherapy to ameliorate psychosocial problems associated with burns such as acute stress disorder, depression and post traumatic stress disorder are discussed. Better analgesics, newer antibiotics and immune stimulating drugs are required to reduce mortality and morbidity in large burns.
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PMID:Current pharmacotherapy for the treatment of severe burns. 1261 89


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