Unusual venous thrombosis.
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ABSTRACT:
SUBMITTER: Douketis JD
PROVIDER: S-EPMC4050000 | biostudies-literature | 2014 Jun
REPOSITORIES: biostudies-literature
Publications
Unusual venous thrombosis.
Douketis James D JD Carrier Marc M Crowther Mark A MA
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 20140601 9
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Project description: Not available
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Project description:GENEVA GWAS of Venous Thrombosis
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Project description:Cerebral venous sinus thrombosis (CVT) consists of partial or complete occlusion of a sinus or a cerebral vein. CVT represents 0.5-1% of all strokes and is more frequent in young women. This review discusses particular aspects of CVT diagnosis and management: decompressive craniectomy (DC), anticoagulation with direct oral anticoagulants (DOACs), CVT after coronavirus-disease 19 (COVID-19) and Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT).
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Project description:The column in this issue is supplied by Whitney Sharp, D.O., and Juan Jose Olivero, M.D. Dr. Sharp is chief medical resident in internal medicine at Houston Methodist Hospital and earned her Doctor of Osteopathic Medicine degree at Nova Southeastern University in Fort Lauderdale, Florida. Dr. Olivero is a nephrologist at Houston Methodist Hospital and a member of the hospital's Nephrology Training Program. He obtained his medical degree from the University of San Carlos School of Medicine in Guatemala, Central America, and completed his residency and nephrology fellowship at Baylor College of Medicine in Houston, Texas.
| S-EPMC6217559 | biostudies-other
Project description:Nonthrombotic iliofemoral venous obstruction, masquerading as deep vein thrombosis, was diagnosed in four patients. In each instance the patient was hospitalized and intravenous heparin therapy was started. Phlebography demonstrated venous outflow obstruction without thrombosis; subsequent CT scanning revealed an obstructing lesion in each case. At surgical exploration, (1) endoaneurysmorrhaphy of a hypogastric artery aneurysm decompressed an obstructed right iliac vein; (2) a primary iliac vein leiomyosarcoma was extirpated; (3) a synovial cyst arising from the right hip joint, which obstructed the femoral vein, was excised; and, (4) a postherniorrhaphy inflammatory mass obstructing the left iliofemoral vein junction was confirmed with biopsy results. Improved diagnostic accuracy with its attendant specific therapy is achieved in suspected cases of iliofemoral vein thrombosis if, in addition to noninvasive venous studies or phlebography, CT scanning of the abdomen and pelvis is performed.
| S-EPMC10131839 | biostudies-literature
Project description:Purpose of reviewCerebral venous thrombosis (CVT) is a rare cause of stroke that most commonly affects younger women. Here, we review new literature relevant to the management and prognosis of individuals with CVT and ongoing areas of uncertainty.Recent findingsDirect-acting oral anticoagulants (DOACs) are being increasingly integrated into routine care but are not yet recommended by guidelines. Recent randomized clinical trials and available case series offer reassuring safety data. Routine use of endovascular therapy is not associated with improved outcomes. The relationship between recanalization and prognosis is uncertain. The evidence base for management of CVT continues to improve. Ongoing areas of uncertainty include duration of therapy and whether certain subgroups of patients may benefit from neurointervention or personalized approaches to antithrombotic strategy. The state of knowledge will continue to benefit from large collaborative international efforts, and integration of patient partnerships to identify research priorities.
| S-EPMC8757924 | biostudies-literature
Project description:ObjectiveVenous thrombosis (VT) damages the vein wall, both physically by prolonged distension and from inflammation. These factors contribute to post-thrombotic syndrome (PTS). Interleukin (IL)-6 might play a role in experimental PTS and vein wall responses. Previous assessments of post-thrombotic vein wall injury used static measures such as histologic examination and immunologic assays. The purpose of the present study was to use myography to quantify the changes in contraction and relaxation of murine vessels exposed to an acute VT.MethodsWild-type (WT) C57BL/6 mice were used to determine the baseline vein wall passive tension on a DMT 610m myograph (DMT-USA, Inc., Ann Arbor, Mich), including dosing concentrations of phenylephrine (Phe) and acetylcholine (Ach). WT and IL-6-/- mice underwent VT using inferior vena cava (IVC) ligation (complete stasis) and stenosis (partial stasis), with no-surgery mice used as controls. The mice were harvested at 2 days (2D) and analyzed using a myograph. The vessels were stimulated with Phe and Ach to stimulate a contraction and relaxation response. The endothelial responses to VT were quantified by CD31 immunohistochemistry, Greiss assay, polymerase chain reaction, and Evans blue assay.ResultsOptimal passive tension was determined to be 2 mN, with an optimal concentration of Phe and Ach of 7E-3M and 1E-5M, respectively. No significant differences were found in the contractions when exposed to Phe between the WT control, WT 2D ligation, and WT 2D stenosis IVC segments and the IL-6-/- mice with and without thrombus (P > .05 for all). When treated with Ach, significantly more relaxation was found in the nonthrombosed control IVC segments than in those IVC segments that had had a 2D thrombus from either ligation- or stenosis-derived thrombotic mechanisms in both WT and IL-6-/- mice. CD31 staining showed ∼20% less luminal endothelium after stasis thrombosis (P ≤ .01) but no loss in the controls (P > .05). Evans blue staining showed a trend toward increased leakiness in post-thrombotic vein walls. No significant difference in the endothelial gene markers or nitric oxide production was found.ConclusionsCompared with the controls, acute thrombosis in the total or partial stasis models did not impair IVC contractile responses, suggesting no effect on the medial vascular smooth muscle response. The relaxation response was significantly reduced in the post-thrombotic groups, likely from direct endothelial injury. These findings suggest, at acute points, that VT impairs the endothelial function of a vein wall while retaining the vascular smooth muscle cell function and might be a mechanism that promotes PTS.
| S-EPMC6928442 | biostudies-literature
Project description:AimsTo explore the effect of nonthrombotic internal jugular venous stenosis (IJVS) exerted on cerebral venous thrombosis (CVT).MethodsPatients with imaging confirmed CVT were enrolled into this real-world case-control study consecutively from January 2018 through April 2021, and were divided into CVT and IJVS-CVT groups, according to whether or not with non-thrombotic IJVS. Chi-square and logistic regression models were utilized for between-group comparison of thrombotic factors.ResultsA total of 199 eligible patients entered into final analysis, including 92 cases of CVT and 107 cases of IJVS-CVT. Chi-square revealed that thrombophilic conditions were found in majority of CVT, while only minority in the IJVS-CVT group (83.7% vs. 20.6%, p < 0.001). Multivariate logistic regression indicated that most identified thrombophilia were negatively related to IJVS-CVT (all p < 0.05), including oral contraceptive use (β = -1.38), hyperhomocysteinemia (β = -1.58), hematology (β = -2.05), protein C/S deficiency (β = -2.28), connective tissue disease (β = -1.18) and infection (β = -2.77). All recruited patients underwent standard anticoagulation, 10 cases in IJVS-CVT group also received jugular angioplasty for IJVS correction. Most participants obtained alleviations during 1-year follow-up. However, both clinical and imaging outcomes in IJVS-CVT group were not as good as those in CVT group (both p < 0.05). Moreover, 8 cases with CVT and 7 cases with IJVS-CVT were rehospitalized for CVT recurrences and underwent customized treatment.ConclusionNonthrombotic IJVS may be one of the risk factors of CVT. Anticoagulation might need to be suggested for IJVS patients.
| S-EPMC8504525 | biostudies-literature
Project description:AbstractPlatelets are key players in cardiovascular disease, and platelet aggregation represents a central pharmacologic target, particularly in secondary prevention. However, inhibition of adenosine diphosphate and thromboxane signaling has low efficacy in preventing venous thromboembolism, necessitating the inhibition of the plasmatic coagulation cascade in this disease entity. Anticoagulation carries a significantly higher risk of bleeding complications, highlighting the need of alternative therapeutic approaches. We hypothesized that procoagulant activation (PA) of platelets promotes venous thrombus formation and that targeting PA could alleviate venous thrombosis. Here, we found elevated levels of procoagulant platelets in the circulation and in thrombi of patients with deep vein thrombosis (DVT) and pulmonary embolism, and in mice developing DVT following inferior vena cava stenosis. Furthermore, we detected PA of recruited platelets within murine venous thrombi and human pulmonary emboli. Mice with platelet-specific deficiency in central pathways of PA-cyclophilin D and transmembrane protein 16F-were more resistant toward low flow-induced venous thrombosis. Finally, we found that a clinically approved carbonic anhydrase inhibitor, methazolamide, reduced platelet procoagulant activity and alleviated murine thrombus formation without affecting trauma-associated hemostasis. These findings identify an essential role of platelet procoagulant function in venous thrombosis and delineate novel pharmacologic strategies targeting platelets in the prevention of venous thromboembolism.
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Project description:Arterial and venous (A/V) thrombosis constitutes the greatest source of morbidity and mortality worldwide. Long considered as distinct entities, accumulating evidence indicates that A/V thrombosis can occur in the same populations suggesting that common mechanisms are likely operative. Although hyperactivation of the immune system is a common forerunner to the genesis of thrombotic events in both vascular systems, the key molecular control points remain poorly understood. Consequently, anti-thrombotic therapies targeting the immune system for therapeutic gain are lacking. Here we show that neutrophils are key effectors of both A/V thrombosis and can be targeted via novel immunoregulatory nanoparticles. Using antiphopholipid antibody syndrome (APS) as a model for devastating A/V thrombosis, we identified the transcription factor Krüppel-like factor 2 (KLF2) as a key regulator of neutrophil activation. Upon activation via genetic loss of KLF2 or administration of antiphospholipid antibodies, neutrophils cluster P-selectin glycoprotein ligand 1 (PSGL-1) via cortical actin remodeling, thereby increasing adhesion potential at thrombosis sites. Targeting clustered PSGL-1 using designer nanoparticles attenuates neutrophil-mediated A/V thrombosis in APS and KLF2 knockout models, illustrating the importance and feasibility of targeting activated neutrophils to prevent pathological thrombosis. Together, our results demosntrate a role for activated neutrophils to prevent pathological thrombosis. Together, our results demonstrate a role for activated neutorphils in both arterial and venous thrombosis and identify key molecular events that serve as potential targets for therapeutics against diverse causes of immunothrombosis.
2022-09-12 | GSE208336 | GEO