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PubMed2005

Myocardial infarction and arterial thrombosis in severe (homozygous) FXII deficiency: no apparent causative relation.

Twenty-one patients (12 female and 9 male) with severe (homozygous) factor XII (FXII) deficiency and 58 (32 female and 26 male) with heterozygous FXII deficiency were observed for an average 16.2 years. No patient with homozygous FXII deficiency experienced myocardial infarction or any other arterial thrombosis. The same was true for heterozygotes. The cases of FXII deficiency and arterial thrombosis reported in the literature were evaluated. In every instance, associated risk factors were present that could justify the arterial thrombosis. Dyslipidemia, hypertension, smoking, and diabetes mellitus were the most frequent findings. The examination of the few papers that dealt with the prevalence of arterial thrombosis in patients with severe FXII deficiency showed that only 1 patient of 61 experienced myocardial infarction. In conclusion, it seems that the role of FXII deficiency in the pathogenesis of arterial thrombosis is minor.

Adolescent↗

PubMed2006

Antiphospholipid-mediated thrombosis: interplay between anticardiolipin antibodies and vascular cells.

The antiphospholipid syndrome (APS) is characterized by thrombosis or pregnancy morbidity in the presence of antiphospholipid autoantibodies (aPL). aPL are a heterogeneous family of autoantibodies with diverse cross-reactivities whose origin and role have not been fully elucidated. Many of the autoantibodies associated with APS are directed against phospholipid-binding plasma proteins, such as beta2-GPI and prothrombin, or phospholipid-protein complexes. The mechanisms by which aPL cause thrombosis are not completely understood. There is no unique mechanism able to explain all symptoms associated with the presence of aPL. Different theories have been proposed, including the effect of aPL on endothelial cells, monocytes, and platelets. aPL are able to recognize, injure, or activate cultured vascular endothelial cells. Cultured endothelial cells incubated with aPL express increased levels of cell adhesion molecules and tissue factor (TF), an effect mediated by beta2-GPI, and may promote inflammation and thrombosis. Overexpression of TF has been also shown in monocytes in vitro and ex vivo. TF is the major initiator of coagulation in vivo; thus, its dysregulation may be one of the most important contributors to thrombosis. Effects of aPL upon platelets are not completely elucidated. aPL bind anionic phospholipid but they are normally in the inner side of cell membranes. When platelets are activated by different agonists, anionic phospholipids are exposed. There is some evidence showing that activated platelets are present in aPL-positive patients. Increased levels of beta-thrombomodulin, and microvesicle formation seem to support this hypothesis. Activated platelets may contribute to thrombosis by persistent exposure of a procoagulant surface.

Antibodies, Anticardiolipin↗

PubMed2003

The incidence of deep vein thrombosis after hip and knee arthroplasties in Japanese patients: a prospective study.

PURPOSE: To document the incidence of proximal deep vein thrombosis and pulmonary embolism in 58 consecutive Japanese patients undergoing total hip arthroplasty or total knee arthroplasty. METHODS: Patients were routinely examined for proximal deep vein thrombosis by B-mode ultrasonography before and after surgery. Those patients who had ultrasonographic findings of deep vein thrombosis were also investigated for pulmonary embolism by ventilation-perfusion lung scan. RESULTS: The incidence of deep vein thrombosis after total hip arthroplasty and total knee arthroplasty were 9.1% and 4.0% respectively, and the incidence of pulmonary embolism were 3.0% and 0%, respectively. There were no cases of fatal pulmonary embolism. CONCLUSION: The incidence of deep vein thrombosis and pulmonary embolism in Japanese patients may have increased over the last few decades.

Aged↗

PubMed2005

Venous thrombosis: the role of genes, environment, and behavior.

Over the last decade we have witnessed an avalanche of newly identified risk factors for venous thrombosis. This has advanced our knowledge of its etiology, because more determinants have been described and because the underlying concepts have received a new and broader understanding. Venous thrombosis is a common multicausal disease occurring as the result of interacting genetic, environmental and behavioral risk factors. Some of these have been known since medieval times, such as the increased risk of thrombosis during immobilization in pregnancy and after childbirth (although retained milk of the breast-feeding mother was seen as the primary cause for the latter). Pregnancy and puerperium still cause thrombosis, as do exogenous hormones in oral contraceptives and hormonal replacement therapy. Furthermore, the immobilization in the puerperium of the old days translates directly to situations of immobilization in current times, such as prolonged travel in airplanes or excessive electronic gaming. While pedigrees with abundant thrombosis were observed in the early 1900s, the first cause of heritable thrombophilia (antithrombin deficiency) was discovered in 1965, with the subsequent identification of deficiencies of protein C and protein S in the early 1980s. These were uncommon and strong risk factors, whereas the more recently discovered genetic variants are common and weak, and cause disease only in the presence of other factors.

Adolescent↗

PubMed2002

Protection against thrombosis in mice lacking PAR3.

The recent observation that knock-out of protease-activated receptor-4 (PAR4) ablates thrombin signaling in mouse platelets and protects against ferric chloride-induced thrombosis of mouse mesenteric arterioles suggests that thrombin's actions on platelets can play an important role in thrombosis. Complete ablation of thrombin signaling would be difficult to achieve in human beings because human platelets have 2 thrombin receptors that are each capable of mediating transmembrane signaling. However, it is possible that complete ablation of thrombin signaling in platelets is not necessary for an antithrombotic effect. In mouse platelets, PAR3 functions as a cofactor that binds thrombin and promotes productive cleavage of PAR4, and thrombin responses are decreased but not absent in Par3(-/-) platelets. We now report that Par3(-/-) mice were protected against ferric chloride-induced thrombosis of mesenteric arterioles and against thromboplastin-induced pulmonary embolism. Surprisingly, Par3(-/-) and Par4(-/-) mice showed similar degrees of protection in these models and similar prolongation of tail bleeding times. Thus, even a partial decrease in mouse platelet responsiveness to thrombin protected against thrombosis and impaired hemostasis in some settings. These results demonstrate the importance of PAR3's unusual cofactor function and underscore the relative importance of thrombin's actions on platelets in vivo. They also suggest that PAR inhibition might be explored for the prevention or treatment of thrombosis in human beings.

Animals↗

PubMed2006

A nonsense polymorphism in the protein Z-dependent protease inhibitor increases the risk for venous thrombosis.

The protein Z-dependent protease inhibitor (ZPI) is a hemostatic serpin with anticoagulant activity. As for antithrombin, deficiency of ZPI could have relevant thrombotic consequences. We have studied 6 genetic modifications affecting the ZPI gene, identifying 5 haplotypes. Haplotype H5 is featured by a stop codon at position 67. The relevance of these genetic modifications and haplotypes in venous thrombosis was evaluated in a case-control study including 1018 patients and 1018 age- and sex-matched controls. Surprisingly, the H5 haplotype was found in 0.9% of controls, supporting that the Arg67Stop change is a low frequency nonsense polymorphism. The prevalence of this haplotype increased significantly in patients (3.0%), one of whom was in a homozygous state. Multivariate analysis confirms that carriers have a 3.3-fold risk of developing venous thrombosis (P = .002; 95% CI: 1.5-7.1). Moreover, we observed a significant association of this polymorphism with familial history of thrombosis (P < .001). Our study supports that the ZPI Arg67Stop nonsense polymorphism might be an independent genetic risk factor for venous thrombosis. This polymorphism has slightly lower prevalence but similar thrombotic risk than the FV Leiden or prothrombin 20210A. Although further studies are required, all available data support that the ZPI is a candidate to play a significant role in thrombosis and should be evaluated in thrombophilic studies.

Adult↗

PubMed2006

Enhanced susceptibility to arterial thrombosis in a murine model of hyperhomocysteinemia.

Hyperhomocysteinemia is a risk factor for thrombosis, but the mechanisms are not well defined. We tested the hypothesis that hyperhomocysteinemia accelerates arterial thrombosis in mice. Mice heterozygous for a targeted disruption of the cystathionine beta-synthase gene (Cbs+/-) and wild-type littermates (Cbs+/+) were fed either a control diet or a high methionine/low folate (HM/LF) diet for 6 to 8 months to produce graded hyperhomocysteinemia. The time to occlusion of the carotid artery after photochemical injury was shortened by more than 50% in Cbs+/+ or Cbs+/- mice fed the HM/LF diet (P < .001 versus control diet). Carotid artery thrombosis was not accelerated in mice deficient in endothelial nitric oxide synthase (Nos3), which suggests that decreased endothelium-derived nitric oxide is not a sufficient mechanism for enhancement of thrombosis. Cbs+/+ and Cbs+/- mice fed the HM/LF diet had elevated levels of reactive oxygen species in the carotid artery, increased aortic expression of the NADPH oxidase catalytic subunit, Nox4, and decreased activation of anticoagulant protein C in the aorta (P < .05 versus control diet). We conclude that hyperhomocysteinemia enhances susceptibility to arterial thrombosis through a mechanism that is not caused by loss of endothelium-derived nitric oxide but may involve oxidative stress and impairment of the protein C anticoagulant pathway.

Animals↗

PubMed2001

Reduced incidence of thrombosis in mice with hereditary spherocytosis following neonatal treatment with normal hematopoietic cells.

Thrombosis is a life-threatening complication of hemolytic anemia in humans. Cardiac thrombi are present in all adult alpha-spectrin-deficient (sph/sph) mice with severe hereditary spherocytosis, providing a model for events preceding thrombosis. The current study evaluated (1) the timing of thrombosis initiation and (2) the effect of postnatal transplantation of normal cells on life span and thrombotic incidence in adult mice. Thrombi are detected histologically following necropsy in untreated sph/sph mice of various ages and are not observed until 6 weeks of age. Thrombotic incidence increases from 50% at 6 to 7 weeks of age to 100% at 9 weeks of age. As a potential therapy, nonablated sph/sph neonates were transfused with either genetically marked normal peripheral blood (PB), bone marrow (BM), or both and assessed for donor cells and thrombosis. A single transfusion of PB, with or without BM, significantly increases the percentage of sph/sph mice that survive to weaning (4 weeks of age). Replacement in all sph/sph recipients is limited to red blood cells (RBCs). RBCs derived from donor PB are lost within 5 weeks. PB plus BM prolongs high-level donor PB cell production better than BM alone. Thrombotic incidence is significantly reduced in all sph/sph mice treated with PB, BM, or both. Hence, the presence of normal blood cells in the peripheral circulation of neonatal and adult sph/sph mice rescues the former and abrogates the development of thrombosis in the latter. (Blood. 2001;97:3972-3975)

Animals↗

PubMed2006

Acute partial Budd-Chiari syndrome and portal vein thrombosis in cytomegalovirus primary infection: a case report.

BACKGROUND: Splanchnic vein thrombosis may complicate inherited thrombotic disorders. Acute cytomegalovirus infection is a rare cause of acquired venous thrombosis in the portal or mesenteric territory, but has never been described extending into a main hepatic vein. CASE PRESENTATION: A 36-year-old immunocompetent woman presented with acute primary cytomegalovirus infection in association with extensive thrombosis in the portal and splenic vein. In addition, a fresh thrombus was evident in the right hepatic vein. A thorough evaluation for a hypercoagulable state was negative. The clinical course, biological evolution, radiological and histological findings were consistent with cytomegalovirus hepatitis complicated by a partial acute Budd-Chiari syndrome and portal thrombosis. Therapeutic anticoagulation was associated with a slow clinical improvement and partial vascular recanalization. CONCLUSION: We described in details a new association between cytomegalovirus infection and acute venous thrombosis both in the portal vein and in the right hepatic vein, realizing a partial Budd-Chiari syndrome. One should be aware that this rare thrombotic event may be complicated by partial venous outflow block.

Acute Disease↗

PubMed2005

Acute cytomegalovirus infection complicated by venous thrombosis: a case report.

BACKGROUND: CMV-induced vasculopathy and thrombosis have been reported, but they are rare conditions usually encountered in immunocompromised patients. However more and more complications of CMV infections are recognized in immunocompetent patients. CASE PRESENTATION: We present a case report of a previously healthy adult with cytomegalovirus infection that was complicated by tibiopopliteal deep venous thrombosis and in whom Factor V Leiden heterozygous mutation was found. CONCLUSION: This new case report emphasizes the involvement of cytomegalovirus in induction of vascular thrombosis in patients with predisposing risk factors for thrombosis. It is necessary to screen for CMV infection in patients with spontaneous thrombosis and an history of fever.

Acute Disease↗

PubMed2004

Dural sinus thrombosis after cardiopulmonary bypass.

Cerebral venous thrombosis in various clinical conditions, such as congenital heart disease (CHD) and hypercoagulable states, have been recognized previously. However, dural sinus thrombosis in a pediatric patient with Antiphospholipid Syndrome (APLS) after the repair of a ventricular septal defect (VSD) has not been reported yet. A child who underwent an operation for the surgical repair of VSD under cardiopulmonary bypass (CPB) developed a stroke after the procedure. A cranial computer tomography (CT) scan of the patient showed dural sinus thrombosis and severe cerebral edema. APLS and CPB were thought to be the only risk factors of dural sinus thrombosis. This observation warrants attention and screening should be taken into consideration in patients with APLS who carry a higher risk for dural sinus thrombosis after CPB.

Antiphospholipid Syndrome↗

PubMed2005

Randomized placebo-controlled study of low-dose warfarin for the prevention of central venous catheter-associated thrombosis in patients with cancer.

PURPOSE: In this multicenter, randomized, placebo-controlled clinical trial, we studied whether warfarin 1 mg daily reduces the incidence of symptomatic central venous catheter (CVC) -associated thrombosis in patients with cancer. PATIENTS AND METHODS: Two hundred fifty-five patients with cancer who required a CVC for at least 7 days were randomly assigned to receive warfarin 1 mg or placebo. RESULTS: There were 11 (4.3%) symptomatic CVC-associated thromboses among 255 patients, with no difference in the incidence of symptomatic CVC-associated thrombosis between patients taking warfarin 1 mg daily (six of 130 patients; 4.6%) and patients taking placebo (five of 125 patients; 4.0%; hazard ratio, 1.20; 95% CI, 0.37 to 3.94). Warfarin had no effect on CVC life span (84 days v 63 days in control and warfarin groups, respectively; 95% confidence limit, -16 to 55 days; P = .09), and it did not affect the number of premature CVC removals (23.2% v 25.4% in control and warfarin groups, respectively; 95% confidence limit of difference -8.34 to 12.71; P = .68) or the frequency of major bleeding episodes (2% v 0% in control and warfarin groups, respectively; P = .5, Fisher's exact test). CONCLUSION: Symptomatic CVC-associated thrombosis in patients with cancer, although significant, is less common than previously reported. In this study, the administration of warfarin 1 mg daily did not reduce the incidence of symptomatic CVC-associated thrombosis in patients with cancer. However, the low rate of symptomatic CVC-associated thrombosis means that a much larger trial is required to address this issue definitively.

Adolescent↗

PubMed1996

The stroke syndrome of cortical vein thrombosis.

Cortical vein thrombosis without sinus involvement is rarely diagnosed, although it may commonly be overlooked. We report four cases of cerebral venous thrombosis limited to the cortical veins. The diagnosis was made on surgical intervention in one patient and by angiography in three patients. Together with a survey of the published cases, the clinical and neuroimaging patterns of our patients allow delineation of several features suggestive of cortical venous stroke. Focal or generalized seizures followed by hemiparesis, aphasia, hemianopia, or other focal neurologic dysfunction in the absence of signs of increased intracranial pressure should suggest this possibility. Neuroimaging (CT, MRI) shows an ischemic lesion that does not follow the boundary of arterial territories and often has a hemorrhagic component, without signs of venous sinus thrombosis. Conventional angiography demonstrates no arterial occlusion but may show cortical vein thrombosis corresponding to the infarct, although these may also be nonspecific findings. The role of MR angiography, which is well-established in sinus thrombosis, remains to be assessed in patients with brain ischemia due to isolated cortical vein occlusion.

Adult↗

PubMed2004

The effects of a polymerized bovine-derived hemoglobin solution in a rabbit model of arterial thrombosis and bleeding.

UNLABELLED: Hemoglobin-based oxygen carriers (HBOCs) have been developed primarily for their oxygenating function and possible use as an alternative to red blood cells during surgery or after major trauma. However, their effect on hemostasis has not been studied extensively. We compared the effects on hemostasis of bovine-derived hemoglobin solution (HBOC-201) with gelatin solution and saline infusion in an experimental model of arterial thrombosis and bleeding. After anesthesia, the Folts model was constructed in 30 rabbits. The common carotid artery was exposed, and a 60% stenosis was induced. A compression injury of the artery was then produced, which triggered a series of cyclic episodes of thrombosis (cyclic flow reductions [CFRs]). After the number of baseline CFRs was counted, animals were assigned randomly to one of three groups (n = 10 each): saline (control), gelatin, or HBOC-201 solution. The effect of studied solutions was observed by recording the number of CFRs during another period and was compared with that of saline. Ear immersion bleeding time was recorded after each CFR period. Gelatin and HBOC-201 had similar effects, manifested by significantly decreased CFRs (from median of 7 to 1 and 6 to 1, respectively) and significantly lengthened bleeding time (from 88 to 98 s and 81 to 102 s, respectively; P < 0.05). Saline infusion had no significant effect on CFRs or bleeding time. HBOC-201 and gelatin had similar effects marked by a reduction in the arterial thrombosis rate and increased bleeding time in rabbits. IMPLICATIONS: In a rabbit thrombosis and hemorrhagic model, a polymerized bovine-derived hemoglobin solution and a gelatin solution infusion decreased arterial thrombosis and lengthened bleeding time.

Animals↗

PubMed1993

Prolonged barbiturate therapy in a patient with closed head injury and jugular venous thrombosis.

The case of a patient who sustained a severe closed head injury complicated by jugular venous thrombosis is presented. Early problems with intracranial pressure were related to bifrontal intracerebral contusions. Jugular vein thrombosis became manifest clinically late in the patient's course and was verified by Doppler ultrasonography. Late problems with intracranial hypertension were presumed to be due to decreased cerebral outflow secondary to the thrombosis. The patient required 4 weeks of a high-dose regimen of pentobarbital to control his intracranial pressure. This is an exceptionally long period of time for a patient to be in barbiturate coma for a closed head injury and still make a satisfactory recovery. The incidence, etiology, prevention, and treatment of upper extremity and jugular venous thrombosis are discussed. The ramifications of jugular venous thrombosis in neurosurgical patients are discussed.

Adult↗

PubMed1993

Sigmoid sinus thrombosis after closed head injury in children.

In the literature, clinical descriptions of sigmoid sinus thrombosis occurring after closed head injury in children are rare. One to 5 days after trauma to the back of the head, five children (aged 1 to 7 yr) presented with gait ataxia, vomiting, and headache. Trauma was mild in four children. Computed tomography of all the children, performed within 5 days after the injury, showed focal hyperdensity in the region of the left sigmoid sinus. Four children had extra-axial hyperdense collections along the left transverse sinus, and three had skull fractures adjacent to the left sigmoid sinus. Magnetic resonance imaging (MRI) of all the children, performed 2 to 6 days after injury, showed left sigmoid-sinus thrombosis and decreased flow or thrombosis within the lateral third of the left transverse sinus. All the children had MRI scans 4 to 6 weeks after their diagnosis and were followed up for 1 to 12 months. In four children whose symptoms subsided completely within 2 to 10 weeks, MRI showed recanalization of the sigmoid sinus within 4 to 6 weeks after injury. In one child whose symptoms resolved after 6 months, sigmoid-sinus thrombosis persisted with the formation of collateral flow. We conclude that traumatic sigmoid-sinus thrombosis should be suspected when a child has persistent or delayed gait ataxia and vomiting after injury to the back of the head. Computed tomography characteristically demonstrated focal hyperdensity within the sigmoid sinus that we term the dense sigmoid-sinus sign. Because the sinus recanalized and the symptoms subsided in most children within 6 weeks, we conclude that prophylactic medical or surgical intervention is not indicated.

Child↗

PubMed2003

MRI diagnosis of bilateral adrenal vein thrombosis.

We report a case of bilateral adrenal vein thrombosis in an adult female who had a history of breast cancer. The patient does not have clinical, serological or imaging evidence of metastatic disease 14 months from the initial diagnosis. Adrenal vein thrombosis is a rare entity. There have been no previous reports specifically stating an association between adrenal vein thrombosis and hypercoaguability, but there are many cases in the literature documenting venous thrombosis elsewhere within the body in patients with hypercoaguable states. Laboratory testing performed to exclude a hypercoaguable state, revealed heterozygosity for the Factor V Leiden mutation/activated protein C resistance and elevated factor VIII levels [3660 IU l(-1) (<1500)]. This is the first reported case of bilateral metachronous adrenal vein thrombosis in which MRI established the diagnosis.

Adrenal Glands↗

PubMed2003

Deep venous thrombosis associated with protein C and/or S deficiency: management with catheter-directed thrombolysis.

We performed this study to evaluate the efficacy of catheter-directed thrombolysis with urokinase in treating acute symptomatic iliofemoral deep venous thrombosis associated with protein C and/or S deficiency. A total of 42 consecutive patients with deep venous thrombosis were seen between September 2000 and August 2002. Of these, catheter-directed thrombolysis via the popliteal vein was performed in 5 patients (11.9%) with acute iliofemoral deep venous thrombosis associated with protein C and/or S deficiency. Average duration of symptoms was 4.2 days (range, 1-7 days). The average urokinase dose was 2.7 million IU (range, 0.6 million to 7.0 million IU) infused over an average of 33.1 h (range, 16-67 h). Lysis was complete in all five treated cases. Two cases had underlying iliac venous stenoses (>50%) that were treated with angioplasty and stent placement. In one patient in whom recanalization of a right iliac vein occlusion was successful, thrombosis occurred in the treated vein within 3 weeks of intervention despite full anticoagulation therapy, and further intervention was required. There were no complications or clinically detectable pulmonary emboli. The technical and clinical success rates were 100%. This initial experience suggests that catheter-directed thrombolysis for treatment of acute symptomatic iliofemoral deep venous thrombosis associated with protein C and/or S deficiency is safe and effective.

Acute Disease↗