Diagnostic value of hemostasis activation markers in acute deep vein thrombosis

The aim of the following study was to evaluate the diagnostic value of selective hemostasis activation markers, prothrombin activation fragment 1 + 2 (F1 + 2), thrombin-antithrombin complex (TAT), plasmin-alpha 2-antiplasmin complex (PAP) and D-dimer in patients with acute deep venous thrombosis (DVT). The study was performed on 56 patients with freshly diagnosed acute DVT confirmed by venography. The study indicated that patients with acute venous thrombosis have increased concentrations of F1 + 2, TAT complex, PAP complex and D-dimer in blood plasma. The statistical analysis showed that F1 + 2 is the most sensitive test while the D-dimer measurement proved to be the most specific in diagnosing DVT. The conducted logistic regression showed that the most reliable parameter that confirms the existence of acute venous thrombosis is the D-dimer test. The measurement of both F1 + 2 and the D-dimer concentrations rises the reliability of the DVT up to 97%.     

Heart failure in patients with deep vein thrombosis

Patients with heart failure (HF) are particularly vulnerable to the development of venous thromboembolism (VTE) and its related complications of pulmonary embolism and right ventricular failure. To improve our understanding of the clinical characteristics, prophylaxis, and initial management of patients with HF and deep vein thrombosis (DVT), we compared 685 patients with a history of HF with 3,890 patients without HF in a prospective registry of 5,451 consecutive patients with ultrasound-confirmed DVT. We excluded 876 patients for whom data regarding HF status were incomplete. Patients with HF had an increased frequency of co-morbid conditions such as neurologic disease including stroke (33% vs 26%, p = 0.0002), acute lung disease including pneumonia (31% vs 15%, p <0.0001), and acute coronary syndrome (11% vs 4%, p <0.0001) contributing to a higher medical acuity than in patients without HF. Furthermore, patients with HF were more likely to have VTE risk factors of immobilization (53% vs 42%, p <0.0001), acute infection (33% vs 27%, p = 0.01), and chronic obstructive pulmonary disease (29% vs 12%, p <0.0001). Patients with and without HF and DVT had a high frequency of recent hospitalization (48% vs 47%, p = 0.96). Fewer than 12 of patients with HF (46%) who subsequently developed DVT received any VTE prophylaxis. In conclusion, the combination of higher medical acuity, increased frequency of VTE risk factors, and low rate of VTE prophylaxis presents a "triple threat" to patients with HF.     

Postoperative deep vein thrombosis in patients with colorectal cancer

Deep vein thrombosis (DVT) is reported to be common among patients undergoing surgery for colorectal cancer. This randomized controlled trial was aimed to determine the efficacy of low molecular-weight heparin in the prophylaxis of DVT in this high-risk group and was truncated early in view of an unexpectedly low incidence of DVT. Between March 2002 and January 2004, a total of 99 patients with colorectal cancer - selected for surgery in the lithotomy position - were randomized before surgery to either receive dalteparin or no drug (51 and 48 patients, respectively) during the perioperative period. Duplex ultrasonography was performed before and after the surgery. We also looked for distal venous thrombosis, pulmonary embolism, hemorrhage and any mortality. No episode of DVT occurred in either the drug arm or the observation arm. There was no death following surgery. The incidence of DVT in Indian patients operated for colorectal cancer in the lithotomy position was negligible.     

Prevention of deep vein thrombosis in cancer patients

Venous thromboembolism (VTE) in patients with cancer follows an aggressive course, and it is often resistant to traditional regimens of pharmacological prophylaxis and treatment. Anticoagulant-related bleeding is also common and can complicate VTE treatment as well as cancer therapy. Consequently, the most effective approach to reducing the burden of VTE and its associated morbidity and mortality is to provide appropriate prophylaxis. Few clinical trials have focused on the prevention of VTE in this high-risk patient population, and they consistently demonstrate the efficacy and safety of anticoagulant prophylaxis in reducing thrombotic complications. Currently, low-molecular-weight heparins and oral vitamin K antagonists are the most commonly used anticoagulants for primary prevention in patients with cancer, but compliance with consensus guidelines is poor. Novel anticoagulants with a convenient and favorable risk/benefit profile may help to improve prophylaxis utilization and treatment. This review will provide a summary of the evidence on the primary prevention of VTE in patients with cancer.     

Suspected acute deep vein thrombosis in patients with rheumatoid arthritis

Real-time venous ultrasound has replaced phlebography for making the diagnosis of clinically relevant lower extremity DVT. Phlebography is still useful in suspected calf vein thrombosis when an immediate diagnosis is required and in the postoperative patient. A combination of sonography and contrast phlebography is used to sort out the extent of chronic and acute venous changes in patients with chronic deep vein thrombosis.     

Ambulatory care for ambulant patients with deep vein thrombosis

A follow-up study is reported on 49 patients with acute deep vein thrombosis (DVT) treated on an ambulatory basis. Venography had shown crural DVT in 27 % and proximal extension in 73 %. The initial treatment consisted of heparin (7,500 U iv, 40,000 U sc), ethylbiscoumacetate (900 mg), phenprocoumon (9 mg), and a ready made compression stocking for the calf. The patients were advised to undertake frequent strolls, the first when leaving the office. Pain, swelling and incapacity for walking vanished within two days. The partial thromboplastintime was prolonged 2.4-times on the first day and the thromboplastintime was in the therapeutic range on the second day already. Until follow-up 4 patients died of other diseases. There was no clinical pulmonary embolism, no secondary hospitalisation and only one new DVT. Of 844 months of patients at risk of recurrence 50 % passed under anticoagulants and 70 % with compression therapy. At an average of 19 months, 82 % of patients were asymptomatic and 45 % showed mild chronic venous insufficiency. In contrast, impaired drainage function (by lightreflectionrheography) was found in 79 % overall and in 100 % after DVT of the proximal veins. The discrepancy is explained by the compliance with compression therapy.     

Inherited coagulation disorders in cirrhotic patients with portal vein thrombosis

The prevalence and pathogenesis of portal vein thrombosis (PVT) in patients with cirrhosis without hepatocellular carcinoma are not clearly defined. The role of thrombophilic genetic factors is well established in other venous thrombotic diseases, as well as in noncirrhotic portal thrombosis. Recently, new, inherited thrombophilic disorders (factor V Leiden [FVL], mutation G20210A of prothrombin [PTHR A(20210)], and mutation TT677 of methylenetetrahydrofolate reductase [MTHFR C677-->T]) have been identified and associated with increased risk of venous thrombosis. The aim of our study was to investigate the role of these thrombophilic disorders in the pathogenesis of PVT in cirrhotic patients. Twenty-three cirrhotic patients with PVT and 40 cirrhotics without PVT were included. A group of 184 patients with deep vein thrombosis (DVT) and 431 healthy persons served as controls. The FVL, PTHR A(20210), and MTHFR C(677)-->T genotypes were identified by a polymerase chain reaction and restriction analysis. The frequencies of FVL, PTHR A(20210) mutation, and homozygous MTHFR C(677)-->T were 13%, 34.8%, and 43.5% in cirrhotic patients with PVT and 7.5%, 2.5%, and 5% in cirrhotic patients without PVT, respectively. Five patients in the former group had associated defects. A thrombophilic genotype was detected in 69.5% of the patients with PVT. Identification of this high-risk group may have implications in patients who are candidates for major surgery or liver transplantation, and may influence the duration of oral anticoagulation.     

Pharmacogenetics of the local thrombolysis in patients with deep vein thrombosis

Thrombophilia, the state of increased tendency for blood clotting, is considered the disorder of a complex etiology, caused by both environmental and genetic factors. As gene variants predisposing to thrombophilia and influencing the increased risk of vein thrombosis might influence response to local thrombolysis, the aim of the work was to characterize the pharmacogenetic conditions for local streptokinase treatment in patients with a deep vein thrombosis (DVT) of lower extremities based on the following polymorphism analyses: G1691A polymorphism of factor V (FV), G20210A polymorphism of prothrombin (PT), A4250G (Thr312Ala) polymorphism of fibrinogen-alpha (FGA), G(-455)A polymorphism of fibrinogen-beta (FGB), 4G/5G polymorphism of plasminogen activator inhibitor type 1(PAI-1) and insertion/deletion (I/D) polymorphism of tissue plasminogen activator (t-PA). The study included 40 DVT patients who underwent a local thrombolytic treatment within 14-day period from diagnosis. Full recanalization was achieved in 20 subjects (50%) [group R(+)], whereas incomplete or total lack of recanalization was identified in the remaining 20 patients [group R(-)]. No major complications of thrombolytic treatment occurred in the studied group. In the case of prothrombin gene all individuals carried homozygous wild type genotype (GG). Prevalence of the genotypes and alleles of the remaining five polymorphisms did not differ significantly between the groups R(+) and R(-). Neither sex nor age, smoking or time period from diagnosis to introduction of the thrombolytic treatment significantly influenced treatment efficacy. The results of the study suggest that a local thrombolysis with streptokinase introduced within two week period from the diagnosis is a safe and efficient method of treatment for deep vein thrombosis of lower extremities. However, size of the group is insufficient to clearly determine the association between investigated polymorphisms and efficacy of local treatment with streptokinase.     

High prevalence of anti-prothrombin antibody in patients with deep vein thrombosis

The present study was designed to determine the prevalence of lupus anticoagulant (LA) antibody and several antibodies for antiphospholipid syndrome (APS) in patients with deep vein thrombosis (DVT)/pulmonary embolism (PE) (n = 48), cerebral thrombosis (CT, n = 30), systemic lupus erythematosus (SLE, n = 22), and idiopathic thrombocytopenic purpura (ITP, n = 30). The presence of antibodies was examined by using the respective ELISA kits. LA was positive in 38.6% of patients with DVT/PE, suggesting that LA is one of the most important risk factors in DVT/PE. The highest prevalence of anti-beta(2) glycoprotein I (beta(2)GPI) IgG was in CT and SLE, followed by DVT, and none in ITP and healthy volunteers (control, n = 40), suggesting that it is related to thrombosis, particularly arterial thrombosis. The highest prevalence of anti-prothrombin (aPT) IgG antibody was in DVT, followed by CT and SLE, and none in ITP and the control, suggesting that it is related to thrombosis, especially venous thrombosis. The highest prevalence of antiphospholipid (aPL) IgG was in DVT, CT, and SLE, but 0% in ITP and control. On the other hand, aPL IgM, anti-annexin V IgG, and anti-annexin V IgM were positive in patients both with and without thrombosis, suggesting that they are not related to thrombosis. Our results indicated that among the anti-phospholipid antibodies, LA is the most sensitive marker for APS while anti-beta(2)GPI IgG, aPT IgG, and aPL IgG are risk factors for thrombosis. In particular, aPT IgG is a significant marker for DVT/PE.     

Noninvasive diagnosis of deep vein thrombosis in postoperative patients

The accuracy of noninvasive testing for the diagnosis of deep vein thrombosis (DVT) generally is less in asymptomatic patients than it is in those with symptoms suggestive of thrombosis. This is because asymptomatic DVT often is confined to the distal veins and, when it involves the proximal veins, the thrombi usually are smaller than in symptomatic patients with proximal thrombosis. Because the positive predictive value of noninvasive tests for asymptomatic DVT generally is 80% or less, abnormal results should be confirmed by venography. There are two main reasons why asymptomatic DVT is sought in the postoperative period: (1) to identify the need for full-dose anticoagulant therapy to prevent symptomatic episodes of venous thromboembolism (VTE), including fatal pulmonary embolism (this represents a form of secondary prophylaxis), and (2) to use this outcome as a surrogate for episodes of clinically important VTE in studies that are designed to evaluate methods of venous thrombosis prophylaxis. In relation to the first of these indications, evidence suggests that routine surveillance of high-risk patients to detect asymptomatic postoperative DVT does not result in improved clinical outcomes in patients who received appropriate VTE prophylaxis. In relation to the second indication, there is concern that asymptomatic VTE may not be a reliable surrogate for clinically important VTE, particularly if the effectiveness of different antithrombotic agents is being compared. Coupled with the comparatively low accuracy of noninvasive testing for asymptomatic DVT, this suggests that the results of such testing are unsuitable for the evaluation of new methods of prophylaxis in clinical trials.     

Plasma and urine beta-thromboglobulin concentration in patients with deep vein thrombosis

Plasma and urine beta-thromboglobulin (BTG) were measured in 52 patients with established deep vein thrombosis (DVT) and in 100 patients with clinically suspected DVT but with a negative venogram. Both plasma BTG (geometric mean 54: 95% range 12--239 ng/ml) and urine BTG (0.25; 0.03--3.1 ng/ml) were significantly elevated (p less than 0.005) in patients with DVT compared to symptomatic patients with a negative venogram (plasma BTG 32, 9--112 ng/ml; urine BTG 0.12, 0.02-- 0.58 ng/ml). Sensitivity (35%) and specificity (80%) of the plasma BTG assay for the diagnosis of DVT were low. The urine BTG assay had a sensitivity of 37% but a specificity of 100%. There was a significant correlation between plasma and urine BTG (r = 0.68, p less than 0.005). Serial BTG measurements were made in urine (40 patients) and plasma (20 patients) from high-risk neurosurgical cases who were screened with 125I-fibrinogen leg scanning and impedance plethysmography. BTG was elevated postoperatively and returned to normal within 2 or 3 days, but rose again in 10 patients in association with the development of DVT. The rise of BTG preceded the uptake of 125I-fibrinogen and lasted for only a few days. The return to normal of BTG was not related to treatment with anticoagulants. While measurement of BTG in plasma and urine is of limited value in the clinical diagnosis of venous thrombosis, the data indicate platelet activation occurs in venous thrombosis, but is maximal or perhaps limited to the initial phase of thrombus development.     

Ruling out deep vein thrombosis in patients with superficial vein thrombosis: external validation of the ICARO score

Journal of Thrombosis and Thrombolysis - A clinical score was recently proposed to rule out concomitant DVT in patients with a clinical suspicion of SVT. This study aimed to assess the external...     

Distal deep vein thrombosis

Received from the Section of General Internal Medicine, University of Wisconsin Medical Center, 600 Highland Avenue, Madison, Wisconsin 53792.     

下肢深静脉血栓形成患者血小板活化状态的变化及意义

为探讨下肢深静脉血栓形成(DVT)思考血小板活化状态的变化及其临床意义，用流式细跑术(PCM)，以单克隆抗体为探针，对35例下肢DVT患者(DVT组)及3l例健康人(对照组)血小板活化标记物溶酶体颗粒糖蛋白(CD63)、血小板表面选择素(CD62p)及凝血酶敏感蛋白(TSD)进行了检测。结果显示，DVT组3种血小板活化标志物阳性表达率均高于对照组(P均＜0．001)，溶栓治疗后3种血小板活化标志物的阳性表达率均呈降低趋势。提示DVT患者体内血小板活化亢进；FCM可作为活化血小板的良好检测手段。