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PubMed2006

Transjugular intrahepatic portosystemic shunt for portal vein thrombosis with and without cavernous transformation.

BACKGROUND: Treatment options for patients with portal vein thrombosis are limited. AIM: To evaluate the feasibility and efficacy of transjugular intrahepatic portosystemic shunt for portal vein thrombosis with/without cavernomatous transformation. METHODS: A survey of such patients, referred for transjugular intrahepatic portosystemic shunt between 1994 and 2005, was performed. Success rates, complications, transjugular intrahepatic portosystemic shunt patency and clinical progression were examined. RESULTS: Transjugular intrahepatic portosystemic shunt was attempted in 28 patients (13 cirrhotics). Indications were: presurgery/transplantation (2), worsening of ascites (2), variceal bleeding (15 - 8 elective), refractory ascites (3), portal biliopathy (3) and portal vein thrombosis complicating Budd-Chiari syndrome (2). Transjugular intrahepatic portosystemic shunt was placed successfully in 19 of 28 (73%); 23 of 28 had complete portal vein thrombosis and 9 of 23 had cavernous transformation and transjugular intrahepatic portosystemic shunt was successfully placed in six of these. In the 19 patients with transjugular intrahepatic portosystemic shunt, the mean follow-up was 18.1 months (range 5-70): six patients had stent revisions; three had liver transplantation, one died of bleeding. Most cirrhotic patients had an improvement in the Child-Pugh score. In the failed transjugular intrahepatic portosystemic shunt group, two of nine died, and three had further bleeding. CONCLUSIONS: Transjugular intrahepatic portosystemic shunt should be considered for selected patients with symptomatic complete portal vein thrombosis with/without cavernous transformation, as clinical improvement and less rebleeding occur when transjugular intrahepatic portosystemic shunt placement is successful.

Adolescent↗

PubMed1986

Lack of pathogenetic role of proteins C and S in thrombosis associated with asparaginase-prednisone-vincristine therapy for leukaemia.

Plasma levels of protein C and protein S antigens were measured in eight children who developed thrombosis following asparaginase-prednisone-vincristine treatment for acute lymphoblastic leukaemia and in nine similarly treated children without this complication. Protein C antigen levels were below normal in three of the eight patients with thrombosis and in three of the nine patients without the complication (P = 0.38). Low protein S antigen levels were found in five of six patients with thrombosis and in two of seven patients without thrombosis (P = 0.10). Plasma factor IX and factor X antigen levels, other vitamin K dependent factors, were also measured in the two groups of patients. In general, reduced levels of protein C, protein S or both antigens (anticoagulant vitamin K dependent proteins) were associated with reduced levels of factor IX, factor X, or both of these factors (procoagulant vitamin K dependent clotting proteins). The ratios of protein C and protein S antigens to each other and to factor IX and factor X antigens did not differ between the two groups. Thus, there is no clear evidence that reduced levels of protein C and (or) protein S cause thrombosis in leukaemia patients treated with this drug combination.

Adolescent↗

PubMed1986

Thrombosis following percutaneous radial artery cannulation.

A prospective study of the arterial supply of the hand was carried out in 100 ICU patients after cannulation of the radial artery. Patency of the radial artery was checked using a reversed Allen's test and Doppler ultrasonic technique. Furthermore, radial artery angiography was carried out in 15 patients with suspect thrombosis, and the artery was examined by microscopy in four patients at autopsy. Signs of thrombosis, Allen's test and Doppler technique, were found in 33/100 patients. In 10/15 angiograms a thrombosis was visualized, and in 3/4 patients at autopsy a thrombosis was found. The incidence of thrombosis was not correlated to sex, age, size of artery (judged by wrist circumference), cannulation technique or the presence of hypotension. It did, however, correlate to the presence of haematoma at the puncture site. After removal of the cannula recanalisation occurred soon in the majority of cases.

Adolescent↗

PubMed2002

The influence of platelet glycoprotein polymorphisms on receptor function and risk for thrombosis.

With regard to hemostasis and thrombosis, collagens are among the most important physiologic components of the extracellular matrix in their role as platelet activators. Differences in the rate of platelet activation markedly influence normal hemostasis and the pathological outcome of thrombosis. Thus, collagen receptors, such as the integrin alpha2beta1 and indirectly, GPIb alpha, represent a relatively unexploited target of pharmacological control and are only recently becoming appreciated as potential factors in the generic risk for thrombosis. In general, the importance platelet glycoprotein polymorphisms as genetic risk factors for arterial thrombosis is a new area of human genomics that needs to be carefully addressed. Discrepancies in the degree to which they are reported to contribute to risk for clinical thrombosis will only be resolved once there is a universal standard for clinical study design. Most of the clinical studies differ by patient population size, ethnicity, bias in the selection of patients and controls, plurality in clinical endpoints and variation of environmental factors. Despite these differences, there is substantial evidence that the integrin beta3 PlA2 haplotype, the GPIb alpha Met145 haplotype, the GPIb alpha -5C haplotype and the integrin alpha2 haplotype 1 (807T) each contribute to the risk for and morbidity of thrombotic disease. There may remain dispute as to the extent of their contribution. However, well-designed, large, prospective, genetic and epidemiologic studies are needed to clarify the role of these and other platelet receptor polymorphisms. Most importantly, the cumulative effects of multiple platelet and plasma glycoproteins SNPs to thrombotic risk must be evaluated concurrently. Additional in vitro studies of the functional relevance underlying these polymorphisms are needed to provide a sound biological explanation for the results of clinical correlations. The opportunity now exists to make significant inroads into the development of strategies for the prevention of thrombotic disease.

Genetic Predisposition to Disease↗

PubMedDate not supplied

Ultrasound-guided fine needle aspiration biopsy of portal vein thrombosis in liver cirrhosis: results in 15 patients.

Between 1988 and 1992 ultrasound-guided fine needle aspiration biopsies of thromboses in the main branches of the portal vein were carried out in 15 patients with liver cirrhosis. The aims of the study were to evaluate the usefulness, feasibility and diagnostic accuracy of this procedure in cirrhotics with known or suspected hepatocellular carcinoma. The procedure was carried out only in patients with a platelet count > or = 40,000/microL and prothrombin activity > or = 40%. A single pass, with a 22 gauge spinal needle, was performed in the portal vein lumen. Diagnosis of the aetiology of the portal vein thrombosis was obtained in all 15 cases. In 12 cases, a cytological diagnosis of hepatocellular carcinoma was made. In one case, the neoplastic cells aspirated were compatible with adenocarcinoma, and a subsequent colonoscopy confirmed the presence of colonic cancer. The material aspirated was compatible with chemically-induced thrombosis in one patient who had undergone several percutaneous ethanol injection sessions for treatment of hepatocellular carcinoma, and in the last case only blood was aspirated, thus ruling out the coexistence of hepatic cancer. We conclude that fine needle aspiration biopsy of portal vein thrombosis is a feasible, low risk procedure that facilitates the diagnosis of hepatocellular carcinoma when fine needle biopsy of focal liver lesions fails. Fine needle aspiration biopsy of portal vein thrombosis is also useful in excluding neoplastic aetiology of portal vein thrombosis.

Adenocarcinoma↗

PubMed1995

Activated protein c resistance (APC) and inherited factor V (FV) mis-sense mutation in patients with venous and arterial thrombosis in a haematology clinic.

BACKGROUND: Inherited factor V (FV) mis-sense point mutation has recently been identified as a major cause of familial venous thrombosis. The incidence of this congenital haemostatic disorder in Australia is unknown. AIM: To examine the incidence of this congenital defect in patients with thrombosis attending a haematology clinic. METHODS: Individuals investigated or treated for venous and arterial thrombosis over a four month period, as well as those who were on anticoagulant for valvular replacement or arrhythmia were studied for the presence of FV mis-sense point mutation, FV Q506 (G to A at nucleotide position 1691) by a polymerase chain reaction based test, and activated protein C (APC) resistance using an APTT based coagulation assay. RESULTS: Forty-five patients with venous thromboembolism (VTE), 20 patients with coronary artery disease and 25 patients with valvular replacement or arrhythmia who were on anticoagulant were examined. The frequency of FV mis-sense point mutation in these three groups was 26.7%, 15% and 4% respectively. In this study, patients with FV Q506 were of a younger age and had a higher incidence of extensive thrombosis or recurrence as compared to those with the normal factor V gene. This mutation was found in a diverse group of people (four of the 12 patients were of non-European origin). Nearly 50% of these patients had other risk factors for VTE. The number of patients with a family history of VTE was similar for those with the FV mutation and the normal FV. CONCLUSION: This study confirms the high incidence of FV Q506 mutation in patients with VTE reported overseas. Several clinical features, i.e. young age of onset of VTE, high recurrence rate, diverse ethnic background and importance of associated risk factors are highlighted. The findings in this study also raise the possibility that this mutation may be a risk factor for arterial thrombosis. Large studies are required to substantiate these findings.

Adult↗

PubMed1990

Late symptoms after pregnancy-related deep vein thrombosis.

Thromboembolism during pregnancy is a rare complication with a potential fatal outcome. Very little is known about long-term effects and therefore 104 women with thrombosis during pregnancy or puerperium were identified and their subjective complaints were assessed in a questionnaire. All had their thrombosis diagnosed by objective methods and the median follow-up time was 11 years. In spite of anticoagulant treatment only 22% were without complaints; 4% had ulceration, all occurring in the group with thrombosis during pregnancy. Significantly more women who had had their thrombosis during pregnancy used compression bandages than those who had their thrombosis during puerperium. The severity of the symptoms increased with the increasing number of thromboses. Anticoagulant therapy of the acute episode does not appear to alter the degree of long-term handicap in the lower limbs.

Adolescent↗

PubMedDate not supplied

Vascular access thrombosis prophylaxis.

Vascular access thrombosis in the hemodialysis patient leads to significant cost and morbidity. Fistula patency supersedes graft patency, therefore obtaining a mature functioning fistula in patients approaching end-stage renal disease (ESRD) by early patient education and referral needs to be practiced. Current methods to maintain vascular access patency rely on early detection and radiologic or surgical prevention of thrombosis. Study of thrombosis biology has elucidated other potential targets for the prophylaxis of vascular access thrombosis. The goal of this review is to examine the current available methods for vascular access thrombosis prophylaxis.

Arteriovenous Shunt, Surgical↗

PubMed1994

Thrombosis and fibrinolysis in acute myocardial infarction.

The development of coronary thrombosis in response to rupture of atherosclerotic plaques is the primary determinant of the evolution of stable atherosclerotic coronary disease to unstable ischemic syndromes and acute myocardial infarction. Activation of the tissue factor pathway of coagulation and adhesion of platelets are critical events in the initiation of thrombosis. However, subsequently, other factors may determine the extent of thrombosis by modulating the intensity of procoagulant and fibrinolytic activity. Marked procoagulant activity, attenuation of physiologic fibrinolytic activity, or both appear to be risk factors for myocardial infarction. The results of recent studies have provided considerable insight into potential mechanisms for thrombosis in response to rupture of atherosclerotic plaque and have identified potential novel antithrombotic interventions to inhibit the progression of coronary thrombosis.

Animals↗

PubMed2006

Effects of factor XI deficiency on ferric chloride-induced vena cava thrombosis in mice.

BACKGROUND: Increased plasma levels of coagulation factor (F) XI are a risk factor for venous thrombosis. OBJECTIVE: To further explore the relationship between FXI and venous thrombosis, we evaluated FXI-deficient and wild-type mice in a ferric chloride (FeCl(3))-induced vena cava thrombosis model. METHODS AND RESULTS: Thrombosis was induced by 3-min topical application of filter papers containing increasing concentrations of FeCl(3) and the thrombus was measured at 30 min. In contrast to wild-type mice, FXI-deficient mice failed to form a thrombus with 5% FeCl(3,) and were partially protected against 7.5% and 10% FeCl(3,) respectively. The protective effect was substantially stronger than a high dose of heparin (1,000 units kg(-1), i.v.), clopidogrel (30 mg kg(-1), p.o.) or argatroban (30 mg kg(-1), i.p.). These antithrombotic agents resulted in off-scale bleeding in a tail bleeding time assay, whereas the bleeding time of FXI-deficient mice was unchanged compared to wild-type mice. In addition to its known effect on the coagulation cascade, enhanced clot lysis was demonstrated in FXI-deficient mouse and human plasma compared to those supplemented with FXIa. CONCLUSION: Given the strong antithrombotic efficacy (possibly contributed by strong anticoagulant activity associated with increased fibrinolytic activity) and mild bleeding diathesis associated with FXI deficiency, therapeutic inhibition of FXI may be a reasonable therapeutic strategy to treat or prevent venous thrombosis.

Animals↗

PubMed2001

Rheolytic thrombectomy for in-stent thrombosis: creating a diagnostic window.

Acute-stent thrombosis is a relatively uncommon complication of coronary artery stenting, however, it is a potentially catastrophic event. In this case report of stent thrombosis, rheolytic thrombectomy is used to reestablished flow within the artery and, thereby, facilitate intravascular ultrasound. This documented that inadequate stent expansion, residual disease, and tissue prolapse through the stent at an angulated segment of the artery are factors that may underlie thrombosis. This case illustrates that rheolytic thrombectomy is feasible in subacute thrombosis, and that this approach facilitates diagnostic evaluation and treatment of underlying factors involved in stent thrombosis.

Aged↗

PubMed1998

Arterial thrombosis leading to intestinal infarction in a patient with Behçet's disease associated with protein C deficiency.

Behçet's disease may be a possible cause of both occlusive and aneurysmal arterial involvement as well as recurrent venous thrombosis. A case of Behçet's disease complicated with vascular involvement leading to intestinal infarction is presented. A 41-yr-old man suffering from Behçet's disease for 15 yr presented with a 2-day history of severe abdominal pain and bloody diarrhea. Intestinal infarction secondary to thrombosis of the superior mesenteric artery had been diagnosed during surgical exploration 3 yr previously. He was started on anticoagulation with nutritional support. The patient was readmitted with severe diarrhea and malabsorption symptoms 3 yr after intestinal resection. A thrombus located in the posterior wall of the infrarenal portion of aorta was detected by aortography and ultrasonography. Although thrombosis is a relatively common complication of Behçet's disease caused by vasculitis, protein C deficiency, which is a pertinent laboratory finding in this case, might be a secondary factor in the thrombotic event. This is the first case reported of mesenteric artery thrombosis leading to bowel infarction and abdominal aorta thrombosis associated with protein C deficiency.

Adult↗

PubMed2001

Prothrombotic inherited abnormalities other than factor V Leiden mutation do not play a role in venous thrombosis in inflammatory bowel disease.

OBJECTIVES: Because the incidence of thromboembolism is increased in patients with inflammatory bowel disease, we attempted to assess the role of prothrombotic inherited coagulation abnormalities in the development of thrombosis. METHODS: Four populations were compared: 15 patients with inflammatory bowel disease and a previous venous thrombosis, 58 control patients with inflammatory bowel disease but without thrombosis, 110 patients without inflammatory bowel disease but with previous deep venous thrombosis, and 84 healthy subjects. Inherited and acquired risk factors of venous thrombosis, e.g., factor V Leiden and prothrombin 20210A mutations, C677T methylenetetrahydrofolate reductase polymorphism, a polymorphism located in exon 13 of factor V gene, inflammatory and hypercoagulability markers were studied in each population. RESULTS: In the study, 14.3% of thrombotic patients with inflammatory bowel disease had factor V Leiden mutation versus 0% of control patients with inflammatory bowel disease (p = 0.04), 15.5% of thrombotic patients without inflammatory bowel disease (NS) and 3.6% of the healthy controls. A total of 14% of thrombotic patients with inflammatory bowel disease and 11.8% of thrombotic patients without inflammatory bowel disease carried prothrombin 20210A mutation, compared to 1.7% of control patients with inflammatory bowel disease; however, the difference was just below significance. Other inherited coagulation abnormalities were not statistically significantly different among the four populations. CONCLUSIONS: Our study confirms that factor V Leiden mutation increases the risk for thrombotic events but is not more frequent in patients with inflammatory bowel disease. Our results do not support the role of other thrombotic risk factors.

Adult↗

PubMed2006

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.

Adolescent↗

PubMed2002

Prothrombotic factors in neonates with cerebral thrombosis and intraventricular hemorrhage.

AIM: To investigate whether the factor V Leiden mutation (FVL), the prothrombin gene G20210A variant or the methylenetetrahydrofolate reductase (MTHFR) C677T genotype are risk factors for central nervous system (CNS) thrombosis or intraventricular hemorrhage (IVH) in neonates. METHODS: Thirteen full-term infants with cerebral infarct documented with magnetic resonance imaging were assessed with the whole spectrum of assays for thrombophilia including the three DNA-based prothrombotic factors. The frequency of congenital defects was compared with that observed in 38 healthy full-term infants. The genetic defects were also assessed in 55 premature neonates, gestational age <32 wk, 17 of whom developed IVH, grade II-IV. The remaining 38 premature neonates without IVH were used as controls. RESULTS: In the CNS thrombosis group: a prothrombotic factor was detected in 53% of patients and an underlying disease or a triggering event in 61.5%. The frequency of FVL in thrombosed neonates was higher (23%) than in the group of healthy full-term infants (10.5%), although it did not reach statistical significance. IVH developed in 30.9% of premature neonates. Apart from several maternal or neonatal risk factors for IVH, FII G20210A was found in a considerably higher prevalence in the cohort of neonates with IVH (12%) than in those without (2%), although the difference was not statistically significant. CONCLUSION: The pathogenesis of cerebral thrombosis or IVH in neonates is multifactorial. Along with underlying diseases or triggering events, congenital prothrombotic factors (FVL or FII G20210A) showed a trend towards a higher frequency in full-term infants with CNS thrombosis or premature neonates with IVH than in controls. However, their contribution to neonatal cerebral thrombosis or IVH remains to be determined.

Birth Weight↗

PubMed2005

Honokiol inhibits arterial thrombosis through endothelial cell protection and stimulation of prostacyclin.

AIM: To study the effect of honokiol on arterial thrombosis and endothelial cells. METHODS: Rabbit platelet aggregation was performed with Borns turbid method. Thrombosis was produced by the endothelial injury stimulated with electric current. Rat aortic endothelial cells (RAEC) were cultured and cell viability was assessed using the MTT assay. Nitric oxide (NO) concentrations in serum-free media of RAEC were determined using the kinetic cadmium-reduction method. The stable metabolite prostacyclin was measured in serum-free media of RAEC by radioimmunoassay. RESULTS: Honokiol (37.6-376 micromol/L) decreased rabbit platelet aggregation in vitro in a concentration-dependent manner, while intravenously injection of honokiol (0.12-12 microg/kg) significantly inhibited rabbit platelet aggregation induced by collagen ex vivo. In the electrical current-stimulated carotid thrombosis model in rats, honokiol (5-50 microg/kg, iv) prolonged the thrombus occlusion time in a does-dependent manner. In vitro honokiol (0.376-37.6 micromol/L) effectively protected cultured RAEC against oxidized low density lipoprotein (ox-LDL) injury, and significantly increased 6-keto-PGF1alpha (the stable metabolite of prostacyclin) in serum-free media of RAEC. Honokiol also increased NO level in RAEC serum-free medium at a lower concentration range (0.0376-0.376 micromol/L), but honokiol 3.76 micromol/L decreased NO level. CONCLUSION: Honokiol is a potent arterial thrombosis inhibitor. Endothelial cell protection and the stimulation of prostacyclin release may be its main anti-thrombosis mechanism. Stimulation of NO release in endothelial cells may play a role, but it is not a key factor.

6-Ketoprostaglandin F1 alpha↗

PubMed2000

Aortic and iliac thrombosis in six dogs.

Six dogs had signs of pelvic limb weakness, pain and collapse as a result of occlusion of the distal aorta and/or the iliac arteries by a thrombus. Antemortem diagnosis was made on the basis of clinical signs, angiography and ultrasonography. Five dogs had concurrent disease that probably predisposed to thrombosis, including hyperadrenocorticism (three dogs), neoplasia and cardiac disease. Two dogs died shortly after the episode of thrombosis. Dogs that survived the acute episode received aspirin in an attempt to prevent thrombosis occurring again and all regained pelvic limb function. For dogs that survived longer than one month after the acute episode, repeat thrombosis was uncommon; hence the prognosis was related to the underlying disease. Aortic and iliac thrombosis in dogs is an uncommon condition that usually arises secondarily to a predisposing disease process; it carries a more favourable prognosis than feline aortic thromboembolism.

Adrenocortical Hyperfunction↗

PubMed1995

Inferior vena cava thrombosis as a complication of femoral vein catheterisation.

Indwelling femoral venous catheters were prospectively studied by ultrasonography to define the frequency and evolution of inferior vena cava (IVC) thrombosis. IVC thrombosis was identified in six of 56 catheters (54 children). Only one patient with a positive ultrasound scan had clinical signs of thrombosis. All children with IVC thrombosis had had catheters in place for over six days. It is recommended that either the femoral central venous catheters are routinely changed at six days or ultrasound studies are routinely performed twice a week in all patients with catheters in situ for six or more days and that the catheter is removed immediately if evidence of thrombosis appears.

Catheterization, Central Venous↗