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Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients with and Without Cirrhosis Nicolas M

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Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients with and Without Cirrhosis Nicolas M Gastroenterology 2019;156:1582–1599 PERSPECTIVES REVIEWS AND REVIEWS IN BASIC AND CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Douglas J. Robertson and Vincent W. Yang, Section Editors Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients With and Without Cirrhosis Nicolas M. Intagliata,1 Stephen H. Caldwell,1 and Armando Tripodi2 1Division of Gastroenterology and Hepatology, University of Virginia Medical CenterCharlottesville, Virginia; and 2Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Cà Granda Ospedale Maggiore Policlinico, Angelo Bianchi Bonomi Hemophilia and Thrombosis Center and Fondazione Luigi Villa, Milano, Italy Portal vein thrombosis unrelated to solid malignancy is also central to estimating prognosis and to aid therapeutic common in patients with cirrhosis, but less frequently decision-making. observed in patients without cirrhosis. Prompt diagnosis and management of acute symptomatic portal vein throm- bosis are essential. Failure to detect and treat thromboses Pathophysiology and Risk Factors of can result in mesenteric ischemia, chronic cavernous Cirrhotic and Non-Cirrhotic Portal Vein transformation, and complications of portal hypertension. Thrombosis In patients with cirrhosis, development of portal vein The low-pressure, slow-flow, and high-volume hemody- thrombosis is often insidious and remains undetected until its incidental detection. Management of portal vein throm- namics of the portal venous system results in a unique bosis in patients with cirrhosis is more controversial. vascular environment. All venous thromboses are ’ — However, there are data to support treatment of specific multifactorial due to components of Virchow s triad patients with anticoagulation agents. We review the com- hypercoagulability, endothelial injury, and reduced blood mon and distinct features of portal vein thromboses in pa- flow. Dominant risks for PVT in patients with or without tients without liver tumors, with and without cirrhosis. cirrhosis can be broadly classified into risks arising from local or systemic processes (Table 1). In patients without cirrhosis, a systemic hypercoagulable Keywords: Hepatic; Therapy; Fibrosis; Anticoagulation. state is often implicated in PVT.5,6 Local risk factors in this setting include malignancy, intra-abdominal infections, abdominal trauma, and intra-abdominal surgery (eg, sple- istorically, clinicians in the late 19th and early 20th nectomy). In patients with cirrhosis, development of PVT is H century recognized the association of portal vein closely associated with static portal blood flow from thrombosis (PVT) with a variety of disorders, including advancing PH, coupled with spontaneous development of cirrhosis and portal hypertension (PH), malignancy, intra- portosystemic shunts. PV velocity is associated with risk of abdominal infection, and as a sequela of abdominal sur- PVT in cirrhosis and consequently as patients develop – gery.1 3 The liver has a unique circulatory system evolved to advancing PH, thrombosis becomes more likely.7 Other local protect against ischemic injury. However, when portal blood inciting factors common to cirrhosis (eg, infection, surgery, flow is impeded, considerable consequences can ensue or large portosystemic shunts) can enhance this risk. (Figure 1). At the sinusoidal level, deprivation of blood flow from portal venous microthrombi is proposed as a cause of Biology of Hypercoagulability in Portal Vein fi 4 brosis, organ atrophy, and PH. Termed parenchymal Thrombosis extinction, this concept emphasizes the consequences of Thrombophilia defines a condition characterized by ischemia to the liver from interruption of blood flow via the inherited or acquired hypercoagulability secondary to splanchnic mesenteric veins. Non-tumoral thrombosis of the PV and associated splanchnic tributaries can occur from a variety of underly- ing etiologies, including PH, hypercoagulability, and vascular Abbreviations used in this paper: CT, computed tomography; DOAC, endothelial injury (Table 1). At initial diagnosis, it is direct-acting oral anticoagulant; EASL, European Association for the Study of Liver Disease; FVIII, factor VIII; LMWH, low-molecular-weight important to distinguish between the common cirrhosis- heparin; MPN, myeloproliferative neoplasm; MRI, magnetic resonance related PVT and the uncommon non-cirrhotic PVT. This imaging; PC, protein C; PH, portal hypertension; PS, protein S; PVT, portal vein thrombosis; TIPS, transjugular intrahepatic portosystemic shunt; US, distinction is critical, as the evaluation, prognosis, and ultrasound; VKA, vitamin K antagonist. treatment are different. Careful evaluation for associated Most current article primary hepatic malignancy is essential. Establishing the © 2019 by the AGA Institute timing of thrombosis (acute vs chronic) and the anatomical 0016-5085/$36.00 extent within the splanchnic mesenteric venous system are https://doi.org/10.1053/j.gastro.2019.01.265 May 2019 PVT in Patients With and Without Cirrhosis 1583 REVIEWS AND PERSPECTIVES Figure 1. Types of portal vein thrombosis. hemostasis defects leading to venous (rarely arterial) throm- demonstrated by in vitro thrombin generation studies.19–21 bosis. Hypercoagulability is evident in both non-cirrhotic and This balance is mainly due to decreased levels of PC and cirrhotic PVT, but is often dominated by different pathways. increased levels of factor VIII (FVIII).19,22,23 Activated PC is Inherited genetic mutations, such as factor V Leiden and the physiological inhibitor to FVIII, the latter being the most prothrombin gene G20210A polymorphisms are more potent driver of thrombin generation. Therefore, high common in patients with both cirrhotic8,9 and non-cirrhotic levels of FVIII, low levels of PC, and the FVIII/PC ratio are an PVT.10,11 These common mutations are relatively weak index of hypercoagulability in cirrhosis. These changes are pro-coagulant factors compared to inherited deficiencies of associated with unfavorable outcome in patients with anticoagulant factors, such as antithrombin, protein C (PC), cirrhosis.24 Furthermore, patients with cirrhosis who are and protein S (PS). Among acquired thrombophilic condi- resistant to the anticoagulant action of thrombomodulin tions, the anti-phospholipid syndrome is characterized by (in vitro) are more likely to develop de novo PVT.25 persistent positivity of lupus anticoagulant and/or solid- Thrombophilia may occur via other mechanisms, phase antibodies to cardiolipin or b2-glycoprotein-I.12 including increased levels of circulating cell-derived micro- Deficiencies of the naturally occurring anticoagulants,13 particles containing negatively charged phospholipids or high levels of procoagulant factors,14 or the presence of tissue factor derived from the parent cells (eg, platelets or – the anti-phospholipid syndrome15 17 in patients with PVT monocytes). In addition, activated neutrophils in areas are reported. However, the phenotypic activity of naturally of inflammation cause release of neutrophil external traps occurring anticoagulants cannot be easily measured in that can increase thrombin generation without affecting cirrhotic PVT due to impaired synthetic capacity of the liver. levels of the pro- or anticoagulant factors.26,27 Neutrophil Similarly, tests of lupus anticoagulants in anti-phospholipid external traps have been associated with increased risk of syndrome may be prolonged beyond the upper limit of the thrombosis in both non-cirrhotic subjects28,29 and in reference range in cirrhosis. Moreover, the solid-phase an- cirrhosis.30 High levels of gut-derived bacterial lipopolysac- tibodies to cardiolipin or b2-glycoprotein-I have been charide are common in cirrhosis and could also contribute to measured only sporadically in patients with PVT and not hypercoagulability31 and platelet hyperactivity.32 according to the most recent standards.18 Thus, these Isolated assessment of any of the individual components associations remain uncertain. of the Virchow’s triad is insufficient to entirely define Evidence is accumulating that the rebalanced hemostasis individual risk.25 Nonetheless, there are shared features system in cirrhosis is prone to hypercoagulability, as between cirrhotic and non-cirrhotic PVT beyond anatomical 1584 Intagliata et al Gastroenterology Vol. 156, No. 6 Table 1.Risk Factors for Portal Vein Thrombosis PERSPECTIVES REVIEWS AND Common risk factors in non-cirrhotic PVTa Common risk factors in cirrhosis PVTb Systemic disorder (approximately 50%–60% of cases) Systemic disorder MPNsa (polycythemia vera, essential thrombocytemia, primary Advanced portal hypertension with reduced portal flow velocity myelofibrosis) Steal syndrome from large spontaneous portosystemic shunts JAK2 V617F mutation Malignancy Malignancy Inherited thrombophiliab Inherited thrombophilia Factor V Leiden Factor V Leiden Prothrombin gene G20210A mutation Prothrombin gene G20210A mutationa Acquired thrombophilia Protein C and S deficiency Increased Factor VIII Antithrombin deficiency Protein C and S deficiency, antithrombin deficiency Acquired thrombophilia Other systemic risk factors Antiphospholipid syndromea Non-alcohol steatohepatitis Paroxysmal nocturnal hemoglobinuria Other extrinsic factors Other systemic risk factors Local Autoimmune disease and vasculitis Abdominal malignancy (HCC) Inflammatory bowel disease Intrabdominal surgery (hepatectomy, surgical shunt) Pregnancy Local regional therapy for HCC (TACE, radioembolization) Exogenous hormone supplementation TIPS Local (approximately 20%–25%
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