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JHEP Reports : Innovation in Hepatology Apr 2023The expression splanchnic vein thrombosis encompasses Budd-Chiari syndrome and portal vein thrombosis. These disorders have common characteristics: they are both rare... (Review)
Review
The expression splanchnic vein thrombosis encompasses Budd-Chiari syndrome and portal vein thrombosis. These disorders have common characteristics: they are both rare diseases which can cause portal hypertension and its complications. Budd-Chiari syndrome and portal vein thrombosis in the absence of underlying liver disease share many risk factors, among which myeloproliferative neoplasms represent the most common; a rapid comprehensive work-up for risk factors of thrombosis is needed in these patients. Long-term anticoagulation is indicated in most patients. Portal vein thrombosis can also develop in patients with cirrhosis and in those with porto-sinusoidal vascular liver disease. The presence and nature of underlying liver disease impacts the management of portal vein thrombosis. Indications for anticoagulation in patients with cirrhosis are growing, while transjugular intrahepatic portosystemic shunt is now a second-line option. Due to the rarity of these diseases, studies yielding high-grade evidence are scarce. However, collaborative studies have provided new insight into the management of these patients. This article focuses on the causes, diagnosis, and management of patients with Budd-Chiari syndrome, portal vein thrombosis without underlying liver disease, or cirrhosis with non-malignant portal vein thrombosis.
PubMed: 36941824
DOI: 10.1016/j.jhepr.2022.100667 -
Journal of Clinical and Experimental... 2022Patients with cirrhosis of the liver are at high risk of developing portal vein thrombosis (PVT), which has a complex, multifactorial cause. The condition may present... (Review)
Review
Patients with cirrhosis of the liver are at high risk of developing portal vein thrombosis (PVT), which has a complex, multifactorial cause. The condition may present with a myriad of symptoms and can occasionally cause severe complications. Contrast-enhanced computed tomography (CT) is the gold standard for the diagnosis of PVT. There are uncertainties regarding the effect on PVT and its treatment outcome in patients with cirrhosis. The main challenge for managing PVT in cirrhosis is analyzing the risk of hemorrhage compared to the risk of thrombus extension leading to complications. All current knowledge regarding non-tumor PVT in cirrhosis, including epidemiology, risk factors, classification, clinical presentation, diagnosis, impact on natural history, and treatment, is discussed in the present article.
PubMed: 35677518
DOI: 10.1016/j.jceh.2021.11.003 -
RoFo : Fortschritte Auf Dem Gebiete Der... Feb 2022Portal vein thrombosis (PVT) is a rare but severe entity that can cause clinically significant sequela such as worsening portal hypertension or mesenteric ischemia.... (Review)
Review
BACKGROUND
Portal vein thrombosis (PVT) is a rare but severe entity that can cause clinically significant sequela such as worsening portal hypertension or mesenteric ischemia. Those cases refractory to medical management may be referred for endovascular intervention. Several technical considerations have been described in the literature, but a cohesive comparison of these multiple techniques is lacking.
METHODS
The purpose of this article is to review the diagnosis and endovascular management of PVT, including areas in which further research is warranted.
RESULTS
Cases of PVT can be readily diagnosed using ultrasound, computed tomography, or magnetic resonance imaging. Treatment often begins with systemic anticoagulation and endovascular interventions may be used in selected cases. Determining the optimal approach to accessing the portal venous system depends on the underlying disease and chronicity of the thrombus and the degree of occlusion. Once access to the portal venous system is established, catheter-directed therapy may be performed to achieve recanalization.
CONCLUSION
Despite the heterogeneity in patient presentation, cases of PVT can be readily diagnosed across several imaging modalities. Strategizing interventional approaches involves evaluation of the underlying disease and the chronicity of the thrombus.
KEY POINTS
· This review will enable interventionalists to establish a framework for treating portal vein thrombosis by identifying patient risk factors and thrombus characteristics that determine patient management.. · The unique risks and benefits for transhepatic, transsplenic, and transmesenteric approaches for establishing portal venous access will be discussed.. · Advantages and complications of thrombolysis, thrombectomy, and transjugular intrahepatic portosystemic shunt creation for treating portal vein thrombosis will be reviewed in detail based on our extensive institutional experience..
CITATION FORMAT
· Ju C, Li X, Gadani S et al. Portal Vein Thrombosis: Diagnosis and Endovascular Management. Fortschr Röntgenstr 2022; 194: 169 - 180.
Topics: Endovascular Procedures; Humans; Portal Vein; Portasystemic Shunt, Transjugular Intrahepatic; Thrombosis; Treatment Outcome
PubMed: 34649289
DOI: 10.1055/a-1642-0990 -
Journal of Thrombosis and Haemostasis :... Jun 2022Activated coagulation factor XI (FXIa) contributes to the development and propagation of thrombosis but plays only a minor role in hemostasis; therefore, it is an...
BACKGROUND
Activated coagulation factor XI (FXIa) contributes to the development and propagation of thrombosis but plays only a minor role in hemostasis; therefore, it is an attractive antithrombotic target.
OBJECTIVES
To evaluate the pharmacology of asundexian (BAY 2433334), a small molecule inhibitor targeting FXIa, in vitro and in various rabbit models.
METHODS
The effects of asundexian on FXIa activity, selectivity versus other proteases, plasma thrombin generation, and clotting assays were evaluated. Antithrombotic effects were determined in FeCl - and arterio-venous (AV) shunt models. Asundexian was administered intravenously or orally, before or during thrombus formation, and with or without antiplatelet drugs (aspirin and ticagrelor). Potential effects of asundexian on bleeding were evaluated in ear-, gum-, and liver injury models.
RESULTS
Asundexian inhibited human FXIa with high potency and selectivity. It reduced FXIa activity, thrombin generation triggered by contact activation or low concentrations of tissue factor, and prolonged activated partial thromboplastin time in human, rabbit, and various other species, but not in rodents. In the FeCl -injury models, asundexian reduced thrombus weight versus control, and in the arterial model when added to aspirin and ticagrelor. In the AV shunt model, asundexian reduced thrombus weight when administered before or during thrombus formation. Asundexian alone or in combination with antiplatelet drugs did not increase bleeding times or blood loss in any of the models studied.
CONCLUSIONS
Asundexian is a potent oral FXIa inhibitor with antithrombotic efficacy in arterial and venous thrombosis models in prevention and intervention settings, without increasing bleeding.
Topics: Animals; Anticoagulants; Aspirin; Factor XIa; Fibrinolytic Agents; Hemorrhage; Humans; Platelet Aggregation Inhibitors; Rabbits; Thrombin; Thrombosis; Ticagrelor
PubMed: 35289054
DOI: 10.1111/jth.15700 -
Journal of Veterinary Emergency and... May 2022To expand the number of conditions and interventions explored for their associations with thrombosis in the veterinary literature and to provide the basis for...
OBJECTIVES
To expand the number of conditions and interventions explored for their associations with thrombosis in the veterinary literature and to provide the basis for prescribing recommendations.
DESIGN
A population exposure comparison outcome format was used to represent patient, exposure, comparison, and outcome. Population Exposure Comparison Outcome questions were distributed to worksheet authors who performed comprehensive searches, summarized the evidence, and created guideline recommendations that were reviewed by domain chairs. The revised guidelines then underwent the Delphi survey process to reach consensus on the final guidelines. Diseases evaluated in this iteration included heartworm disease (dogs and cats), immune-mediated hemolytic anemia (cats), protein-losing nephropathy (cats), protein-losing enteropathy (dogs and cats), sepsis (cats), hyperadrenocorticism (cats), liver disease (dogs), congenital portosystemic shunts (dogs and cats) and the following interventions: IV catheters (dogs and cats), arterial catheters (dogs and cats), vascular access ports (dogs and cats), extracorporeal circuits (dogs and cats) and transvenous pacemakers (dogs and cats).
RESULTS
Of the diseases evaluated in this iteration, a high risk for thrombosis was defined as heartworm disease or protein-losing enteropathy. Low risk for thrombosis was defined as dogs with liver disease, cats with immune-mediated hemolytic anemia, protein-losing nephropathy, sepsis, or hyperadrenocorticism.
CONCLUSIONS
Associations with thrombosis are outlined for various conditions and interventions and provide the basis for management recommendations. Numerous knowledge gaps were identified that represent opportunities for future studies.
Topics: Adrenocortical Hyperfunction; Anemia, Hemolytic, Autoimmune; Animals; Cat Diseases; Cats; Consensus; Critical Care; Dirofilariasis; Dog Diseases; Dogs; Fibrinolytic Agents; Protein-Losing Enteropathies; Risk Factors; Sepsis; Thrombosis
PubMed: 35499966
DOI: 10.1111/vec.13204 -
Journal of Clinical and Experimental... Sep 2014Mesenteric vein thrombosis is increasingly recognized as a cause of mesenteric ischemia. Acute thrombosis commonly presents with abdominal pain and chronic type with... (Review)
Review
Mesenteric vein thrombosis is increasingly recognized as a cause of mesenteric ischemia. Acute thrombosis commonly presents with abdominal pain and chronic type with features of portal hypertension. Contrast enhanced CT scan of abdomen is quite accurate for diagnosing and differentiating two types of mesenteric venous thrombosis. Prothrombotic state, hematological malignancy, and local abdominal inflammatory conditions are common predisposing conditions. Over the last decade, JAK-2 (janus kinase 2) mutation has emerged as an accurate biomarker for diagnosis of myeloproliferative neoplasm, an important cause for mesenteric venous thrombosis. Anticoagulation is the treatment of choice for acute mesenteric venous thrombosis. Thrombolysis using systemic or transcatheter route is another option. Patients with peritoneal signs or refractory to initial measures require surgical exploration. Increasing recognition of mesenteric venous thrombosis and use of anticoagulation for treatment has resulted in reduction in the need for surgery with improvement in survival.
PubMed: 25755568
DOI: 10.1016/j.jceh.2014.03.052 -
Nefrologia : Publicacion Oficial de La... Nov 2017Vascular access for haemodialysis is key in renal patients both due to its associated morbidity and mortality and due to its impact on quality of life. The process, from...
Vascular access for haemodialysis is key in renal patients both due to its associated morbidity and mortality and due to its impact on quality of life. The process, from the creation and maintenance of vascular access to the treatment of its complications, represents a challenge when it comes to decision-making, due to the complexity of the existing disease and the diversity of the specialities involved. With a view to finding a common approach, the Spanish Multidisciplinary Group on Vascular Access (GEMAV), which includes experts from the five scientific societies involved (nephrology [S.E.N.], vascular surgery [SEACV], vascular and interventional radiology [SERAM-SERVEI], infectious diseases [SEIMC] and nephrology nursing [SEDEN]), along with the methodological support of the Cochrane Center, has updated the Guidelines on Vascular Access for Haemodialysis, published in 2005. These guidelines maintain a similar structure, in that they review the evidence without compromising the educational aspects. However, on one hand, they provide an update to methodology development following the guidelines of the GRADE system in order to translate this systematic review of evidence into recommendations that facilitate decision-making in routine clinical practice, and, on the other hand, the guidelines establish quality indicators which make it possible to monitor the quality of healthcare.
Topics: Aneurysm; Angioplasty; Antibiotic Prophylaxis; Arteriovenous Shunt, Surgical; Catheterization, Peripheral; Clinical Decision-Making; Constriction, Pathologic; Equipment Failure; Evidence-Based Medicine; Humans; Infection Control; Needles; Physical Examination; Renal Dialysis; Rheology; Spain; Thrombosis; Vascular Access Devices
PubMed: 29248052
DOI: 10.1016/j.nefro.2017.11.004 -
Cell Reports Feb 2022The metabolism of activated macrophages relies on aerobic glycolysis, while mitochondrial oxidation is disrupted. In lipopolysaccharide-activated macrophages, the...
The metabolism of activated macrophages relies on aerobic glycolysis, while mitochondrial oxidation is disrupted. In lipopolysaccharide-activated macrophages, the citrate carrier (CIC) exports citrate from mitochondria to enhance glycolytic genes through histone acetylation. CIC inhibition or Slc25a1 knockdown reduces the occupancy of H3K9ac to hypoxia-inducible factor-1α (HIF-1α) binding sites in promoters of glycolytic genes to restrain glycolysis. HIF-1α also transcriptionally upregulates immune-responsive gene 1 for itaconate production, which is inhibited by CIC blocking. Isotopic tracing of [U-C] glucose shows that CIC blockage prevents citrate accumulation and itaconate production by reducing glycolytic flux and facilitating metabolic flux in the TCA cycle. Isotopic tracing of [U-C] glutamine reveals that CIC inhibition reduces succinate accumulation from glutaminolysis and the gamma-aminobutyric acid shunt by enhancing mitochondrial oxidation. By restraining glycolysis, CIC inhibition increases NAD content to ensure mitochondrial biogenesis for oxidative phosphorylation. Furthermore, blockage of citrate export reduces cerebral thrombosis by inactivation of peripheral macrophages.
Topics: Acetylation; Animals; Biological Transport; Carrier Proteins; Citric Acid; Citric Acid Cycle; Histones; Hydro-Lyases; Hypoxia-Inducible Factor 1, alpha Subunit; Macrophage Activation; Macrophages; Mice, Inbred C57BL; Mitochondria; NAD; Organelle Biogenesis; Oxidation-Reduction; Succinates; Succinic Acid; Thrombosis; Transcription, Genetic; Zebrafish; Mice
PubMed: 35172156
DOI: 10.1016/j.celrep.2022.110391 -
Neurosurgical Review Apr 2022Ventriculoatrial shunts are the most common second-line procedure for cases in which ventriculoperitoneal shunts are unsuitable. Shunting-associated thrombosis is a... (Review)
Review
Ventriculoatrial shunts are the most common second-line procedure for cases in which ventriculoperitoneal shunts are unsuitable. Shunting-associated thrombosis is a potentially life-threatening complication after ventriculoatrial shunt insertion. The overall prevalence of this complication is still controversial because of substantial differences in the numbers found in studies using clinical data and in those analyzing postmortem findings. The etiology of thrombosis may be multifactorial, including shunt catheter itself, contents of cerebrospinal fluid, shunt infection, and genetic disorder. The clinical presentation can vary widely, ranging from asymptomatic to a life-threatening condition. Timely recognition of thromboembolic lesions is critical for treatment. However, early diagnosis and management is still challenging because of a relatively long asymptomatic latency and lack of clear guideline recommendations. The purpose of this review is to provide an overview of ventriculoatrial shunt thrombosis, especially to focus on its etiopathogenesis, diagnosis, treatment, and prevention.
Topics: Cerebrospinal Fluid Shunts; Humans; Hydrocephalus; Thromboembolism; Thrombosis; Ventriculoperitoneal Shunt
PubMed: 34647222
DOI: 10.1007/s10143-021-01656-5