• Advanced cirrhosis
• Ascites
• D-dimers

• Humans
• Fibrin Fibrinogen Degradation Products/analysis
• Fibrin Fibrinogen Degradation Products/metabolism
• Liver Cirrhosis/blood
• Liver Cirrhosis/complications
• Liver Cirrhosis/diagnosis
• Biomarkers/blood
• Venous Thromboembolism/blood
• Venous Thromboembolism/diagnosis
• Venous Thromboembolism/etiology
• Disseminated Intravascular Coagulation/diagnosis
• Disseminated Intravascular Coagulation/blood
• Disseminated Intravascular Coagulation/etiology

• Aggregometry
• Primary hemostasis
• Thrombin generation
• von Willebrand factor

• Humans
• Male
• Female
• Middle Aged
• Blood Platelets/metabolism
• Liver Cirrhosis/blood
• Platelet Function Tests/methods
• Platelet Aggregation
• Platelet Activation/physiology
• Aged
• P-Selectin/blood
• Adult
• Thrombin/metabolism
• Thrombin/analysis

• Incidence
• Liver cirrhosis
• Portal vein thrombosis
• Prevalence
• Risk factors

• Adrenergic beta-Antagonists/adverse effects
• Ascites/pathology
• Cross-Sectional Studies
• Humans
• Liver Cirrhosis/complications
• Liver Cirrhosis/epidemiology
• Portal Vein/pathology
• Prospective Studies
• Venous Thrombosis/complications

• Cirrhosis
• intervention
• narrative review
• portal vein thrombosis (PVT)

• Fibrin fibrinogen degradation products
• Liver cirrhosis
• Splanchnic circulation
• Systematic review
• Venous thrombosis

Rotational thromboelastometry (ROTEM) has been studied in patients with advanced chronic liver disease (ACLD) without considering the impact of portal hypertension. We evaluated the influence of the hepatic venous pressure gradient (HVPG) on ROTEM results in patients with ACLD.

Cross-sectional study; ACLD patients undergoing HVPG measurement within the prospective Vienna Cirrhosis Study (NCT03267615) underwent concomitant ROTEM testing.

Among 159 patients (68% male; Child–Pugh-A: 53%, Child–Pugh-B: 34%, Child–Pugh-C: 13%), 21 patients (13%) had a HVPG between 6 and 10 mmHg, 84 patients (53%) between 10 and 19 mmHg, and 54 patients (34%) ≥ 20 mmHg. Child–Pugh-C patients (vs. Child–Pugh-A and vs. Child–Pugh-B patients, respectively) showed longer clot formation time (CFT: median 187 s vs. 122 s vs. 122 s, p = 0.007) and lower maximum clot firmness (MCF: median: 45 mm vs. 56 mm vs. 56 mm, p = 0.002) in extrinsic thromboelastometry (EXTEM), while platelet counts were similar across Child–Pugh stages. In the overall cohort, ROTEM parameters did not differ by severity of portal hypertension. However, among compensated Child–Pugh-A patients, MCF decreased with increasing portal pressure, i.e. in higher HVPG strata (HVPG 9–10 mmHg: median MCF: 59 mm vs. HVPG 10–19 mmHg: 56 mm vs HVPG ≥ 20 mmHg: 54 mm, p = 0.023). Furthermore, patients with short CFT and high MCF in EXTEM had higher levels of lipopolysaccharide-binding protein, C-reactive protein, and procalcitonin, as well as higher leukocyte counts (all p < 0.05).

Portal hypertension seems to impact ROTEM results only in compensated Child–Pugh-A patients. Bacterial translocation and systemic inflammation may trigger a procoagulant state in patients with ACLD.

The online version of this article (10.1007/s12072-020-10093-3) contains supplementary material, which is available to authorized users.

• Ascites
• Bacterial translocation
• Cirrhosis
• Clinical
• Coagulation
• Hepatic
• Hepatic venous pressure gradient
• Inflammation
• Varices
• Viscoelastic test

Changes in primary hemostasis have been described in patients with chronic liver disease (CLD) and cirrhosis and are still subject to ongoing debate. Thrombocytopenia is common and multifactorial. Numerous studies also reported platelet dysfunction. In spite of these changes, primary hemostasis seems to be balanced. Patients with CLD and cirrhosis can suffer from both hemorrhagic and thrombotic complications. Variceal bleeding is the major hemorrhagic complication and is mainly determined by high portal pressure. Non portal hypertension-related bleeding due to hemostatic failure is uncommon. Thrombocytopenia can complicate management of invasive procedures in CLD patients. Recently, oral thrombopoietin agonists have been approved to raise platelets before invasive procedures. In this review we aim to bundle literature, published over the past decade, discussing primary hemostasis in CLD and cirrhosis including (1) platelet count and the role of thrombopoietin (TPO) agonists, (2) platelet function tests and markers of platelet activation, (3) von Willebrand factor and (4) global hemostasis tests.

• chronic liver disease
• cirrhosis
• platelet
• platelet function
• primary hemostasis
• von Willebrand factor

• cerebral vein thrombosis
• direct oral anticoagulants
• splanchnic vein thrombosis
• vitamin K antagonists

• coagulation, decompensated cirrhosis, fibrinolysis, hepatitis b virus, plasma d-dimer

• Adult
• Aged
• Biomarkers/blood
• Female
• Fibrin Fibrinogen Degradation Products/analysis
• Hepatitis B, Chronic/blood
• Hepatitis B, Chronic/complications
• Hepatitis B, Chronic/diagnosis
• Hepatitis B, Chronic/mortality
• Humans
• Liver Cirrhosis/blood
• Liver Cirrhosis/diagnosis
• Liver Cirrhosis/etiology
• Liver Cirrhosis/mortality
• Male
• Middle Aged
• Predictive Value of Tests
• Prognosis
• Retrospective Studies

Portal vein thrombosis (PVT) represents a well-known complication during the natural course of liver cirrhosis (LC), ranging from asymptomatic cases to life-threating conditions related to portal hypertension and hepatic decompensation. Portal flow stasis, complex acquired hypercoagulable disorders and exogenous factors leading to endothelial dysfunction have emerged as key factors for PVT development. However, PVT occurrence remains unpredictable and many issues regarding its natural history, prognostic significance and treatment are still elusive. In particular although spontaneous resolution or disease stability occur in most cases of PVT, factors predisposing to disease progression or recurrence after spontaneous recanalization are not clarified as yet. Moreover, PVT impact on LC outcome is still debated, as PVT may represent itself a consequence of liver fibrosis and hepatic dysfunction progression. Anticoagulation and transjugular intrahepatic portosystemic shunt are considered safe and effective in this setting and are recommended in selected cases, even if the safer therapeutic option and the optimal therapy duration are still unknown. Nevertheless, their impact on mortality rates should be addressed more extensively. In this review we present the most debated questions regarding PVT, whose answers should come from prospective cohort studies and large sample-size randomized trials.

• Portal vein thrombosis
• Liver cirrhosis
• Hypercoagulability
• Anticoagulation
• Direct oral anticoagulants

• Administration, Oral
• Anticoagulants/administration & dosage
• Anticoagulants/adverse effects
• Disease Progression
• Female
• Humans
• Hypertension, Portal/etiology
• Hypertension, Portal/mortality
• Hypertension, Portal/therapy
• Liver Cirrhosis/complications
• Liver Cirrhosis/mortality
• Liver Cirrhosis/therapy
• Patient Selection
• Portal Vein/pathology
• Portasystemic Shunt, Transjugular Intrahepatic
• Prognosis
• Prospective Studies
• Time Factors
• Treatment Outcome
• Venous Thrombosis/etiology
• Venous Thrombosis/mortality
• Venous Thrombosis/therapy

Portal vein thrombosis (PVT) is a frequent and serious complication in patients with liver cirrhosis (LC). Recently, a new classification of PVT was proposed, although the functional component was not completed included. The status of liver disease (compensated/decompensated) should be added to this classification. Reduced portal flow velocity and the acquired hypercoagulable status associated with LC are the main risk factors for PVT development, although endothelial dysfunction may play an important role that needs to be further evaluated. The European Association for the Study of the Liver and the American Association for the Study of Liver Disease recommend that the anticoagulant treatment should be consider in cirrhotic patients with PVT. Low molecular weight heparin and vitamin K antagonists proved their efficacy and relatively safety in PVT treatment, although in addition to recanalization rates, more complex end-points such as mortality and decompensation rate should be evaluated. The new oral anticoagulant therapies offers the advantage of oral administration in the absence of laboratory monitoring, however, there are a few reports regarding their use in cirrhotic patients, most of them referring to compensated isolated cases. Transjugular intrahepatic portosystemic shunt could be an alternative if thrombosis progresses despite anticoagulatant therapy and/or when PVT is associated with portal hypertension complications. The aim of this editorial is to discuss the different aspects of pathophysiology, clinical relevance, diagnosis and management of PVT in patients with LC.

• Portal vein thrombosis
• Liver cirrhosis
• Classification
• Risk factors
• Anticoagulation

• Administration, Oral
• Anticoagulants/administration & dosage
• Anticoagulants/therapeutic use
• Heparin, Low-Molecular-Weight/administration & dosage
• Heparin, Low-Molecular-Weight/therapeutic use
• Humans
• Hypertension, Portal/etiology
• Hypertension, Portal/therapy
• Liver Cirrhosis/complications
• Portal Vein
• Portasystemic Shunt, Transjugular Intrahepatic
• Severity of Illness Index
• Venous Thrombosis/classification
• Venous Thrombosis/diagnosis
• Venous Thrombosis/etiology
• Venous Thrombosis/therapy
• Vitamin K/antagonists & inhibitors

• D-dimer
• coagulation
• complications
• liver transplant
• thrombosis

• Liver cirrhosis
• ascites
• bacterial translocation
• dysbiosis
• gut microbiota
• hepatic encephalopathy
• immune-inflammatory disorder
• inflammation
• intestinal permeability
• portal hypertension

Portal vein thrombosis (PVT) is a frequent complication in cirrhosis and its prevalence increases with disease severity. Several factors are involved in the development and progression of PVT. The challenge for the management of PVT is the precise evaluation of the bleeding risk as opposed to life-threatening extension of thrombosis. Nevertheless, the impact on the progression and outcome of liver disease is unclear. A critical evaluation of the available data discloses that treating PVT in cirrhotics is safe and effective. However, there are open issues, such as which anticoagulant could represent a safer therapeutic option, and when and for how long this treatment should be administered to cirrhotic patients with PVT.

• Portal vein thrombosis
• anticoagulants
• bleeding
• cirrhosis
• direct oral anticoagulants

• Cirrhosis
• Endotoxin
• Factor VIII
• Hypercoagulability
• LPS
• von Willebrand factor