scholarly journals Portal Vein Aneurysm Complicated by Thrombosis

2019 ◽  
Vol 26 (2) ◽  
pp. 71-76
Author(s):  
Doaa Faleh ◽  
Seraj Nadir Baeshin ◽  
Ghaida Ahmed Alzahrani ◽  
Hesham Tariq Nahhas ◽  
Nouri Abbas Abbas
Keyword(s):  
Portal Vein ◽  
Factor V Leiden ◽  
Factor V ◽  
Liver Pathology ◽  
Factor V Leiden Mutation ◽  
Portal Vein Aneurysm

The current study described a case of portal vein aneurysm at the confluence of the superior mesenteric and splenic veins, complicated by thrombosis in a patient with no liver pathology but with Factor V Leiden mutation.

Portal Vein Thrombosis Complicating Islet Transplantation in a Recipient with the Factor V Leiden Mutation

2004 ◽  
Vol 78 (1) ◽  
pp. 172-173 ◽  
Author(s):  
Daniel C. Brennan ◽  
M Brendan Shannon ◽  
Matthew J. Koch ◽  
Kenneth S. Polonsky ◽  
Niraj Desai ◽  
...  
Keyword(s):  
Portal Vein ◽  
Portal Vein Thrombosis ◽  
Islet Transplantation ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Vein Thrombosis

scholarly journals Utility of Thrombophilia Testing in Portal Vein Thrombosis in a Large Single Institutional Cohort

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 3646-3646
Author(s):  
Douglas Tremblay ◽  
Leonard Naymagon ◽  
Kevin Troy ◽  
Caroline Cromwell ◽  
Colleen Edwards ◽  
...  
Keyword(s):  
Portal Vein ◽  
Portal Vein Thrombosis ◽  
Clinical Management ◽  
Factor V Leiden ◽  
Antiphospholipid Antibody ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Vein Thrombosis ◽  
Mthfr Mutation ◽  
Thrombophilia Testing

Introduction: Patients with portal vein thrombosis (PVT) are frequently referred to hematology for hypercoagulable evaluation. The prevalence of identifiable thrombophilic conditions in patients with PVT is not well reported and the clinical impact of thrombophilia testing is unknown. Methods: We conducted a retrospective review of patients at a single tertiary care center. Patients were identified who had a documented PVT with or without concurrent thrombosis in additional splanchnic vessels, followed between 1/1/2000 and 5/1/2019 with at least 3-month follow-up available. Exclusion criteria included liver transplantation within 6 months of PVT and inadequate documentation. Changes in clinical management were determined by chart review and determination of documented change in choice, dose, or duration of anticoagulant, future thromboprophylaxis, or counseling of asymptomatic family members as documented in the medical chart. Results: Baseline characteristics of the entire cohort are summarized in Table 1. Five-hundred and forty-four unique patients were identified. Most patients had an isolated PVT (55.3%). The most common concurrent vessel thrombosed was the superior mesenteric vein (36.9%). Cirrhosis was the most common predisposing provoking condition, followed by recent abdominal surgery and inflammatory bowel disease. Of note, 106 patients (19.4%) had no identifiable underlying provoking factor. Two-hundred ninety-one patients (53.5%) had at least one hypercoagulable laboratory test performed, with a median number of 8 tests (Table 2). PAI-1 polymorphism was the most common positive thrombophilia test, followed by MTHFR mutation and an elevated homocysteine. Of note, these three test abnormalities have not been consistently linked to increased thrombotic potential. Identification of a JAK2 mutation was noted in 16.7% of patients tested and was detected in 37% of patients without a predisposing provoking factor prior to testing. No patients harbored a mutated CALR and MPL. In patients without a predisposing provoking factor who had thrombophilia testing performed (n=98), thrombophilia testing was positive in 59 patients (60.2%). Of note, 39 patients (40.0%) of these patients had a negative thrombophilia evaluation. In patients with thrombophilia testing (n=291), only 41 (14.1%) patients had a test result which impacted management. By far the most common positive-management altering test was JAK2 mutational testing, with 33 patients receiving further workup including a bone marrow biopsy and/or treatment of an underlying MPN as a result of testing. One patient who was diagnosed with paroxysmal nocturnal hemoglobinuria (PNH) received treatment with eculizumab. Two patients with antiphospholipid antibody syndrome were specifically administered coumadin as a result of testing. One patient with Factor V Leiden was anticoagulated for a longer duration, two received thromboprophylaxis during subsequent high-risk situations (which may have been done regardless of Factor V Leiden mutation), and one had screening performed on an asymptomatic family member. One patient with MTHFR mutation and elevated homocysteine received folate supplementation. Conclusions: These results demonstrate that nearly all hypercoagulable laboratory testing in patients with PVT is not of clinical utility. The most notable exception is JAK2 mutational testing, which appears to be an essential component in the workup of PVT without an obvious provoking factor both because of its relatively high frequency of occurrence and its significant impact on clinical management. In addition, while PNH and APLS are rarely positive in thrombophilia evaluation of PVT, they likely merit evaluation in appropriate clinical settings given their potential to meaningfully impact management. Extensive thrombophilia testing does not appear to reliably impact management. Disclosures Kremyanskaya: Incyte, Celgene, Constellation, Protagonist.: Research Funding; La Jolla: Consultancy.

scholarly journals Portal Thrombosis in Cirrhosis: Role of Thrombophilic Disorders

2020 ◽  
Vol 9 (9) ◽  
pp. 2822
Author(s):  
José Ignacio Fortea ◽  
Inés García Carrera ◽  
Ángela Puente ◽  
Antonio Cuadrado ◽  
Patricia Huelin ◽  
...  
Keyword(s):  
Portal Vein ◽  
Protein C ◽  
Mutational Analysis ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Jak2 V617f ◽  
Prothrombin G20210a ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Vein Thrombosis

In patients with liver cirrhosis the contribution of inherited and acquired prothrombotic disorders in the development of non-malignant portal vein thrombosis (PVT) is inconclusive. The purpose of this retrospective study was to examine the prevalence of thrombophilia in this setting at our center from January 2012 to November 2019. Tests included gene mutational analysis for Factor V Leiden, prothrombin G20210A, JAK2 (V617F), Calreticulin (CARL), in addition to activated protein C resistance, antithrombin III, protein C and S levels, and antiphospholipid antibodies. We included 77 patients, six of whom (7.8%) had a thrombophilic disorder: antiphospholipid syndrome in four patients, prothrombin gene mutation in one and factor V Leiden mutation in one. This latter patient had also been diagnosed with polycythemia vera years before PVT development. Complete thrombosis of the main portal vein and re-thrombosis after stopping anticoagulation were more frequent in patients with thrombophilia, but the rates of recanalization under anticoagulant therapy were similar among groups. No other difference was accounted between groups. The low prevalence of acquired and inherited thrombophilia found in patients with cirrhosis and PVT support testing for these disorders on an individual basis and avoiding universal screening to reduce costs and unwarranted testing.

Portal vein thrombosis in association with factor V Leiden mutation in a patient with hepatocellular carcinoma

1997 ◽  
Vol 29 (3) ◽  
pp. 224-225 ◽  
Author(s):  
Aytemiz Gürgey ◽  
Münever Büyükpamukcu ◽  
Canan Baskut ◽  
Bilgehan Yalcin ◽  
Safiye Gögüş
Keyword(s):  
Hepatocellular Carcinoma ◽  
Portal Vein ◽  
Portal Vein Thrombosis ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Vein Thrombosis

scholarly journals Prevalence of the factor V Leiden mutation in hepatic and portal vein thrombosis.

Gut ◽  
1997 ◽  
Vol 40 (6) ◽  
pp. 798-800 ◽  
Author(s):  
A E Mahmoud ◽  
E Elias ◽  
N Beauchamp ◽  
J T Wilde
Keyword(s):  
Portal Vein ◽  
Portal Vein Thrombosis ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Vein Thrombosis
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