Tamoxifen-associated portal vein thrombosis causing severe oesophageal variceal bleeding.
Ontology highlight
ABSTRACT:
SUBMITTER: Hsu A
PROVIDER: S-EPMC4693120 | biostudies-other | 2015 Aug
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion.
| S-EPMC4415192 | biostudies-other
Project description:BackgroundPortal vein thrombosis (PVT) would exert a further increase in resistance to portal blood flow, resulting in worsening portal hypertension and poor outcome. This study aimed to identify risk factors and develop an clinically applicable dynamic nomogram predicting the occurrence of PVT in cirrhotic patients during primary prophylaxis for variveal hemorrhage (VH).MethodsThe multi-center retrospective study enrolled cirrhotic patients with high-risk varices, which were further divided into training and validation cohorts for 3 years follow-up. A dynamic nomogram based on the Cox proportional hazard regression model was developed with the cutoff value calculated by X-title analysis. The performance of the nomogram was evaluated with Harrell's concordance index (C-index), calibration curve and decision curve analysis.Results91 (34.0%) of the whole cohort were diagnosed with PVT during 3-year follow-up. Variables including carvedilol (P < 0.001), low portal vein velocity (P < 0.001), increased size of esophageal varices (P = 0.005), and high HbA1c (P < 0.001) and procalcitonin (P = 0.015) were identified to be independently associated with PVT, which were further incorporated into the dynamic nomogram with optimal cutoff (8.8 and 14.6) for risk-stratification. The C-indexes (0.894 of internal validation and 0.892 of external validation) and calibration curves demonstrated ideal discrimination and calibration. The thresholds for more reasonable application of the nomogram were 0-0.27, 0-0.66, and 0.04-1.00 at 1, 2, and 3-year, respectively.ConclusionThe dynamic nomogram could be accurately and reliably used for clinical risk-stratification of PVT in cirrhotic patients during primary prophylaxis for VH.
| S-EPMC9203843 | biostudies-literature
Project description: Not available
| S-EPMC10659130 | biostudies-literature
Project description:The rapid global spread as well as the mortality and morbidity associated with COVID-19 has raised increasing concern around the globe. Studies have reported that patients infected with the novel coronavirus are prone to coagulopathy. However, information on portal vein thrombosis in patients with COVID-19 is scarce. In this case report, we depict the abdominal CT findings of a 26-year-old male patient with COVID-19 who developed severe abdominal pain during hospitalization and was later diagnosed with portal vein thrombosis. We also demonstrate the chest CT findings of the same patient, which revealed bilateral pleural effusion, a less common imaging finding, and multifocal patchy consolidations. This paper emphasizes that physicians, particularly radiologists, should be aware of thromboembolic events when examining any suspected patient during the current outbreak.
| S-EPMC7465749 | biostudies-literature
Project description:We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, -0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD40L (Spearman's rank correlation coefficient [rs ], -0.33; P < 0.001), sNox2-dp (rs , -0.57; P < 0.0001), and urinary excretion of isoprostanes (rs, -0.48; P < 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2α-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation.
| S-EPMC6442692 | biostudies-literature
Project description: Not available
| S-EPMC8094621 | biostudies-literature
Project description:A 73-year-old woman with portal vein stenosis caused by tumor recurrence after pancreatoduodenectomy was treated with stent placement without embolization of the jejunal varix. Anticoagulation therapy using heparin followed by rivaroxaban was administered after the procedure. She continued to receive systemic chemotherapy as an outpatient. Neither restenosis nor stent thrombosis was observed after 7 months. Based on the presented case and literature review, portal vein stenting is an effective treatment option for jejunal variceal bleeding caused by malignant portal venous stricture after pancreaticoduodenectomy. Antithrombotic therapy following portal venous stenting is required to prevent stent thrombosis in the majority of cases, although it has a risk of inducing recurrent variceal bleeding. Adjunctive jejunal variceal embolization can possibly be omitted in selected cases to obtain sufficient portal-SMV flow reconstruction.
| S-EPMC9327411 | biostudies-literature
Project description:Portal vein thrombosis (PVT) is associated with inferior pretransplantation and posttransplantation outcomes. We aimed to create a predictive model to risk stratify transplant candidates for PVT. Data on adult transplants in the United States during the Model for End-Stage Liver Disease (MELD) era through September 2016 were reviewed. We constructed and validated a scoring system composed of routine, readily available clinical information to predict the development of incident PVT at 12 months from transplantation listing. A total of 66,568 liver transplant candidates were dichotomized into 2 groups to construct (n = 34,751) and validate (n = 31,817) a scoring system. In general, the derivation and validation cohorts were clinically similar. Although nonalcoholic steatohepatitis was a significant predictor of incident PVT (hazard ratio, 1.29; 95% confidence interval, 1.08-1.54; P < 0.001), age, MELD score, and moderate-to-severe ascites were also associated with increased risk. African American race was associated with decreased risk. A scoring system (PVT risk index [RI]) of these 5 variables had an area under the curve of 0.71 and 0.70 in both derivation and validation cohorts, respectively. By applying the low cutoff score of 2.6, incident PVT could be accurately excluded (negative predictive value 94%). Using the high cutoff score of 4.6 (positive predictive value 85%), PVT could be diagnosed with high accuracy. The PVT-RI predicts which candidates awaiting lifesaving liver transplantation will and will not develop future PVT. Although this scoring system will require prospective validation, it provides a powerful new tool for the clinician when risk stratifying cirrhosis patients prior to liver transplantation for future PVT development.
| S-EPMC6864229 | biostudies-literature
Project description:BackgroundWell-defined guidelines for the treatment of portal vein thrombosis (PVT) in patients with cirrhosis are lacking, given the paucity of robust data. Among the available treatment options the best choice is unknown.MethodsWe conducted a comprehensive search of multiple electronic databases and conference proceedings (through December 2019) to identify studies that reported on the use of anticoagulants in the treatment of PVT in patients with cirrhosis. Our goals were to evaluate the pooled odds ratio (OR) and pooled rate of treatment responders and bleeding events.ResultsA total of 17 studies were included: 648 patients were treated with anticoagulation and 96 were controls. Pooled OR for treatment responders was 5.1 (95% confidence interval [CI] 2.5-10.2, P = 0.001) and pooled OR for bleeding was 0.4 (95%CI 0.1-1.5, P = 0.2) for anticoagulation treatment versus control. Pooled rate of treatment responders with anticoagulation was 66.7% (95%CI 58.3-74.1) compared to 26% (95%CI 14.2-42.7) for the control group. Pooled rate of bleeding seemed comparable (7.8%, 95%CI 4.5-13.3, and 15.4%, 95%CI 4.3-42.7). On subgroup analysis, pooled rates of treatment responders and bleeding events seemed similar between low molecular weight heparin, vitamin K antagonists, and direct oral anticoagulants.ConclusionsOur study demonstrated that anticoagulation is effective and safe in the treatment of PVT in patients with cirrhosis. Owing to the comparable outcomes, direct oral anticoagulants may be considered as first-line treatment, depending on patient preferences.
| S-EPMC7406805 | biostudies-literature
Project description:COVID-19-associated coagulopathy (CAC), mainly characterized by hypercoagulability leading to micro- and macrovascular thrombotic events due to the fibrinolysis shutdown phenomenon, is a life-threatening complication of severe SARS-CoV-2 infection. However, optimal criteria to assess patients with the highest risk for progression of severe CAC are still unclear. Bedside point-of-care viscoelastic testing (VET) appears to be a promising tool to recognize CAC, to support the appropriate therapeutic decisions, and to monitor the efficacy of the treatment. The ClotPro VET has the potential to reveal fibrinolysis resistance indicated by a clot lysis time (LT) > 300 s on the TPA-test. We present a case of severe SARS-CoV-2 infection complicated by CAC-resulting portal vein thrombosis (PVT) and subsequent liver failure despite therapeutic anticoagulation. Since fibrinolysis shutdown (LT > 755 s) caused PVT, we performed a targeted systemic fibrinolytic therapy. We monitored the efficacy of the treatment with repeated TPA assays every three hours, while the dose of recombinant plasminogen activator (rtPA) was adjusted until fibrinolysis shutdown completely resolved and portal vein patency was confirmed by an ultrasound examination. Our case report highlights the importance of VET-guided personalized therapeutic approach during the care of severely ill COVID-19 patients, in order to appropriately treat CAC.
| S-EPMC10525483 | biostudies-literature