Portal thrombosis: Percutaneous transhepatic treatment with urokinase — A case report

We present a case report of a patient suffering from portal and superior mesenteric vein thrombosis secondary to splenectomy. No surgical procedure could be performed due to the extension of thrombus.Local fibrinolysis treatment with urokinase through a percutaneous transhepatic approach was decided upon, and this procedure had a successful patient outcome.     

Inhibition and reversal of platelet-rich arterial thrombus in vivo: direct vs. indirect factor Xa inhibition

BACKGROUND/OBJECTIVE: The efficacy of a direct factor (F)Xa inhibitor, ZK-807834, was compared with indirect inhibition by enoxaparin for inhibition and deaggregation of acute platelet-rich thrombi in a well-characterized porcine carotid injury model. METHODS: A crush injury was performed on a randomly chosen carotid artery and the thrombus allowed to propagate for 30 min. Pigs then received intravenous drug for 35 min: ZK-807834-Dose 1 (40 microg kg(-1) bolus + 1.5 microg kg(-1) min(-1) infusion, n=6); ZK-807834-Dose 2 (20 microg kg(-1) bolus + 0.75 microg kg(-1) min(-1) infusion; n=6); enoxaparin (1 mg kg(-1) bolus; n=6); or saline (n=6). Five minutes after drug initiation, the contralateral artery was injured. Thrombus size was monitored by scintillation detection of autologous 111In-platelets. RESULTS: The prothrombin time ratio was 2.2 +/- 0.1; 1.4 +/- 0.3; 1.2 +/- 0.9 and 1.1 +/- 0.2, respectively. ZK-807834-Dose 1 significantly inhibited carotid platelet deposition (525 +/- 226 x 10(6) cm(-2); P = 0.008), whereas ZK-807834-Dose 2 (2325 +/- 768) and enoxaparin (1236 +/- 383) were not different from saline (2776 +/- 642). Thrombus deaggregation was greatest for animals receiving ZK-807834-Dose 1 (473 +/- 185). Neither ZK-807834-Dose 2 (1588 +/- 480) nor enoxaparin (1618 +/- 686) was different from saline control (2222 +/- 598). CONCLUSIONS: Direct FXa inhibition with ZK-807834, at a prothrombin time ratio of 2.2, effectively inhibits thrombosis and promptly deaggregates thrombi induced by arterial injury. In contrast, indirect FXa inhibition with enoxaparin was ineffective.     

Interobserver Agreement for the Diagnosis of Venous Thromboembolism on Computed Tomography Chest Angiography and Indirect Venography of the Lower Extremities in Emergency Department Patients

Objectives: To determine interobserver agreement between radiologists for computed tomography (CT) angiography and venography. CT venography of the lower extremities combined with standard CT angiography of the chest may result in an increased overall diagnosis rate of venous thromboembolism (pulmonary embolism or deep venous thrombosis).
Methods: The study had a retrospective cohort design. The population consisted of emergency department patients who were evaluated for suspected pulmonary embolism. A random sample of 50 patients diagnosed and treated for venous thromboembolism and 50 age- and gender-matched patients whose CT angiograms and venograms were read as negative were enrolled. The original reading (R1) was compared with readings of two study radiologists: R2, a general radiologist, and R3, a radiologist with fellowship training in cross-sectional imaging. All readers were blinded to each other.
Results: Both R2 and R3 found both CT angiogram and venogram components technically adequate in 95% (95% CI = 89% to 98%) and 86% (95% CI = 78% to 92%) of studies, respectively. The agreement was very good for CT angiography (lowest agreement = 92%; lowest κ = 0.83) and was good for CT venography (85%, κ = 0.65). In nine cases, R1 read the CT angiogram as negative but the venogram as positive for DVT, whereas both R2 and R3 read both components as negative in four of these nine, suggesting a false-positive isolated DVT rate of 44% (95% CI = 19% to 73%). In no case did R1 read both scan components as negative when R2 and R3 agreed on presence of pulmonary embolism or DVT.
Conclusions: Diagnosis of pulmonary embolism on CT angiography is more reliable than diagnosis of isolated DVT on CT venography.     

在深静脉血栓—肺栓塞病程中腔静脉滤器的应用价值分析

目的：探讨腔静脉滤器(Vena cava filter VCF)在深静脉血栓(Deep venous thrombosis DVT)—肺栓塞(Pulmonary embolism PE)病程中的应用价值。方法：结合本组25例高危深静脉血栓一肺栓塞患者，对其中24例置放5种构型的永久型或临时型下腔静脉滤器(IVCF)26枚的临床疗效、影响病程与预后因素及病生理改变，复习文献分析讨论。结果：DVT有可能脱落导致PE或致死性肺栓塞；置放IVCF可有效预防肺栓塞，早期进行溶栓治疗，改变预后。结论：严格按适应证植入IVCF，对DVT—PE的早期治疗和预防致死性肺栓塞有重要意义，但其应用价值需进行综合评价和进一步探讨。     

完全性肺静脉异位引流的手术治疗经验

为评估影响完全性肺静脉异位引流（ＴＡＰＶＤ）手术纠治的因素，本组纳入了２８例在中度低温体外循环和１５例在深低温停循环下手术纠治者。结果手术死亡４例，死亡率９．３％。随访３２例，２例肺静脉回流梗阻分别于术后５个月和２年３个月死亡。结论认为，ＴＡＰＶＤ必须早期手术防止肺血管阻塞性病变；术后定期随访；改进手术方法，防止心房内补片粘连所致肺静脉回流梗阻。     

Analysis thrombolysis with anticoagulation treatment for early stage of deep vein thrombosis in the lower extremities

Objective:To explore the effect of thrombolysis with anticoagulation treatment forearly stage of deep vein thrombosis of lower extremity.Methods:The clinical data of 10 patients at the early stage of deep vein thrombosis(DVT)in the lower extremuites treated by thrombolysis with anticoagulation and dispersion drugs were analyzed retrospectively.Results:The thrombolytic effect was significant.After treatment,the deep veins were recanalized without regurgitation in 75.3% of the patients.The total effective rate was 100%.Only three patients had hemorrhagic complication,but none of the patients died.Conclusion:Thrombolysis with anticoagulation treatment is an effective and safe method for DVT at the early stage.     

急性肠系膜静脉血栓形成16例临床分析

目的　分析急性肠系膜静脉血栓形成 (ASMVT)的临床特征和诊断方法。方法　对北京友谊医院 1985年 10月至 2 0 0 2年 10月确诊的 16例ASMVT的临床资料进行分析 ,并结合文献 ,总结ASMVT的临床特征和诊断方法。结果 16例ASMVT患者 ,年龄 19～ 6 4岁 (平均 4 5 9岁 )。主要症状有腹痛 ( 16 / 16 )、腹胀 ( 16 / 16 )、呕吐 ( 10 / 16 )、发热 ( 8/ 16 ) ,主要体征有腹部膨隆 ( 16 / 16 )、腹膜刺激征( 16 / 16 )。误诊率 75 % ( 12 / 16 ) ,死亡率 4 4 % ( 7/ 16 )。结论　ASMVT的临床表现有一定的特征 ,早期彩色超声检查、诊断性腹腔穿刺、结合CT或肠系膜上动脉造影异常发现可对ASMVT做出正确的诊断 ,早期手术可以降低死亡率     

Characterization of an immunologic polymorphism (D79H) in the heavy chain of factor V.

BACKGROUND: During the study of a family with hereditary factor (F)V deficiency (FV Amersfoort, 1102 A > T in exon 7) we identified an individual with 5% FV heavy chain antigen (FV(HC)) and 50% FV light chain antigen (FV(LC)). Further testing revealed that apart from the FV Amersfoort allele a second variant FV allele was segregating in this family, which encodes for a FV molecule with a reduced affinity for mAb V-23 used in the FV heavy chain ELISA (ELISA(HC)). OBJECTIVE: Identification and characterization of the molecular basis responsible for the reduced affinity of the variant FV for mAb V-23. METHODS: Family members of the proband were screened for mutations in the exons coding for the heavy chain of FV, after which the recombinant variant FV could be generated and characterized. Next, the cases and controls of the Leiden Thrombophilia Study (LETS) were genotyped for carriership of the variant FV. RESULTS: In the variant FV allele a polymorphism in exon 3 (409G > C) was identified, which predicts the replacement of aspartic acid 79 by histidin (D79H). Introduction of this mutation in recombinant FV confirmed that it reduces the affinity for binding to mAb V-23. The substitution has no effect on FV(a) stability and Xa-cofactor activity. In Caucasians the frequency of the FV-79H allele is approximately 5%. Analysis of the LETS revealed that the FV-79H allele is not associated with FV levels (FV(LC)), activated protein C sensitivity (using an activated partial thromboplastin time-based test) or risk of venous thrombosis (OR 1.07, CI 95: 0.7-1.7). CONCLUSION: The D79H substitution in FV should be considered as a neutral polymorphism. The monoclonal antibody V-23, which has a strongly reduced affinity for FV-79H, is not suitable for application in diagnostic tests.     

Von Willebrand factor, platelets and endothelial cell interactions

Summary.  The adhesive protein von Willebrand factor (VWF) contributes to platelet function by mediating the initiation and progression of thrombus formation at sites of vascular injury. In recent years there has been considerable progress in explaining the biological properties of VWF, including the structural and functional characteristics of specific domains. The mechanism of interaction between the VWF A1 domain and glycoprotein Ibα has been elucidated in detail, bringing us closer to understanding how this adhesive bond can oppose the fluid dynamic effects of rapidly flowing blood contributing to platelet adhesion and activation. Moreover, novel findings have been obtained on the link between regulation of VWF multimer size and microvascular thrombosis. This progress in basic research has provided critical information to define with greater precision the role of VWF in vascular biology and pathology, including its possible involvement in the onset of atherosclerosis and its acute thrombotic complications.     

Decreased Risk of Renal Allograft Thrombosis Associated With Interleukin-2 Receptor Antagonists: A Report of the NAPRTCS

Graft thrombosis is the most common cause of first year graft failure in pediatric renal transplantation. The North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) database was analyzed for cases of graft failure due to thrombosis among patients transplanted from 1998 to 2004. The impact of interleukin-2 (IL-2) receptor antagonists as induction therapy was determined. There were a total of 51 graft failures due to thrombosis among the 2750 reported renal transplants (1.85%) (95% CI (1.39%, 2.41%)). This represents the most common cause of graft loss during the first year post-transplant accounting for 35% of first year losses and 18% of all graft losses. The incidence of thrombosis among patients who received IL-2 receptor antibodies was 1.07% (12/1126) compared to 2.40% (39/1624) among patients who did not (OR 0.44, 95% CI 0.23, 0.84, p = 0.014). Use of IL-2 receptor blockade was the only significant prognostic factor in a multivariate model with previously identified risk factors. Analysis of NAPRTCS data found that the use of IL-2 receptor antibodies as induction therapy is associated with a significantly decreased risk of graft failure due to thrombosis. This provocative finding requires further investigation to determine whether thrombotic failure can be decreased by this therapeutic strategy.