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 diagnostic strategies and clinical characteristics of thrombophilia associated with heterozygous or homozygous factor V Leiden mutation have been determined according to the literature and to a personal study in 51 families. Factor V mutation was present in the 51 propositi and in 84 out of 125 family members (81 heterozygous, 3 homozygous). Venous thrombosis was observed in all the propositi, in 17 of the 84 family members with the mutation and in 6 of the 41 with a normal APC resistance test and no mutation. An associated protein C or protein S deficiency was present in 5 families (10%). The most frequent clinical manifestations were superficial or deep vein thrombosis and/or pulmonary embolism, but also thrombosis at an unusual site (cerebral, mesenteric or central retinal vein). A causal relationship is frequently difficult to demonstrate. A precipitating factor was observed in 84% of cases and a recurrent thrombotic episode occurred in 50% of propositi. The risk of thrombosis associated with pregnancy was high in the post-partum period, especially in homozygous women. In the 28 homozygous subjects, markers of coagulation activation were frequently elevated in untreated patients. Finally, the efficacy of anticoagulant treatment is suggested but the long period often observed between treatment interruption and a recurrence does not militate in favour of long term treatment.
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PMID:Diagnosis and clinical characteristics of inherited activated protein C resistance. 897 37

In the UK, the Committee for Safety of Medicines (CSM) issued a warning in October 1995 about the possible increased risk of nonfatal deep venous thrombosis (DVT) among users of oral contraceptives (OCs) containing the third generation progestogens, desogestrel and gestodene. Subsequent media coverage increased the number of consultations and enquiries about these OCs. CSM had concluded that, overall, the third generation OCs are safe. CSM recommended their continued use. Nevertheless, many women stopped using them and induced abortions increased by 11%. In April 1996, the Committee for Proprietary Medicinal Products issued a more cautious statement about the OCs and called for further evaluation. Chance, confounding, and bias may account for the increased risk observed in the studies in question. Yet, it is possible that these OCs may increase the risk of DVT. The increased risk may be offset by a reduced risk of acute myocardial infarction. Physicians need to conduct careful and thorough counseling and to allow the patient to be involved and to take responsibility in making a decision about OC use. They should document all counseling with a note that the patient understands and accepts the increased risk of DVT. They should not prescribe the third generation OCs to women with any of the absolute contraindications to OC use (ischemic heart disease, hypertension, atherogenic lipid disorders, focal or crescendo migraine, cigarette smoking, transient ischemic attacks, past cerebral/subarachnoid hemorrhage, history of vascular thrombosis, prothrombotic abnormalities [e.g., Factor V Leiden], conditions predisposing to thrombosis [e.g., systemic lupus erythematosus], and obesity. Women who are intolerant of second generation OCs may prefer third generation OCs. Physicians should selectively screen women with a family history of a first-degree relative younger than 45 with thromboembolism for Factor V Leiden. They should also screen for protein C, protein S, and antithrombin III deficiency and for acquired antiphospholipid antibodies.
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PMID:Oral contraceptives and the risk of DVT. 898 64

One hundred and thirty unrelated patients with recurrent deep venous thrombosis were studied over a period of 4 years (1986-1990) in order to determine the possible etiology. Protein C levels were estimated in plasma both by chromogenic substrate assay and by immunoassay. Protein S levels in plasma was determined by immunoassay using antisera to human protein S. Antithrombin III (AT-III) was assayed using monospecific rabbit antiserum to human AT-III. Fifteen patients were found to have hereditary protein C deficiency (11.52%). Family studies revealed autosomal recessive inheritance in one patient and a dominant pattern in the remaining 14 patients. Protein S deficiency was found in eight cases (6.1%), AT-III deficiency was established in five cases (3.8%) and a fibrinolytic defect in 33 cases (25.4%). Thrombosis of visceral and cerebral vessels and a positive family history were more frequently found among patients who had hereditary deficiency of one or the other antithrombotic factor. Thrombophlebitis of superficial veins was found to be very common in patients with protein C and protein S deficiency and virtually absent in AT-III deficiency. The high frequency of protein C and protein S deficiency in this ethnic group is attributed to the high frequency of consanguinity.
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PMID:Thrombophilia in ethnic Arabs in Kuwait. 900 58

The authors report a study on the hemostatic status of a group of patients with deep venous thrombosis in order to highlight the possible pathogenetic responsibility of blood coagulative disorders in the genesis of thrombosis. The group consisted of 27 patients (14 males, 13 females, mean age 48 +/- 4 years) with deep venous thrombosis of the lower limbs (clinical symptoms were primary in 21 cases, secondary in 6 cases) diagnosed on the basis of clinical data and ultrasonographic instrumental findings. Fourteen normal subjects were also examined as a control group (12 males, 2 females, mean age 28 +/- 5 years). Venous blood was collected on fasting from patients and controls to examine the following parameters: fibrinogen (F), factor VII (F VII), antithrombin III (AT III), protein C (PC), protein S (PS) using coagulometric methods (IL), and tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1), fibrinopeptide A (FPA), betathromboglobulin (BTG) and dimer-D (D-D) using ELISA methods (Boehringer). Patients with deep venous thrombosis showed a significant increase in F, FVII, tPA and D-D levels compared to controls, whereas a significant reduction was observed in PAI-1. Nonsignificant variations were found for AT III, PC, PS and BTG. In the light of these results the authors affirm that: high fibrinogen and factor VII levels are highly prognostic for thrombosis in patients with deep venous thrombosis; the importance of the lack of inhibitory factors (AT III, PC, PS) is confined to individual genetically predisposed cases; there is an efficacious hyperfibrinolytic reactive response to the presence of thrombus (increase in tPA and D-D, reduction of PAI-1).
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PMID:[Hemostatic status in subjects with deep venous thrombosis]. 905 19

Ovarian cancer cells appear to be capable of both thrombin formation and induction of fibrin degradation which may be essential prerequisites for the development of deep vein thrombosis (DVT) as well as the spread of malignancy. To study further this coagulation-cancer interaction in 60 patients with untreated ovarian cancer of FIGO stage I-IV the incidence of DVT was recorded pre-operatively, post-operatively on day 1, 3, 5, 7, 10, before each of six cycles of Cisplatinum/ Epirubicin/Cyclophosphamide chemotherapy, during follow-up and in the post-operative period of second look surgery. In addition, blood coagulation tests results were determined prospectively. Two patients were excluded from these calculations due to previous DVT 5 to 6 weeks before the diagnosis of ovarian cancer but all patients were eligible for surgery and randomized to receive either daily low molecular weight heparin (LMWH) (n = 28) or unfractionated heparin (UFH) (n = 32) for perioperative thrombosis prophylaxis until the 7th post-operative day. According to the FIGO stage, patients were equally distributed in the 2 heparin treatment groups. The predictive value of pre-operative coagulation test results, clinical parameters, and type of heparin used were tested in univariate and multivariate analysis for development of post-operative DVT and overall patients survival. Impedance plethysmography for DVT screening was used. The presence of DVT was then confirmed by phlebography. Only D-dimer and fibrinogen levels were correlated significantly with the FIGO stage while antithrombin, protein C, and plasminogen activator inhibitor activity were not. The incidence of DVT was 6.7% (4/60) up to the 7th and 8.3% (5/60) between the 8th and 29th post-operative day. DVT occurred in 10.6% (5/47) during chemotherapy. Pre-operative coagulation test results, the type of heparin used, and clinical parameters were not significant risk factors for post-operative DVT development in univariate analysis. The D-dimer and fibrinogen levels were significant risk factors for reduced overall survival in univariate analysis but only the FIGO stage was an independent predictor (in multivariate analysis). After a median follow up of 26.5 months (min. 8 months, max. 41 months), 21.4% of LMWH treated and 37.5% of UFH-treated patients died of cancer (p = 0.26). Pre-operative test results were neither predictive for DVT nor the outcome of cancer but patients showed an improved though not statistically significant overall survival after LMWH treatment.
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PMID:Blood coagulation and thrombosis in patients with ovarian malignancy. 906 93

Deep vein thrombosis (DVT) is a frequent event in patients with spinal cord injury, even with prophylactic anticoagulant therapy. Lower limb paralysis is a known major risk factor for venous thrombosis, supposedly due to the venostasis in relation with total immobility. The main goal of this study was to evaluate the endothelial response to anoxia to determine whether recovery of fibrinolytic potential occurs in patients subjected to forced bedrest because of a spinal cord injury and whether this recovery is related to the incidence and/or evolution of DVT. We evaluated vascular endothelium reactivity in the lower limbs no longer submitted to the hydrostatic pressure of the erected position in 15 patients with paraplegia or tetraplegia and in 10 normal volunteers after venous occlusion produced by the application of 10 cm Hg pressure to the lower limb for 15 min comparatively to the upper limb used as reference. Among the 15 patients, 10 whose spinal cord injury had occurred 1 to 6 months earlier were still receiving prophylactic anticoagulant therapy, whereas the five other patients were not receiving prophylactic anticoagulants because the injury dated back 6 months or more. After venostasis, tissue plasminogen activator (tPA) increased significantly in both patients and controls in the upper limb (tPA levels twofold and threefold respectively in controls and patients) but showed no significant changes in the lower limb; prolonged immobility did not allow recovery in the lower limbs of a level of fibrinolytic responsiveness identical to that in the upper limbs. The plasminogen activator inhibitor (PAI1) remained unchanged after anoxia, although wide interindividual variations were seen. Natural coagulation inhibitors and circulating blood stigmates of hypercoagulability were measured. None of the patients had abnormally low levels of coagulation inhibitors (ie, antithrombin III, protein C and protein S levels were normal). Seventy-five per cent of patients (prophylactically anticoagulated or not) had very high levels of fibrin degradation products (D. Dimer levels sevenfold to eightfold those of the controls), but all patients had normal levels of thrombin-antithrombin complexes and prothrombin fragments 1 + 2. The permanence of the thrombotic process characterized by an increase in D. Dimer levels without recovery of fibrinolytic potential suggests a proposal for the patients an indefinite antithrombotic treatment at curative doses.
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PMID:Endothelial fibrinolytic reactivity and the risk of deep venous thrombosis after spinal cord injury. 907 65

Thromboprophylaxis with oral anticoagulants up to six months is established in patients after a first venous thromboembolic event (VTE). The risk of recurrent VTE is still considerable thereafter, and it is uncertain whether some patients might benefit from extended anti-coagulation. We performed a prospective, multicenter trial (4 thrombosis centers) and evaluated in 380 patients with a first or recurrent VTE (patients with a deficiency of antithrombin, protein C, protein S or plasminogen; cancer; or an antiphospholipid antibody syndrome were excluded) the risk of recurrence after discontinuation of secondary thromboprophylaxis with oral anticoagulants. It was the aim of the study to evaluate whether patients, with factor V Leiden are at an increased risk of recurrent VTE. 112 (29.5%) patients were carriers of factor V Leiden (26.9% heterozygous, 2.6% homozygous). After a median observation time of 19.3 months the overall recurrence rate of VTE was 9.9%. Recurrent deep vein thrombosis and/or pulmonary embolism occurred in 26 of 268 patients without factor V Leiden (9.7%) and in 10 of 112 patients with factor V Leiden (8.9%). The probability of recurrent VTE two years after discontinuation of oral anticoagulants was 12.4% (95% CI 7.8-17) in patients without factor V Leiden and was 10.6% (95% CI 3.8-17.4) in carriers of the mutation. This difference was statistically not significant. Patients with factor V Leiden are not at a higher risk of recurrent VTE within two years after discontinuation of oral anticoagulants than patients without factor V Leiden. Balancing the risk of recurrent VTE and bleeding from oral anticoagulants, patients with factor V Leiden are not likely to benefit from oral anticoagulant therapy extended beyond six months.
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PMID:The risk of recurrent venous thromboembolism in patients with and without factor V Leiden. 913 32

We examined the incidence of thrombophilia in deep vein thrombosis (DVT). Of 38 cases, we found 4 cases of protein C abnormality, 2 cases each of protein S abnormality and lupus anticoagulant, 1 case of antithrombin III abnormality. The total incidence was 23.7%, whereas only 2 cases (6.2%) of plasminogen abnormality were found among 32 healthy individuals. The incidence of thrombophilia was apparently higher among patients with DVT than that of healthy subjects, although the incidence of Japanese DVT was lower than that of Caucasian DVT, as previously reported. By SSCP analysis in one case of protein C abnormality, we demonstrated an abnormality of exon 9-3. To establish laboratory diagnosis of thrombophilia, it is recommended that (1) severe liver diseases, DIC, and oral anticoagulant be ruled out, (2) abnormality be confirmed by repeated examination, (3) family study determine inheritance mode, if possible. It was strongly suggested that laboratory examination of thrombophilia should be routinely applied to cases of venous thrombosis including DVT, not only for diagnostic interest but also for appropriate treatment of these cases.
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PMID:[Laboratory diagnosis of congenital thrombophilia]. 913 96

While many studies have demonstrated the pathogenetic role of inherited deficiency of natural clotting inhibitors in patients in the development of deep vein thrombosis of lower limbs, no data are available on the prevalence of these abnormalities in patients with upper vein thrombosis. In this study, antithrombin III, protein C, protein S, plasminogen, resistance to activated protein C and factor V Leiden mutation were assayed in 27 consecutive patients with thrombosis of upper extremities. Only two patients (7.4%) showed a congenital defect (one patient with deficiency of protein C, confirmed by family study, and one patient with factor V Leiden mutation). Anticardiolipin antibodies were also measured and four patients (14.8%) had increased levels, confirmed on a subsequent occasion 3 months later. Eighteen out of 27 (67%) had a predisposing or triggering factor, thus emphasizing the role of physical stress in the development of upper vein thrombosis. At variance with what is observed in deep vein thrombosis of the lower limbs, inherited clotting abnormalities seem to be rarely responsible for upper vein thrombosis, whereas anticardiolipin antibodies and cancer are implicated in a significant proportion of cases.
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PMID:Low prevalence of thrombophilic coagulation defects in patients with deep vein thrombosis of the upper limbs. 916 20

Although venous thromboembolism is a rare complication of pregnancy, it is one of the leading causes of maternal mortality. As many as 40% of asymptomatic women with deep venous thrombosis may indeed have a pulmonary embolism. Therefore, pregnant women with thromboembolic disease, a history of thromboembolic disease, or those who are at increased risk of thromboembolism (mechanical cardiac valve prostheses, antithrombin II, or protein C or S deficient) should receive anticoagulant therapy. The choice of anticoagulant therapy in a pregnant woman as well as the dose and duration will depend on the specific condition being treated. Although anticoagulant therapy is beneficial, it is not without risks to both mother and fetus. This article discusses the use of anticoagulants and thrombolytics in pregnant women.
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PMID:Anticoagulants and thrombolytics during pregnancy. 920 21


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