Liver cirrhosis complicated by portal vein thrombosis (PVT) is a fatal complication with no specific manifestations but often misdiagnosed, it crucially increases the mortality worldwide. This study aimed to identify risk factors and establish a predictive model for diagnosis of venous thrombosis clinical by routine blood tests and endoscopic characteristics.

Patients from Gansu Provincial Hospital from October 2019 to December 2023 were enrolled. The retrospective modelling cohort was screened by propensity score matching (PSM) at a 1:1 ratio from the baseline characteristics before endoscopic diagnosis. Variables were collected from blood test and endoscopic signs using machine learning method (ML). Logistic regression determined risk factors. The predictive performance was evaluated by receiver operation curve (ROC), calibration curve, clinical decision analysis (DCA) and influence curve (CIC). Furthermore, external cohort was used for validation, an online nomogram was established.

A total of 1,058 patients were enrolled, and 470 patients were included after PSM 1: 1. The model identified 7 factors, including splenectomy, blood urea nitrogen (BUN), serum sodium, activated partial thromboplastin time (APTT), thrombin time (TT), D-dimer, and degree of oesophageal varices. The area under the curve (AUC) was 0.907 (95% CI, 0.877-0.931). The calibration curve, decision and clinical impact curves showed the model demonstrated a good predictive accuracy and clinical benefits. The validation got an AUC of 0.890 (95% CI, 0.831-0.934), A nomogram tool was finally established for application.

Blood test combined endoscopic characters could preliminarily predict the liver cirrhosis with portal vein thrombosis for cirrhotic patients undergoing endoscopic examination.

The clinical utility of thrombomodulin-modified thrombin generation (TM-TG) in cirrhosis is uncertain. We conducted a prospective study to evaluate the prognostic value of TM-TG in cirrhosis.

Patients were recruited during outpatient clinics (compensated and stable decompensated cirrhosis) or if admitted to our inpatient service (acutely decompensated cirrhosis). We performed whole blood (WB) and platelet-poor plasma (PPP) TM-TG at recruitment. All patients were prospectively followed-up for bleeding/thrombosis, hepatic decompensation, and liver-related death.

We included 231 patients: 80 with compensated, 70 with stable decompensated, and 81 with acutely decompensated cirrhosis. Median follow-up was 414 days (range: 77-668). Eleven patients, all with acutely decompensated cirrhosis, experienced procedure-related bleeding. Both WB-TG and PPP-TG were more altered in bleeding vs. non-bleeding individuals (lower endogenous thrombin potential [ETP] and peak-height). However, only WB-TG could identify - at the individual patient level - those experiencing major bleeding (all having pre-procedural ETP <350 nmol/L∗min). In acutely decompensated cirrhosis, the AUC of WB-TG ETP for bleeding was 0.854 (95% CI 0.732-0.976), which was higher than that of PPP-TG ETP (0.676; 95% CI 0.524-0.809). Neither WB-TG nor PPP-TG could predict development of thrombosis, mostly portal vein thrombosis (n = 15). In compensated cirrhosis, WB-TG and PPP-TG were comparable between patients who experienced decompensation and those who did not. In decompensated cirrhosis, WB-TG and PPP-TG were more significantly altered in patients experiencing further decompensation/ACLF/liver-related death. A higher WB-TG ETP was linked to a lower risk of progression independently of MELD, Child-Pugh, and C-reactive protein (hazard ratio 0.4, 95% CI 0.21-0.79, p <0.01).

In compensated cirrhosis, WB-TG and PPP-TG do not improve risk stratification. In decompensated cirrhosis, WB-TG may be a promising tool for estimating procedure-related bleeding risk.

Thrombomodulin-modified thrombin generation (TM-TG) in cirrhosis is a well-established research tool to assess the complex coagulopathy of cirrhosis; however, its clinical utility is uncertain. In acutely decompensated cirrhosis, a TM-modified whole blood (WB)-TG ETP <350 nmol/L∗min predicted major bleeding after invasive procedures, whereas platelet-poor plasma TG indicated a hypo-coagulable state in bleeding patients but could not identify those at risk. Neither WB-TG nor platelet-poor plasma-TG could predict development of portal vein thrombosis, which was predicted by cirrhosis and portal hypertension severity. In decompensated cirrhosis, a better WB-TG capacity was associated with a lower risk of further decompensation, acute-on-chronic liver failure, and liver-related death independently of MELD score/Child-Pugh stage and C-reactive protein.

Thrombophilia is characterized by a hypercoagulable state that predisposes individuals to venous and arterial thrombotic events, posing significant challenges for clinical evaluation and management. This narrative review critically examines the current landscape of thrombophilia testing, focusing on the utility and limitations of both circulating and genetic biomarkers. Circulating biomarkers-such as D-dimer, antithrombin, protein C, and protein S-offer dynamic insights into the coagulation process yet often suffer from low specificity in varied clinical settings. In contrast, genetic biomarkers, notably Factor V Leiden and the prothrombin G20210A mutation, provide stable risk stratification but are limited by their low prevalence in the general population. Emerging markers, including selectins, Factor VIII, Factor XI, neutrophil extracellular traps, and extracellular vesicles, are also discussed for their potential to refine thrombotic risk assessment. By integrating evidence-based guidelines from international health organizations, this review underscores the need for a personalized approach to thrombophilia evaluation that balances comprehensive risk assessment with the avoidance of over-testing. Such an approach is crucial for optimizing patient outcomes and informing the duration and intensity of anticoagulant therapy.

The exact pathophysiology of portal vein thrombosis (PVT), a common complication of cirrhosis, remains largely unknown. We previously found that cirrhotic PVT consists of fibrotic intimal thickening of the portal vein wall rather than of true fibrin-rich thrombus. We hypothesized that this intimal thickening of portal vein is secondary to portal hypertension and/or to local inflammatory responses.

To investigate the portal vein intimal thickness in cirrhotic patients, and its relationship with clinical and laboratory parameters associated with portal hypertension and inflammation.

The intimal thickness of right and left portal branches was measured in hilar liver samples from 232 cirrhotic patients without PVT who underwent liver transplantation. The relation between intimal thickness and pretransplant clinical variables was studied with linear regression. Computed tomography scans of 25 patients prior to liver transplantation were reanalyzed for portal vein and portal hypertension related characteristics.

Median right intimal thickness was 129 (1-300 [IQR]) μm; median left intimal thickness was 112 (1-230) μm, and there was a correlation between the intimal thickness of the right and left branches in individual patients (r = 0.30, P < .001). Intimal thickness of the portal vein was associated with a history of variceal bleeding, hepatic encephalopathy or ascites, etiology of disease, and statin use. Other factors, including duration of liver disease, presence of infection, or radiological characteristics were not significantly associated with intimal thickness.

Intrahepatic portal vein intimal thickness is highly variable in patients with cirrhosis, but relatively consistent between right and left portal branches. The association between intimal thickness and history of variceal bleeding suggests that portal hypertension may contribute to initiation of intimal thickening, and consequently to the development of PVT.

Portal vein thromboses (PVT) is a common clotting disorder that can be seen in patients with and without cirrhosis. There are no current clinical guidelines on management of portal vein thromboses in these two distinct populations given most studies are retrospective and comprised of heterogenous cohorts.

When evaluating PVT, patients must first be stratified into those with cirrhosis and those without cirrhosis. In addition, a novel nomenclature can help categorize specific PVT types and determine the need and response to anticoagulation. The management of PVT in patients with cirrhosis varies and is primarily dependent on whether the PVT is recent or chronic. In contrast, patients without cirrhosis are almost always anticoagulated to avoid complications of PVT. Direct oral anticoagulants, low-molecular weight heparin, and vitamin-K antagonists have all been used in patients with and without cirrhosis, without clear guidance on optimal treatment duration and surveillance.

Direct oral anticoagulants are increasingly used for patients with PVT though there is limited data on the safety and efficacy of these medications. The risk/benefit profiles of various anticoagulants must be considered when choosing a therapeutic anticoagulant. There are ongoing studies evaluating outcome measures of different anticoagulants in patients with PVT. Large, multicenter, randomized controlled trials may help elucidate the efficacy of anticoagulants on various outcome measures in PVT, including recanalization, bleeding, and survival.

Two main stages are differentiated in patients with advanced chronic liver disease (ACLD), one compensated (cACLD) with an excellent prognosis, and the other decompensated (dACLD), defined by the appearance of complications (ascites, variceal bleeding and hepatic encephalopathy) and associated with high mortality. Preventing the progression to dACLD might dramatically improve prognosis and reduce the burden of care associated with ACLD. Portal hypertension is a major driver of the transition from cACLD to dACLD, and a portal pressure of ≥10 mmHg defines clinically significant portal hypertension (CSPH) as the threshold from which decompensating events may occur. In recent years, innovative studies have provided evidence supporting new strategies to prevent decompensation in cACLD. These studies have yielded major advances, including the development of noninvasive tests (NITs) to identify patients with CSPH with reasonable confidence, the demonstration that aetiological therapies can prevent disease progression and even achieve regression of cirrhosis, and the finding that non-selective β-blockers can effectively prevent decompensation in patients with cACLD and CSPH, mainly by reducing the risk of ascites, the most frequent decompensating event. Here, we review the evidence supporting new strategies to manage cACLD to prevent decompensation and the caveats for their implementation, from patient selection using NITs to ancillary therapies.

Portal vein thrombosis (PVT) is a common complication in patients with end-stage liver disease (ESLD). The portal vein in patients with ESLD is proposedly an inflammatory vascular bed due to translocation of endotoxins and cytokines from the gut. We hypothesized that a proinflammatory gut microbiome and elevated trimethylamine N-oxide (TMAO), a driver of thrombosis, may contribute to PVT development.

We investigated whether gut microbiome diversity, bacterial species, metabolic pathways, and TMAO levels are associated with PVT in patients with ESLD.

Fecal samples, plasma samples, and data from patients with ESLD and healthy controls were collected through the TransplantLines Biobank and Cohort Study. PVT was defined as a thrombus in the portal vein within a year prior to or after fecal sample collection. Fecal samples were analyzed using Shotgun Metagenomic Sequencing, and TMAO levels were measured in plasma using a Vantera Clinical Analyzer.

One hundred two patients with ESLD, of which 23 with PVT, and 246 healthy controls were included. No significant difference in gut microbiome diversity was found between patients with PVT and without PVT (P = .18). Both ESLD groups had significantly lower alpha diversity than controls. Bacteroides fragilis and 3 Clostridiales species were increased in patients with PVT compared with without PVT. TMAO levels between the 3 groups were not significantly different.

We observed profound differences in gut microbiota between patients with ESLD and controls, but minimal differences between patients with ESLD with or without PVT. In our cohort, a gut-derived proinflammatory state was not associated with presence of PVT in patients with ESLD.

Von Willebrand factor (vWF) plays a key role in hemostasis and is reported to be related to the outcome of advanced chronic liver disease. The present study aimed to investigate the relationship between vWF and other potential variables and portal vein thrombosis (PVT) in patients with decompensated cirrhosis.

Consecutive cirrhotic patients with gastroesophageal varices were admitted to our hospital between January 2020 and September 2022. Patients were prospectively recruited and divided into PVT and non-PVT groups. We collected clinical tests, biochemical tests, coagulation tests, and hemostatic protein profile data to explore the associated factors of PVT.

A total of 128 patients were enrolled including 60 patients with PVT and 68 patients without PVT. Plasma levels of vWF [odds ratio (OR) = 1.015, 95% confidence interval (CI): 1.005-1.025, P = 0.005], D-dimer (OR = 1.967, 95% CI: 1.141-3.389, P = 0.015), and decreased portal vein velocity (PVV) (OR = 0.852, 95% CI: 0.769-0.944, P = 0.002) were the variables independently associated with the existence of PVT. Area under the curve (AUC) analyses for vWF, D-dimer, and PVV were 0.779, 0.848, and 0.832, respectively. A nomogram model was established involving the three parameters, and the AUC was 0.919 (95% CI: 0.869-0.969). In the internal validation using bootstrap, the AUC was 0.919 (95% CI: 0.868-0.970).

Higher vWF levels were related to PVT in patients with decompensated cirrhosis, indicating that vWF might serve as a relevant factor for PVT, and a nomogram containing vWF, D-dimer, and PVV could be an important tool for PVT identification in cirrhotic patients.

Portal vein thrombosis (PVT) is associated with increased mortality post-transplant, but treatment of the clot is not definitively associated with improvement in mortality. We aimed to assess the effect of anticoagulation (AC), transjugular intrahepatic portosystemic shunt (TIPS), or best supportive care only (SCO) as treatment options in patients with PVT and cirrhosis.

This was a retrospective controlled cohort study from a large urban health system. Patients with cirrhosis and PVT were identified and analyzed based on treatment provided (1) AC, (2) TIPS, and (3) SCO. Outcomes included patent portal vein at the end of follow-up and overall mortality.

150 patients on AC, 93 who underwent TIPS, and 172 who received SCO were analyzed. Final portal vein (PV) patency was not significantly different by treatment group in those with partial obstruction at presentation (p = 0.64), while any treatment improved final patency over SCO in those presenting with complete obstruction (p = 0.01). Rate of survival, transplant-free survival, and successful liver transplantation were not different between treatment groups.

In our cohorts, treatment of PVT versus SCO showed no impact on survival in those presenting with partial obstruction of the PV. In those with complete obstruction, any treatment was more effective than SCO in achieving patency of the PV, but overall survival was no different. PVT may not be a pathologic mechanism that causes worsening of liver disease but may be an event in the progression that in itself is not directly responsible for worsening liver function.

Splanchnic vein thrombosis (SpVT) is an uncommon site of venous thrombosis that is associated with complications including portal hypertension and hepatic dysfunction. The evaluation and management of this patient population has evolved in recent years, but there are limited data from clinical trials to guide management. Given the various acquired and biologic risk factors leading to the development of SpVT and the potential complications that can arise from it, input from a multidisciplinary team can be valuable in managing such patients, including thrombosis specialists or hematologists, gastroenterologists or hepatologists, interventional radiologists, and surgeons. In this article, we present 4 cases that highlight important issues and considerations in the evaluation of SpVT, including initial diagnostic approach in a patient with a new diagnosis of SpVT, considerations for anticoagulant therapy, management of SpVT in patients with myeloproliferative neoplasms, and the role of interventional vascular procedures in the management of SpVT. By reviewing the current literature, we address clinically relevant questions that are posed to clinicians managing patients with SpVT; we also point out gaps in our current knowledge that merit future investigation.

Portal vein thromboses (PVTs) are common in patients with cirrhosis and are associated with advanced portal hypertension and mortality. The treatment of PVTs remains a clinical challenge due to limited evidence and competing risks of PVT-associated complications vs bleeding risk of anticoagulation. Significant heterogeneity in PVT phenotype based on anatomic, host, and disease characteristics, and an emerging spectrum of therapeutic options further complicate PVT management. This Clinical Practice Update (CPU) aims to provide best practice advice for the evaluation and management of PVT in cirrhosis, including the role of direct oral anticoagulants and endovascular interventions.

This expert review was commissioned and approved by the American Gastroenterological Association (AGA) Institute CPU Committee and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership, and underwent internal peer review by the CPU Committee and external peer review through standard procedures of Gastroenterology. These Best Practice Advice statements were drawn from a review of the published literature and from expert opinion. Because systematic reviews were not performed, these Best Practice Advice statements do not carry formal ratings regarding the quality of evidence or strength of the presented considerations. Best Practice Advice Statements BEST PRACTICE ADVICE 1: Asymptomatic patients with compensated cirrhosis do not require routine screening for PVT. BEST PRACTICE ADVICE 2: Patients with cirrhosis with PVTs identified on Doppler ultrasound should undergo cross-sectional imaging with computed tomography or magnetic resonance imaging to confirm the diagnosis, evaluate for malignancy, and document the degree of lumen occlusion, clot extent, and chronicity. BEST PRACTICE ADVICE 3: Patients with cirrhosis and PVT do not require a hypercoagulable workup in the absence of additional thromboemboli or laboratory abnormalities or family history suggestive of thrombophilia. BEST PRACTICE ADVICE 4: Patients with cirrhosis and PVT with evidence of intestinal ischemia require urgent anticoagulation to minimize ischemic injury. If available, these patients should be managed by a multidisciplinary team, including gastroenterology and hepatology, interventional radiology, hematology, and surgery. BEST PRACTICE ADVICE 5: Consider observation, with repeat imaging every 3 months until clot regression, in patients with cirrhosis without intestinal ischemia and recent (<6 months) thrombosis involving the intrahepatic portal vein branches or when there is <50% occlusion of the main portal vein, splenic vein, or mesenteric veins. BEST PRACTICE ADVICE 6: Anticoagulation should be considered in patients with cirrhosis without intestinal ischemia who develop recent (<6 months) PVT that is >50% occlusive or involves the main portal vein or mesenteric vessels. Patients who have increased benefit of recanalization include those with involvement of more than 1 vascular bed, those with thrombus progression, potential liver transplantation candidates, and those with inherited thrombophilia. BEST PRACTICE ADVICE 7: Anticoagulation is not advised for patients with cirrhosis with chronic (>6 months) PVT with complete occlusion with collateralization (cavernous transformation). BEST PRACTICE ADVICE 8: Patients with cirrhosis and PVT warrant endoscopic variceal screening if they are not already on nonselective beta-blocker therapy for bleeding prophylaxis. Avoid delays in the initiation of anticoagulation for PVT, as this decreases the odds of portal vein recanalization. BEST PRACTICE ADVICE 9: Vitamin K antagonists, low-molecular-weight heparin, and direct oral anticoagulants are all reasonable anticoagulant options for patients with cirrhosis and PVT. Decision making should be individualized and informed by patient preference and Child-Turcotte-Pugh class. Direct oral anticoagulants may be considered in patients with compensated Child-Turcotte-Pugh class A and Child-Turcotte-Pugh class B cirrhosis and offer convenience as their dosages are independent of international normalized ratio monitoring. BEST PRACTICE ADVICE 10: Patients with cirrhosis on anticoagulation for PVT should have cross-sectional imaging every 3 months to assess response to treatment. If clot regresses, anticoagulation should be continued until transplantation or at least clot resolution in nontransplantation patients. BEST PRACTICE ADVICE 11: Portal vein revascularization with transjugular intrahepatic portosystemic shunting may be considered for selected patients with cirrhosis and PVT who have additional indications for transjugular intrahepatic portosystemic shunting, such as those with refractory ascites or variceal bleeding. Portal vein revascularization with transjugular intrahepatic portosystemic shunting may also be considered for transplantation candidates if recanalization can facilitate the technical feasibility of transplantation.

 Clot waveform analysis (CWA) provides a global assessment of hemostasis and may be useful for patients with cirrhosis with complex hemostatic abnormalities. This study aimed to assess the association between prothrombin time (PT-) and activated partial thromboplastin time (aPTT-) based CWA parameters and cirrhosis severity and prospectively evaluate the role of CWA in predicting mortality and acute decompensation (AD) over 1 year.

 This prospective study included adult patients with cirrhosis between June 2021 and December 2023 at Chulalongkorn University Hospital. The PT- and aPTT-based CWA parameters were obtained using an automated coagulation analyzer.

 A total of 560 patients with cirrhosis were included; 165 (29.5%) and 47 (11.5%) had Child-Turcotte-Pugh (CTP) B and C cirrhosis, respectively. The PT- and aPTT-based CWA parameters, including maximum velocity (min1), maximum acceleration (min2), and maximum deceleration (max2), were significantly lower (p ≤ 0.05) in patients with decompensated cirrhosis than in those with compensated cirrhosis. Additionally, CWA values were significantly higher in patients with higher CTP and Model for End-Stage Liver Disease (MELD) scores. Multivariable analysis revealed that liver stiffness (LS) and max2 of PT-based CWA assay were independently associated with CTP B/C. In addition, min2 and max2 of PT-based CWA assay were independently associated with 1-year mortality. No significant differences in CWA parameters were observed between patients with and without portal vein thrombosis. CWA parameters were not related to AD during the 1-year follow-up.

 A hypocoagulable profile based on CWA parameters is associated with advanced-stage cirrhosis. CWA may be a useful objective marker for assessing cirrhosis severity and predicting 1-year mortality.

Portal vein thrombosis (PVT) is a challenging complication in liver cirrhosis, with no currently available sensitive diagnostic markers. This study aimed to investigate the potential of neutrophil extracellular traps (NETs) and Deoxyribonuclease (DNase) as diagnostic indicators for PVT in chronic hepatitis B (CHB)-related decompensated cirrhosis.

We analyzed 145 CHB-related decompensated cirrhosis patients from the Ditan study and 33 from the Changgung validation study, categorizing them based on PVT occurrence. Plasma samples were assessed for NET markers, including cell-free DNA (cfDNA) and histone-DNA complexes, along with DNase activity.

PVT patients exhibited elevated levels of cfDNA and histone-DNA complexes, and reduced DNase activity. This pattern persisted regardless of hepatocellular carcinoma (HCC) status. Histone-DNA levels, DNase activity, and hemoglobin were identified as independent risk factors for PVT. Receiver operating characteristic curve analysis revealed that high histone-DNA levels may serve as a potential diagnostic marker for PVT, with an area under the curve of 0.8628 in the Ditan study and 0.7521 in the Changgung study. When combined with cfDNA and DNase activity, the area under the curve improved to 0.8774 in the Ditan study and 0.7975 in the Changgung study.

Imbalances in NET homeostasis are associated with PVT in CHB-related decompensated cirrhosis, including cases involving HCC. Histone-DNA complexes, a significant risk factor for PVT, show potential as a diagnostic marker for PVT in decompensated cirrhosis, particularly in HBV-related HCC.

Portal vein thrombosis (PVT) is thought to arise from stagnant blood flow, yet conclusive evidence is lacking. Relative residence time (RRT) assessed using 4D Flow MRI may offer insight into portal flow stagnation.

To explore the relationship between RRT values and the presence of PVT in cirrhotic participants.

Prospective.

Forty-eight participants with liver cirrhosis (27 males, median age 67 years [IQR: 57-73]) and 20 healthy control participants (12 males, median age 45 years [IQR: 40-54]).

3 T/4D Flow MRI.

Laboratory (liver and kidney function test results and platelet count) and clinical data (presence of tumors and other imaging findings), and portal hemodynamics derived from 4D Flow MRI (spatiotemporally averaged RRT [RRT-mean], flow velocity, and flow rate) were analyzed.

We used multivariable logistic regression, adjusted by selected covariates through the Lasso method, to explore whether RRT-mean is an independent risk factor for PVT. The area under the ROC curve (AUC) was also calculated to assess the model's discriminative ability. P < 0.05 indicated statistical significance.

The liver cirrhosis group consisted of 16 participants with PVT and 32 without PVT. Higher RRT-mean values (odds ratio [OR] 11.4 [95% CI: 2.19, 118]) and lower platelet count (OR 0.98 per 1000 μL [95% CI: 0.96, 0.99]) were independent risk factors for PVT. The incorporation of RRT-mean (AUC, 0.77) alongside platelet count (AUC, 0.75) resulted in an AUC of 0.84. When including healthy control participants, RRT-mean had an adjusted OR of 12.4 and the AUC of the combined model (RRT-mean and platelet count) was 0.90.

Prolonged RRT values and low platelet count were significantly associated with the presence of PVT in cirrhotic participants. RRT values derived from 4D Flow MRI may have potential clinical relevance in the management of PVT.

2 TECHNICAL EFFICACY: Stage 2.

Non-selective β blockers (NSBBs) may negatively influence renal function through decreasing heart rate and cardiac output. This study aimed to systematically investigate their association.

PubMed, EMBASE, and Cochrane library databases were searched to identify all relevant studies evaluating the association of NSBBs with renal dysfunction in cirrhotic patients. Unadjusted and adjusted data were separately extracted. Odds ratios (ORs) and hazard ratios (HRs) were pooled. Subgroup meta-analyses were performed according to the proportions of ascites and Child-Pugh class B/C and the mean model for end-stage liver disease (MELD) score. Quality of evidence was assessed using the Grading of Recommendations Assessment, Development, and Evaluation framework.

Fourteen studies were finally included. Based on unadjusted data, NSBBs significantly increased the risk of developing renal dysfunction (OR = 1.49; p = 0.03), and this association remained significant in subgroup analyses of studies where the proportions of ascites was >70% and Child-Pugh class B/C was 100%. Based on adjusted data with propensity score matching (adjusted OR = 0.61; p = 0.08) and multivariable regression modelling (adjusted HR = 0.86; p = 0.713), NSBBs did not increase the risk of developing renal dysfunction, and this association remained not significant in subgroup analyses of studies where the proportions of ascites was >70% and <70%, the proportion of Child-Pugh class B/C was <100%, and the mean MELD score was <15. The quality of evidence was very low for all meta-analyses.

NSBBs may not be associated with the development of renal dysfunction in liver cirrhosis. However, more evidence is required to clarify their association in specific populations.

Factor XI (FXI) is associated with thrombosis in patients without liver disease, but it alterations and prognostic value in cirrhosis are uncertain.

We studied a prospective cohort of cirrhosis patients determining FXI and its association with portal vein thrombosis (PVT), bleeding, and hepatic decompensation/ACLF during 1-year follow-up. Odds ratios (OR) and 95 % CIs were calculated using logistic regression.

We included 183 patients (Child-Pugh [CP] A/B/C 57/59/57). FXI was reduced in cirrhosis, decreasing with CP stage (78 % [66-94] vs. 58 % [44-78] vs. 41 % [30-52] in CP A, B, and C, respectively; p < 0.001). FXI was correlated with MELD score (rho: -0.6, p < 0.001), INR (rho: -0.6, p < 0.001), and platelet count (rho: 0.4, p < 0.001). Sixteen patients (8.7 %) experienced PVT, which only predictor was baseline platelet count (OR: 0.94; CI95 %: 0.91-0.97, p < 0.001). Bleeding occurred in 7 patients (3.8 %). Cirrhosis severity, platelet count, fibrinogen, and FXI (60% vs. 78 %; p = 0.2) were comparable between bleeding and non-bleeding individuals. Finally, no association was found between FXI and hepatic decompensation/ACLF, which were predicted by lower albumin and platelet count, respectively.

FXI seems not to be responsible for thrombosis and cirrhosis progression. The lack of association between low FXI and bleeding events, however, indirectly opens to future studies evaluating FXI inhibitors in cirrhosis.

There are lots of risk factors reported for cirrhotic portal vein thrombosis (PVT) development, however, the relationship between hepatic venous pressure gradient (HVPG) and PVT development remains unclear.

The clinical outcomes of cirrhotic patients who had no PVT and underwent HVPG measurement at baseline between March 2018 and March 2022 were analyzed retrospectively. Screening for non-tumoral PVT development was implemented by contrast-enhanced computed tomography and/or magnetic resonance imaging every 6-12 months.

Eighty-two cirrhotic patients were evaluated over a follow-up period. Of these, 12 patients (14.6%) experienced the development of PVT. The occurrence of non-tumoral PVT at one, two, and three years were 6.6%, 11.7%, and 22.2% respectively. HVPG (p=0.038;HR 1.07;95%CI 1.00-1.14) and alcohol liver disease (ALD) (p=0.019;HR 4.20;95%CI 1.27-13.89) were independently associated with a high PVT risk. The cutoff value of HVPG was 17.52 mmHg. The cumulative incidence of PVT differed significantly among groups stratified by HVPG thresholds of 16mmHg (P=0.011). The sensitivity and specificity of HVPG≥16mmHg in predicting PVT development were 100.0% and 35.7%.

In patients with liver cirrhosis, the value of HVPG was the independent predictive factor of PVT development. Screening for PVT was recommended during follow-up in patients with HVPG≥16 mmHg.

Esophageal-gastric variceal bleeding (EGVB) is a serious complication in patients with liver cirrhosis, characterized by high mortality and rebleeding rates. The effect of sequential endoscopic therapy on patient mortality and rebleeding rates remains unclear.

This study aimed to evaluate the effects of sequential endoscopic therapy on mortality and rebleeding rates in patients with EGVB.

In this single-center retrospective study, 373 hospitalized cases of EGVB caused by liver cirrhosis, collected between November 2019 and November 2023, were divided into four groups according to different treatment methods: a sequential endoscopy group, emergency endoscopy group, emergency endoscopy plus transjugular intrahepatic portosystemic shunt (TIPS) group and control group.

Mortality and rebleeding rates were compared among the four groups using statistical analyses.

The mortality and rebleeding rates of the sequential endoscopy group (3.7% and 19%, respectively) were significantly lower than those of the emergency endoscopy (22% and 36%, respectively), emergency endoscopy plus TIPS (33% and 28%, respectively), and control groups (33% and 51%, respectively) (p = 0.013 and p = 0.013, respectively).

Sequential endoscopic therapy may significantly reduce the mortality and rebleeding rates of patients with EGVB compared to other conventional treatment strategies. The findings of the study could help develop approaches benefiting EGVB treatment.

Patients with cirrhosis show alterations in primary hemostasis, yet prognostic implications of changes in platelet activation remain controversial, and assay validity is often limited by thrombocytopenia. We aimed to study the prognostic role of platelet activation in cirrhosis, focusing on bleeding/thromboembolic events, decompensation, and mortality.

We prospectively included 107 patients with cirrhosis undergoing a same-day hepatic venous pressure gradient (HVPG) and platelet activation measurement. Platelet activation was assessed using flow cytometry after protease-activated receptor (PAR)-1, PAR-4, or epinephrine stimulation. Over a follow-up of 25.3 (IQR: 15.7-31.2) months, first/further decompensation occurred in 29 patients and 17 died. More pronounced platelet activation was associated with an improved prognosis, even after adjusting for systemic inflammation, HVPG, and disease severity. Specifically, higher PAR-4-inducible platelet activation was independently linked to a lower decompensation risk [adjusted HR per 100 MFI (median fluorescence intensity): 0.95 (95% CI: 0.90-0.99); p =0.036] and higher PAR-1-inducible platelet activation was independently linked to longer survival [adjusted HR per 100 MFI: 0.93 (95% CI: 0.87-0.99); p =0.040]. Thromboembolic events occurred in eight patients (75% nontumoral portal vein thrombosis [PVT]). Higher epinephrine-inducible platelet activation was associated with an increased risk of thrombosis [HR per 10 MFI: 1.07 (95% CI: 1.02-1.12); p =0.007] and PVT [HR per 10 MFI: 1.08 (95% CI: 1.02-1.14); p =0.004]. In contrast, of the 11 major bleedings that occurred, 9 were portal hypertension related, and HVPG thus emerged as the primary risk factor.

Preserved PAR-1- and PAR-4-inducible platelet activation was linked to a lower risk of decompensation and death. In contrast, higher epinephrine-inducible platelet activation was a risk factor for thromboembolism and PVT.

In clinical practice, the d-dimer levels rule out venous thromboembolism and diagnose disseminated intravascular coagulation. d-dimers increase in both physiological and pathological conditions. Liver cirrhosis, especially in the final stages, is characterized by complex coagulation and fibrinolysis factor disorders. Multiple mechanisms tried to explain the increased d-dimer levels in patients with liver cirrhosis and ascites. The d-dimer cut-off level used to rule out venous thromboembolism in cirrhosis is higher than that used to confirm the diagnosis of VTE or DIC in noncirrhotic patients. The cut-off d-dimer level used for the prognosis of thrombotic events is not standardized in advanced liver cirrhosis. Thus, it is necessary to update the clinical guidelines regarding the usefulness of d-dimer testing in advanced liver cirrhosis and the cut-off d-dimer levels, which should vary based on the detection method.

Venous thromboembolism (VTE), particularly portal vein thrombosis, is common in patients with cirrhosis. Misconceptions around the increased bleeding risk in this patient group may lead to delayed and/or inadequate anticoagulation. This nutshell review focusses on the approach to management including the role of direct oral anticoagulants in the treatment of VTE in patients with cirrhosis.

Portal vein thrombosis (PVT) is a common thrombotic complication of cirrhosis. It can lead to variceal bleeding and bowel ischemia and also complicate liver transplantation. Identifying the possible risk factors associated with PVT can aid in identifying patients at high risk, enabling their screening and potentially preventing PVT through the rational use of anticoagulants. This study focuses on examining the clinical characteristics of PVT in cirrhotic patients and identifying the clinical and biochemical factors that are linked to the development of PVT. Consecutive hospitalized cirrhotic patients between 2015 and 2023 were identified through the hospital's computerized medical records based on the Tenth Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) coding system and retrospectively analyzed. 928 individuals were included in this study; 783 (84.3%) without PVT and 145 (15.7%) with benign PVT. Hepatitis B virus (HBV) was significantly more common in the PVT group (P-value = .02), while alcohol and primary sclerosing cholangitis (PSC) were less common in this group (P-value = .01 and .02, respectively). Hepatocellular carcinoma (HCC) (P-value < .01), ascites (P-value = .01), and spontaneous bacterial peritonitis (SBP) (P-value = .02) were more common in the PVT group. Patients with PVT had a higher international normalized ratio (INR) level (P-value = .042) and lower plasma albumin (P-value = .01). No differences were identified in white blood cell, hemoglobin, platelet, and bilirubin levels. However, patients with PVT had higher model for end-stage liver disease (MELD) (P-value = .01) and Child-Pugh scores (P-value = .03). This study demonstrated a higher likelihood of PVT presence in cirrhotic patients with advanced age, HBV, and HCC, along with ascites, SBP, splenomegaly, hypoalbuminemia, elevated INR, and a higher MELD score. Nevertheless, additional research endeavors are necessary to accurately ascertain and validate supplementary risk factors within a broader demographic.

To date, there is an ongoing debate regarding the ability to predict PVT development using markers of FVIII or FVIII/PC ratio. This study presents evidence-based medical findings on the influence of FVIII activity levels and FVIII/PC values in the formation of PVT in cirrhosis.

The search for original studies on risk factors for portal vein thrombosis (PVT) associated with cirrhosis was conducted, which primarily focused on comparing circulating FVIII activity levels or FVIII/PC ratio in cirrhotic patients with and without PVT. The quality of evidence from each study was assessed using the Newcastle-Ottawa Scale.

The meta-analysis included a total of 10 original studies. In total, 2250 cirrhotic patients were included, with 414 having PVT and 1836 without PVT. The pooled analysis using a random-effects model showed no significant difference in standardized mean difference (SMD) for FVIII activity levels in cirrhotic patients with or without PVT (SMD = 0.12, 95% CI=-0.46 to 0.70, P = 0.68), but there was significant heterogeneity (I2 = 95.52%, P = 0.00). Meta-regression analysis indicated that differences in mean FVIII activity levels in the PVT group, the number of cases in the non-PVT group, and the study design methods partially contributed to the heterogeneity (P < 0.05). However, compared to the non-PVT group, the PVT group had higher FVIII/PC ratio with a statistically significant difference (SMD = 0.39, 95% CI: 0.15 to 0.63, P = 0.00), and there was no significant heterogeneity (I2 = 28.62%).

In conclusion, the FVIII/PC ratio not only reflects the severity of liver disease, but also can be used as one of the predictors of PVT development.

Portal vein thrombosis (PVT) refers to the development of a non-malignant obstruction of the portal vein, its branches, its radicles, or a combination. This Review first provides a comprehensive overview of all aspects of PVT, namely the specifics of the portal venous system, the risk factors for PVT, the pathophysiology of portal hypertension in PVT, the interest in non-invasive tests, as well as therapeutic approaches including the effect of treating risk factors for PVT or cause of cirrhosis, anticoagulation, portal vein recanalisation by interventional radiology, and prevention and management of variceal bleeding in patients with PVT. Specific issues are also addressed including portal cholangiopathy, mesenteric ischaemia and intestinal necrosis, quality of life, fertility, contraception and pregnancy, and PVT in children. This Review will then present endpoints for future clinical studies in PVT, both in patients with and without cirrhosis, agreed by a large panel of experts through a Delphi consensus process. These endpoints include classification of portal vein thrombus extension, classification of PVT evolution, timing of assessment of PVT, and global endpoints for studies on PVT including clinical outcomes. These endpoints will help homogenise studies on PVT and thus facilitate reporting, comparison between studies, and validation of future studies and trials on PVT.

While advanced liver disease was previously considered to be an acquired bleeding disorder, there is increasing recognition of an associated prothrombotic state with patients being at higher risk of atrial fibrillation (AF) and stroke and venous thromboembolism (VTE) including portal vein thrombosis (PVT). We review the available literature on epidemiology, pathophysiology, and risk factors and provide guidance on anticoagulant management of these conditions in adults with cirrhosis. In patients with Child-Pugh A or B cirrhosis and AF, we recommend anticoagulation with standard-dose direct oral anticoagulants (DOACs) in accordance with cardiology guideline recommendations for patients without liver disease. In those with Child-Pugh C cirrhosis, there is inadequate evidence with respect to the benefit and risk of anticoagulation for stroke prevention in AF. In patients with cirrhosis and acute deep vein thrombosis or pulmonary embolism, we recommend anticoagulation and suggest use of either a DOAC or low-molecular-weight heparin (LMWH)/vitamin K antagonist (VKA) in Child-Pugh A or B cirrhosis and LMWH alone (or as a bridge to VKA in patients with a normal baseline international normalized ratio) in Child-Pugh C cirrhosis. We recommend anticoagulation for patients with cirrhosis and symptomatic PVT. We suggest anticoagulation for those with asymptomatic, progressing PVT and recommend continuing extended anticoagulation for liver transplant candidates with PVT.

Portal vein thrombosis (PVT) is a challenging and controversial complication of cirrhosis. Experimental models that reproduce cirrhotic PVT and effective pharmacological therapies are limited. We aimed to investigate the nature course and mechanisms of PVT in cirrhosis. A novel PVT model was developed via two-step total portal vein ligation in healthy and thioacetamide (TAA)-cirrhotic rats. Circulating and liver-infiltrating neutrophils were isolated from individuals with cirrhosis to examine neutrophil extracellular traps (NETs) and explore their unique characteristics and implications in PVT-associated fibrosis in cirrhosis. We further validated macrophage-myofibroblast transition (MMT) via multiplex immunofluorescence and single-cell sequencing. In the experimental model, cirrhosis promoted PVT development and portal vein intimal thickening. Interestingly, cirrhosis promoted spontaneous resolution of PVT due to instability of thrombus structure, along with pulmonary and intrahepatic clots. NETs-MMT mediate cirrhotic PVT and PVT-associated fibrosis, including fibrotic thrombus remodeling and increased hepatic collagen deposition. Mechanistically, caspase-4-dependent activation of neutrophils and GSDMD mediated the formation of NETs. The extracellular DNA of NETs promoted TGF-β1/Smad3-driven MMT. Inhibiting GSDMD with disulfiram suppressed cirrhotic PVT and prevented associated fibrosis. The cirrhotic PVT model reflected the following three main characteristics of cirrhotic PVT: spontaneous resolution, immunothrombosis, and intimal fibrosis. Targeting NETs with GSDMD inhibitors may serve as a new therapeutic concept to treat cirrhotic PVT.

Cirrhosis is a major health concern worldwide with a complex pathophysiology affecting various biological systems, including all aspects of haemostasis. Bleeding risk is mainly driven by portal hypertension, but in end-stage liver disease it is further increased by alterations in haemostatic components, including platelet function, coagulation, and fibrinolysis. Concurrently, patients with cirrhosis are prone to venous thromboembolic events (VTE) because of the altered haemostatic balance, in particular an increase in thrombin generation. In patients with cirrhosis, vitamin K antagonists (VKA) and low molecular weight heparins (LMWH) are currently the standard of care for VTE prevention, with VKA also being standard of care for stroke prevention in those with atrial fibrillation. However, direct oral anticoagulants (DOAC) could have specific advantages in this patient population. Clinical experience suggests that DOAC are a safe and possibly more effective alternative to traditional anticoagulants for the treatment of VTE in patients with compensated cirrhosis. In addition, emerging data suggest that primary prophylactic treatment with anticoagulants may improve clinical outcomes in patients with cirrhosis by reducing the risk of hepatic decompensation. The selection of the most appropriate DOAC remains to be clarified. This review focuses on the rationale for the use of DOAC in patients with cirrhosis, the specific effects of the different DOAC (as assessed by in vitro and in vivo pharmacokinetic and pharmacodynamic studies), as well as clinical outcomes in patients with cirrhosis on DOAC.

There is heterogeneous data on whether metabolic-associated steatohepatitis is an independent risk factor for portal vein thrombosis (PVT). We aim to compare the incidence of PVT in patients with cirrhosis with and without metabolic dysfunction-associated steatotic liver disease (MASLD).

This is a single-center retrospective study of patients with cirrhosis seen between 1 January 2016 and 31 January 2021. Patients with a history of hepatocellular cancer, liver transplant, Budd-Chiari syndrome, and intra-abdominal malignancies were excluded. Patients with cirrhosis were followed from their first hepatology visit for 180 days to determine the incidence of PVT. Cox proportional hazard regression was used to determine the relationship between MASLD with PVT.

We analyzed data from 2785 patients with cirrhosis who met inclusion and exclusion criteria [mean age: 61.0 ± 12.3 years, 44.3% female, 63.8% Whites and mean model for end-stage liver disease-sodium (MELD-Na) score: 11.7 ± 6.1]. MASLD was present in 21.7% of patients. A total of 89 patients developed PVT during the follow-up, which was fewer in patients with MASLD [2.0% vs. 3.5%, P  = 0.04, unadjusted heart rate (HR): 0.60, 95% confidence interval (CI): 0.27-0.96, P  = 0.04]. After adjusting for the demographics, MASLD-related comorbid conditions and MELD-Na score, MASLD was associated with a lower incidence of PVT as compared to non-MASLD cirrhosis (HR: 0.44, 95% CI: 0.21-0.92, P  = 0.03). After adjusting for the indicators of Child-Pugh Turcotte score, the risk of PVT in patients with MASLD compared to non-MASLD was not statistically significant (HR: 0.50, 95% CI: 0.22-1.13, P  = 0.096).

PVT incidence was lower in patients with MASLD cirrhosis as compared to non-MASLD cirrhosis. However, the difference was not significantly different after adjusting for liver decompensation.

Patients with liver cirrhosis often exhibit complex alterations in their hemostatic system that can be associated with both bleeding and thrombotic complications. While prophylactic correction of abnormal coagulation parameters should be avoided, an individualized approach is recommended prior to invasive procedures, whereby specific preventive measures to stabilize hemostasis should be based on the periprocedural bleeding risk. While the haemostatic system of patients with compensated cirrhosis is often in a rebalanced haemostatic state due to a parallel decline in both pro- and anti-haemostatic factors, a decompensation of liver cirrhosis can lead to destabilization of this fragile equilibrium. Since conventional coagulation tests do not adequately capture the complex changes in the hemostatic system in cirrhosis, functional analysis methods such as viscoelastic tests or thrombin generation assays can be used for evaluating the coagulation status. This review describes the underlying pathophysiological changes in the hemostatic system in liver cirrhosis, provides an overview of diagnostic methods and discusses therapeutic measures in case of bleeding and thrombotic complications.

Hospitalized patients with cirrhosis frequently require critical care management for sepsis, HE, respiratory failure, acute variceal bleeding, acute kidney injury (AKI), shock, and optimization for liver transplantation, while outpatients have unique care considerations. Point-of-care ultrasonography (POCUS) enhances bedside examination of the hepatobiliary system and relevant extrahepatic sites. POCUS includes cardiac US and is used to assess volume status and hemodynamic parameters like cardiac output, systemic vascular resistance, cardiac contractility, and pulmonary artery pressure, which aid in the early and accurate diagnosis of heart failure, cirrhotic cardiomyopathy, porto-pulmonary hypertension, hepatopulmonary syndrome, arrhythmia, and pulmonary embolism. This also helps in fluid management and vasopressor use in the resuscitation of patients with cirrhosis. Lung ultrasound (LUS) can help in differentiating pneumonia, effusion, and edema. Further, US guides interventions such as line placement, drainage of abdominal collections/abscesses, relief of tension pneumothorax, drainage of pleural and pericardial effusions, and biliary drainage in cholangitis. Additionally, its role is essential to assess liver masses foci of sepsis, for appropriate sites for paracentesis, and to assess for vascular disorders such as portal vein or hepatic vein thrombosis. Renal US can identify renal and postrenal causes of AKI and aid in diagnosis of prerenal AKI through volume assessment. In this review, we address the principles and methods of POCUS in hospitalized patients and in outpatients with cirrhosis and discuss the application of this diverse modality in clinical hepatology.

Nonselective β blockers (NSBBs) facilitate the development of portal vein thrombosis (PVT) in liver cirrhosis. Considering the potential effect of NSBBs on neutrophils and neutrophil extracellular traps (NETs), we speculated that NSBBs might promote the development of PVT by stimulating neutrophils to release NETs.

Serum NETs biomarkers were measured, use of NSBBs was recorded, and PVT was evaluated in cirrhotic patients. Carbon tetrachloride and ferric chloride (FeCl3) were used to induce liver fibrosis and PVT in mice, respectively. After treatment with propranolol and DNase I, neutrophils in peripheral blood, colocalization and expression of NETs in PVT specimens, and NETs biomarkers in serum were measured. Ex vivo clots lysis analysis was performed and portal vein velocity and coagulation parameters were tested.

Serum MPO-DNA level was significantly higher in cirrhotic patients treated with NSBBs, and serum H3Cit and MPO-DNA levels were significantly higher in those with PVT. In fibrotic mice, following treatment with propranolol, DNase I significantly shortened the time of FeCl3-induced PVT formation, lowered the peripheral blood neutrophils labelled by CD11b/Ly6G, inhibited the positive staining of H3Cit and the expression of H3Cit and MPO proteins in PVT tissues, and reduced serum nucleosome level. Furthermore, the addition of DNase I to tissue plasminogen activator (tPA) significantly accelerated clots lysis as compared with tPA alone. Propranolol reduced portal vein velocity in fibrotic mice, but did not influence coagulation parameters.

Our study provides a clue to the potential impact of NETs formation on the association of NSBBs with the development of PVT.

Statin use has shown a reduction in hepatic decompensation and portal hypertension. Its association with portal vein thrombosis (PVT) incidence is unknown. We aim to compare the incidence of PVT in patients with and without statin use.

We excluded patients with a history of hepatocellular cancer, liver transplants, Budd-Chiari syndrome, and intra-abdominal malignancies. Patients with cirrhosis were followed from their first hepatologist clinical encounter (January 1, 2016, to January 31, 2021) for 180 days to determine PVT incidence. We tested the association of statin use with PVT using 1:1 propensity score (PS) matching and Cox proportional hazard regression.

We analyzed 2785 patients with cirrhosis (mean age:61.0 ± 12.3 years, 44.3% female, 63.8% White, mean MELD-Na score:11.7 ± 6.1, and statin use:23.1%). A total of 89 patients developed PVT during the follow-up, which was lower in patients with statin use as compared to no statin use (1.3% vs 3.8%, P = 0.001, unadjusted HR:0.28, 95% CI: 0.13-0.62, P = 0.001). After matching for demographics, comorbidities, and hepatic decompensation events, patients with statin use had a lower risk of developing PVT in 180-day follow-up as compared to those without statin use (HR:0.24, 95% CI: 0.10-0.55, P = 0.001). Subgroup analysis showed that statin use was associated with lower PVT incidence in non-NASH (HR: 0.20, 95% CI: 0.07-0.54, P = 0.002) and decompensated cirrhosis (HR: 0.12, 95% CI:0.03-0.53, P = 0.005) than no statin use.

PVT incidence was lower in decompensated cirrhosis patients with statin use than in those with no statin use. However, this finding needs to be further tested in randomized control trials.

Acute portal vein thrombosis (PVST), a serious complication of liver cirrhosis, is characterized as abdominal pain secondary to intestinal ischemia, and even intestinal necrosis. Anticoagulation is recommended for the treatment of acute PVST, but is often postponed in cirrhotic patients with acute variceal bleeding or those at a high risk of variceal bleeding. Herein, we reported a 63-year-old male with a 14-year history of alcoholic liver cirrhosis who developed progressive abdominal pain related to acute portal vein and superior mesenteric vein thrombosis immediately after endoscopic variceal ligation combined with endoscopic cyanoacrylate glue injection for acute variceal bleeding. Fortunately, acute PVST was successfully recanalized by the use of low molecular weight heparin. Collectively, this case suggests that acute symptomatic PVST can be secondary to endoscopic variceal therapy in liver cirrhosis, and can be safely and successfully treated by anticoagulation.

Portal vein thrombosis (PVT), a complication of liver cirrhosis, is a major public health concern. PVT prediction is the most effective method for PVT diagnosis and treatment.

To develop and validate a nomogram and network calculator based on clinical indicators to predict PVT in patients with cirrhosis.

Patients with cirrhosis hospitalized between January 2016 and December 2021 at the First Hospital of Lanzhou University were screened and 643 patients with cirrhosis who met the eligibility criteria were retrieved. Following a 1:1 propensity score matching 572 patients with cirrhosis were screened, and relevant clinical data were collected. PVT risk factors were identified using the least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression analysis. Variance inflation factors and correlation matrix plots were used to analyze multicollinearity among the variables. A nomogram was constructed to predict the probability of PVT based on independent risk factors for PVT, and its predictive performance was verified using a receiver operating characteristic curve (ROC), calibration curves, and decision curve analysis (DCA). Finally, a network calculator was constructed based on the nomograms.

This study enrolled 286 cirrhosis patients with PVT and 286 without PVT. LASSO analysis revealed 13 variables as strongly associated with PVT occurrence. Multivariate logistic regression analysis revealed nine indicators as independent PVT risk factors, including etiology, ascites, gastroesophageal varices, platelet count, D-dimer, portal vein diameter, portal vein velocity, aspartate transaminase to neutrophil ratio index, and platelet-to-lymphocyte ratio. LASSO and correlation matrix plot results revealed no significant multicollinearity or correlation among the variables. A nomogram was constructed based on the screened independent risk factors. The nomogram had excellent predictive performance, with an area under the ROC curve of 0.821 and 0.829 in the training and testing groups, respectively. Calibration curves and DCA revealed its good clinical performance. Finally, the optimal cutoff value for the total nomogram score was 0.513. The sensitivity and specificity of the optimal cutoff values were 0.822 and 0.706, respectively.

A nomogram for predicting PVT occurrence was successfully developed and validated, and a network calculator was constructed. This can enable clinicians to rapidly and easily identify high PVT risk groups.

Nonmalignant portal vein thrombosis (PVT) is a common complication of cirrhosis especially at the stage of decompensations. The diagnosis of PVT in cirrhosis is often incidental and it may be detected during routine semestral abdominal ultrasound with Doppler during screening for hepatocellular carcinoma or during hospitalization for decompensated cirrhosis. After detection of PVT on abdominal ultrasound, it is important to evaluate patients with cross-sectional imaging to determine the age of thrombus, whether acute or chronic, the extent and degree of luminal occlusion of the portal vein, and to rule out hepatocellular carcinoma or other underlying malignancy. Factors influencing management include the degree and extent of luminal occlusion of PVT, potential listing for liver transplantation, and portal hypertension (PHT) complications such as variceal hemorrhage and refractory ascites, severity of thrombocytopenia, and other comorbidities including chronic kidney disease. Anticoagulation is the most common therapeutic option and it is specially indicated in patients who are candidates for liver transplantation. Interventional procedures including transjugular intrahepatic portosystemic shunt (TIPS) placement and mechanical thrombectomy may be used on a case-by-case basis in patients with contraindications or adverse events related to anticoagulation, who develop worsening PVT while on anticoagulant therapy, or have chronic PVT and PHT complications that are not manageable medically or endoscopically.