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.

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.

Patients with decompensated liver cirrhosis suffering from esophagogastric variceal bleeding (EGVB) face high mortality.

To investigate the risk factors for EGVB in patients with liver cirrhosis and establish a diagnostic nomogram.

Patients with liver cirrhosis who met the inclusion criteria were randomly divided into training and validation cohorts in a 6:4 ratio in this retrospective research. Univariate analysis, least absolute shrinkage and selection operator regression, and multivariate analysis were employed to establish the nomogram model. Calibration curve, the area under the receiver operating characteristic curve (AUC), and decision curve analysis (DCA) were applied to assess the discrimination, accuracy, and clinical practicability of the nomogram, respectively.

A total of 1115 patients were enrolled in this study. The nomogram was established based on white blood cells (P < 0.001), hemoglobin (P < 0.001), fibrinogen (P < 0.001), total bilirubin (P = 0.007), activated partial thromboplastin time (P = 0.002), total bile acid (P = 0.012), and ascites (P = 0.006). The calibration curve indicated that the actual observation results were in good agreement with the prediction results of the model. The AUC values of the diagnostic model were 0.861 and 0.859 in the training and validation cohorts, respectively, which were higher than that of the aspartate aminotransferase-to-platelet ratio index, fibrosis index based on 4 factors, and aspartate aminotransferase-to-alanine aminotransferase ratio. Additionally, DCA indicated that the net benefit value of the model was higher than that of the other models.

This research constructed and validated a nomogram with perfect performance for predicting EGVB events in patients with liver cirrhosis, which could help clinicians with timely diagnosis, individualized treatment, and follow-up.

 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.

This study aimed to explore a modified direct intrahepatic portocaval shunt (DIPS) technique as an alternative approach for patients with portal vein occlusion (PVO) and cirrhosis who were not candidates for traditional transjugular intrahepatic portosystemic shunt (TIPS) due to anatomical challenges.

Three patients with esophageal or gastric fundus variceal hemorrhage complicated by severe PVO were treated using innovative DIPS approaches. Preoperative contrast-enhanced computed tomography was employed to assess anatomical feasibility. The modified DIPS techniques involved targeting dilated varicose veins or the confluence of the superior mesenteric and splenic veins to access the inferior vena cava. For broader clinical applications, we outlined the anatomical conditions necessary for adopting the method proposed in this study. Following the puncture, portal hypertension was effectively alleviated, and bleeding was controlled. There were no obvious complications during the follow-up period.

Modified DIPS targeting different vessels appears to be a feasible alternative for the treatment of severe PVO when conventional TIPS by ultrasound-guided percutaneous transhepatic or transsplenic pathway and DIPS are unsuccessful. Future validation in a larger patient population is needed.

Level 4, Case Series.

To evaluate the new preoperative Changgung classification (CC) system of portal vein thrombosis (PVT) in choosing suitable operative procedures to reconstruct portal veins during liver transplantation (LT) in patients with portal vein cavernous transformation (PVCT).

This retrospective observational study analyzed data from allograft LTs performed for various liver diseases.

The study included 22 males and 4 females with LT indications comprising cirrhosis (n = 9), hepatocellular carcinoma (n = 12), PVCT (n = 2), liver failure from fulminant hepatitis B (n = 1), dysfunction of transplanted liver (n = 1), and chronic rejection of transplanted liver (n = 1). Patients were classified according to Yerdel (21 Yerdel II and 5 Yerdel III) and CC (C1-C5). In total 16 simple operations were performed on C1-C3 cases and 9 complex operations on C4-C5 cases, with one additional simple operation. The distribution according to the Yerdel classification was 16 simple and 5 complex operations in Yerdel II cases and 1 simple and 4 complex operations in Yerdel III cases. The median follow-up time was 27.5 months with overall one-year and three-year OS rates of 88.1% and 83.9% for the cohort. Specifically, the one-year OS rates for patients classified as C1-3 vs. C4-5 were 93.3% and 80.0%, while the three-year OS rates were 86.7% and 80.0%, respectively (p = 0.526).

The CC proposed in this study shows comparable potential to the Yerdel classification in preoperatively identifying the need for complex surgical techniques in LT patients with PVCT and may also have predictive power for the survival benefits following LT.

Portal vein thrombosis (PVT) is one of the common complications of cirrhosis. The incidence of PVT correlates with liver disease severity-higher incidence in patients with Child-Turcotte-Pugh (CTP) C, large spontaneous portosystemic shunts, hepatofugal portal flow, and in the presence of hepatocellular carcinoma. PVT may worsen ascites, increase the risk and poor control of variceal bleeding. The occurrence of PVT may increase morbidity and lower survival after a liver transplant. Using statins prevents the occurrence of PVT, whereas beta-blockers may aggravate its occurrence. Cross-sectional imaging is mandatory for the precise diagnosis and classification of PVT. Symptomatic, occlusive PVT and candidacy for liver transplantation are the main indications for anticoagulation. Vitamin K antagonists, low-molecular-weight heparin, and newer anticoagulants are effective and safe in cirrhosis. Direct-acting oral anticoagulants are agents of choice in early cirrhosis (CTP A, B). The duration of anticoagulant therapy, predictors of response, and management of complications of cirrhosis while on therapy require in-depth knowledge and individualized treatment. Transjugular intrahepatic porto-systemic shunt can be considered in nonresponsive cases or when anticoagulants are contraindicated. This manuscript reviews the latest updated knowledge about managing PVT in cirrhosis.

Gallbladder rupture, though rare, is a serious complication often arising from choledocholithiasis and subsequent interventions such as endoscopic retrograde cholangiopancreatography (ERCP). In this case, the patient presented with acute choledocholithiasis and underwent ERCP with sphincterotomy and stone extraction, followed by placement of a fully covered metal stent in the common bile duct (CBD). While the use of covered stents is appropriate, it is important to note that these stents can obstruct the cystic duct orifice in patients with a gallbladder. This occurs in more than 33% of patients with a low cystic duct junction, leading to obstructive acute cholecystitis, as seen in patients with pancreatic ductal adenocarcinoma (PDAC) or distal cholangiocarcinoma who receive metal biliary stents. In this case, the patient developed a liver abscess following a gallbladder rupture, likely due to the stent obstructing the cystic duct. The liver abscess was managed with percutaneous drainage, and cultures grew Streptococcus anginosus, a common pathogen in hepatobiliary infections. The patient was treated with IV piperacillin-tazobactam, followed by oral amoxicillin-clavulanate for a 4-6 week course. Additionally, portal vein thrombosis, a known complication of severe infection, was identified and treated with anticoagulation. This case highlights the need for careful stent selection and possible prophylactic cholecystectomy in patients with a functioning gallbladder to prevent post-ERCP complications like cholecystitis and abscess formation. Early diagnosis, timely drainage, and appropriate antibiotic therapy are critical to managing such complex hepatobiliary conditions.

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.

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.

Sustained virological response (SVR) by direct-acting antivirals (DAAs) may reverse the hypercoagulable state of HCV cirrhosis and the portal vein thrombosis (PVT) risk. We evaluated the incidence and predictive factors of de novo, non-tumoral PVT in patients with cirrhosis after HCV eradication.

Patients with HCV-related cirrhosis, consecutively enrolled in the multi-center ongoing PITER cohort, who achieved the SVR using DAAs, were prospectively evaluated. Kaplan-Meier and competing risk regression analyses were performed.

During a median time of 38.3 months (IQR: 25.1-48.7 months) after the end of treatment (EOT), among 1609 SVR patients, 32 (2.0%) developed de novo PVT. A platelet count ≤120,000/μL, albumin levels ≤3.5 mg/dL, bilirubin >1.1 mg/dL, a previous liver decompensation, ALBI, Baveno, FIB-4, and RESIST scores were significantly different (p < 0.001), among patients who developed PVT versus those who did not. Considering death and liver transplantation as competing risk events, esophageal varices (subHR: 10.40; CI 95% 4.33-24.99) and pre-treatment ALBI grade ≥2 (subHR: 4.32; CI 95% 1.36-13.74) were independent predictors of PVT. After HCV eradication, a significant variation in PLT count, albumin, and bilirubin (p < 0.001) versus pre-treatment values was observed in patients who did not develop PVT, whereas no significant differences were observed in those who developed PVT (p > 0.05). After the EOT, esophageal varices and ALBI grade ≥2, remained associated with de novo PVT (subHR: 9.32; CI 95% 3.16-27.53 and subHR: 5.50; CI 95% 1.67-18.13, respectively).

In patients with HCV-related cirrhosis, a more advanced liver disease and significant portal hypertension are independently associated with the de novo PVT risk after SVR.

Endothelial dysfunction and portal hypertension (PH) are reflected by increased von Willebrand factor antigen (VWF-Ag) levels in advanced chronic liver disease (ACLD). This study investigated VWF release and cleavage and their association with PH and clinical outcomes.

Levels of VWF-Ag, VWF-N (VWF-propeptide), and VWF-A (VWF processed by the main VWF-cleaving protease ADAMTS13) were assessed in 229 patients with clinically stable ACLD (hepatic venous pressure gradient [HVPG] ≥ 6 mmHg; absence of bacterial infections or acute decompensation) undergoing HVPG-measurement. Liver-healthy individuals served as controls (n = 24).

VWF-Ag and VWF-N were similarly accurate for the identification of clinically significant PH (CSPH; HVPG ≥ 10 mmHg) in compensated ACLD (AUROC: VWF-Ag 0.748; VWF-N 0.728). ADAMTS13 activity was similar between patients with ACLD and controls and did not correlate with PH and disease severity, whereas VWF cleavage decreased in patients with CSPH (i.e., VWF-Ag/-A-ratio increased). In vitro VWF activity strongly reflected VWF-Ag levels (Spearman's r = 0.874, p < 0.001), but decreased (vs. controls) in patients with CSPH when normalized to VWF-Ag levels (VWF-activity/-Ag-ratio). VWF-Act/-Ag ratio correlated negatively with ADAMTS13 activity (r =- 0.256, p < 0.001). ADAMTS13 activity was independently predictive for (i) portal vein thrombosis (PVT) and (ii) hepatic decompensation or liver-related death.

VWF-Ag levels and its propeptide are similarly suitable surrogates of PH in patients with compensated ACLD. ADAMTS13-Act was not linked to disease and PH severity, however, when normalized to VWF-Ag, both VWF cleavage and VWF activity were decreased in patients with CSPH, as compared to liver-healthy individuals. Low ADAMTS13-Act was associated with presumably more procoagulant VWF and adverse outcomes.

NCT03267615.

Chronic liver disease very often culminates into cirrhosis and its associated complications. One of the serious complications is portal venous thrombosis, which can occur due to a variety of risk factors. One significant factor contributing to portal hypertension is portal vein thrombosis (PVT). In this study, we aimed to investigate the prevalence of PVT among patients with liver cirrhosis in a tertiary hospital and identify the factors associated with this complication.

This was a cross-sectional observational study of 93 diagnosed liver cirrhosis patients treated at Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER) hospital in southern India between June 2020 and January 2021. A thorough evaluation of the clinical condition of the patients and associated comorbidities was done. The patients then underwent Doppler ultrasound/CECT/MRI to look for PVT and its extent. The collected data were analyzed using Statistical Product and Service Solutions (SPSS, version 24) (IBM SPSS Statistics for Windows, Armonk, NY). Comparison between two proportions was done using two two-tailed Z-test/Fisher's exact tests.

Our study found a PVT prevalence of 17.2% in cirrhotic patients, with a higher prevalence of acute PVT than chronic PVT. Ascitic fluid infection, longer duration of cirrhosis, and increased cirrhosis severity were significantly associated with PVT development. We found no significant associations between PVT and gender, hypertension, smoking, diabetes, or the duration of alcohol intake.

This study highlights the importance of early screening for PVT using Doppler USG in all patients diagnosed with cirrhosis. Additionally, anticoagulation therapy for acute PVT may be considered in patients without bleeding risks.

Although portal vein thrombosis (PVT) was thought to deteriorate portal hypertension and contribute to poor prognosis, risk stratification remains unclear. This study aimed to evaluate its effect on the risk of variceal rehemorrhage and to develop a competitive risk model in cirrhotic patients with PVT.

Cirrhotic patients with and without PVT admitted for acute variceal hemorrhage were retrospectively included after matching (1:1) for age, gender and etiology of cirrhosis from two tertiary centers with 1-year follow-up. Those with PVT were subsequently divided into the training and validation cohorts. Cox regression analysis was performed to identify risk factors and develop a competitive risk model, of which the predictive performance and optimal decision threshold were evaluated by C-index, competitive risk curves, calibration curves and decision curve analysis.

Among 398 patients, PVT significantly increased the variceal rehemorrhage risk. Multivariate Cox regression analysis identified that the Child-Turcotte-Pugh score (P = 0.013), chronic PVT (P = 0.025), C-reactive protein (P < 0.001), and aspartate aminotransferase (P = 0.039) were independently associated with variceal rehemorrhage, which were incorporated into the competitive risk model, with high C-index (0.804 and 0.742 of the training and validation cohorts, respectively), risk stratification ability, and consistency. The optimal decision range of the threshold probability was 0.2-1.0.

We confirmed the adverse effect of PVT on variceal rehemorrhage and developed a competitive risk model for variceal rehemorrhage in cirrhotic patients with PVT, which might be conveniently used for clinical decision-making.

Baveno VII workshop recommends management of acute variceal bleeding (AVB) in cirrhotic patients with nonmalignant portal vein thrombosis (PVT) should be performed according to the guidelines for patients without PVT. Nevertheless, whether PVT affects the outcome of patients with cirrhosis and AVB remains unclear. The aim of this study was to assess the clinical impact of PVT on the outcomes in the pre-emptive TIPSS eligible patients with cirrhosis and AVB.

From December 2010 to June 2016, 1219 consecutive cirrhotic patients admitted due to AVB with (n = 151; 12.4%) or without PVT (n = 1068; 87.6%), who received drug plus endoscopic treatment (a combination of vasoactive drugs, antibiotics, and endoscopic ligation for AVB, followed by beta-blockers plus variceal ligation for prevention of rebleeding) were retrospectively included. Fine and Gray competing risk regression models were taken to evaluate the impact of PVT on clinical outcomes after adjusting for potential confounders.

During follow-up, 211 patients (17.3%) died, 490 (40.2%) experienced further bleeding, and 78 (6.4%) experienced new or worsening ascites within 1 year. Compared with those without PVT, patients with PVT had a similar risk of mortality (PVT vs no-PVT: 19.9% vs 16.7% at 1 year; adjusted HR 0.88, 95%CI 0.51-1.52, p = 0.653), further bleeding (47.0% vs 39.2% at 1 year, adjusted HR 1.19, 95% CI 0.92-1.53, p = 183), and new or worsening ascites (7.9% vs 9.6%, adjusted HR 0.70, 95% CI 0.39-1.28, p = 0.253) after adjusting for confounders in multivariable models. These findings were consistent across different relevant subgroups and confirmed by propensity score matching analysis.

Our study showed no evidence that the PVT was associated with an improved or worsened outcome among cirrhotic patients with AVB who received standard treatment.

Patients with end-stage liver disease (ESLD) undergoing liver transplantation (LT) are prone to thromboses both while on the waiting list and in the perioperative period. This hypercoagulability is associated with significant endothelial dysfunction (ED) due to nitric oxide dysregulation. ED and increased thrombin generation are the main factors responsible for this hypercoagulability. Sepsis alone can significantly alter a patient's coagulation profile. In combination with ESLD, however, sepsis or septic shock are responsible for very complex changes. This makes both the assessment and management of coagulation in septic patients with ESLD very challenging. Viscoelastic testing (VET) is the preferred method of coagulation management in patients with cirrhosis because, as with standard laboratory testing, VET can assess the entire coagulation system including the interaction between both pro- and anticoagulants and platelets.

Occlusive portal vein thrombosis (PVT) often causes portal hypertension-related complications in cirrhotic patients. Transjugular intrahepatic portosystemic shunt (TIPS) is an effective treatment for this difficult problem. However, the factors influencing TIPS success and overall survival in patients with occlusive PVT are unknown. This study investigated the factors influencing TIPS success and overall survival in cirrhotic patients with occlusive PVT.

Cirrhotic patients with occlusive PVT were selected from a prospective database of consecutive patients treated with TIPS in Xijing Hospital between January 2015 and May 2021. Baseline characteristics, TIPS success rate, complications, and survival were collected, and the factors associated with the TIPS success rate and transplant-free survival were analyzed.

A total of 155 cirrhotic patients with occlusive PVT were enrolled. TIPS succeeded in 126 (81.29%) cases. The 1-year survival rate was 74%. Compared with those without, patients with portal fibrotic cord had a lower TIPS success rate (39.02% vs. 96.49%, p<0.001), shorter median overall survival (300 vs. 1,730 days, p<0.001) and more operation-related complications (12.20% vs. 1.75%, p<0.01). Logistic regression analysis found that portal fibrotic cord (odds ratio 0.024) was a risk factor for TIPS failure. Univariate and multivariate analysis showed that portal fibrotic cord was an independent predictor of death (hazard ratio 2.111; 95% CI: 1.094-4.071, p=0.026).

Portal fibrotic cord increased the TIPS failure rate and is a risk factor for poor prognosis in cirrhotic patients.

Vascular liver disorders (VLDs) comprise a wide spectrum of clinical-pathological entities that primarily affect the hepatic vascular system of both cirrhotic and non-cirrhotic patients. VLDs more frequently involve the portal and the hepatic veins, as well as liver sinusoids, resulting in an imbalance of liver homeostasis with serious consequences, such as the development of portal hypertension and liver fibrosis. Surprisingly, many VLDs are characterized by a prothrombotic phenotype. The molecular mechanisms that cause thrombosis in VLD are only partially explained by the alteration in the Virchow's triad (hypercoagulability, blood stasis, and endothelial damage) and nowadays their pathogenesis is incompletely described and understood. Studies about this topic have been hampered by the low incidence of VLDs in the general population and by the absence of suitable animal models. Recently, the role of coagulation imbalance in liver disease has been postulated as one of the main mechanisms linked to fibrogenesis, so a novel interest in vascular alterations of the liver has been renewed. This review provides a detailed analysis of the current knowledge of molecular mechanisms of VLD. We also focus on the promising role of anticoagulation as a strategy to prevent liver complications and to improve the outcome of these patients.

Acute esophageal variceal hemorrhage (AEVH) is a common complication of cirrhosis and might precipitate multi-organ failure, causing acute-on-chronic liver failure (ACLF).

To analyze if the presence and grading of ACLF as defined by European Society for the Study of the Liver-Chronic Liver Failure (EASL-CLIF) is able to predict mortality in cirrhotic patients presenting AEVH.

Retrospective cohort study executed in Hospital Geral de Caxias do Sul. Data from medical records from 2010 to 2016 were obtained by searching the hospital electronic database for patients who received terlipressin. Medical records were reviewed in order to determine the diagnosis of cirrhosis and AEVH, including 97 patients. Kaplan-Meier survival analysis was used for univariate analysis and a stepwise approach to the Cox regression for multivariate analysis.

All- cause mortality for AEVH patients was 36%, 40.2% and 49.4% for 30-, 90- and 365-day, respectively. The prevalence of ACLF was 41.3%. Of these, 35% grade 1, 50% grade 2 and 15% grade 3. In multivariate analysis, the non-use of non-selective beta-blockers, presence and higher grading of ACLF and higher Model for End-Stage Liver Disease scores were independently associated with higher mortality for 30-day with the addition of higher Child-Pugh scores for 90-day period.

Presence and grading of ACLF according to the EASL-CLIF criteria was independently associated with higher 30- and 90-day mortality in cirrhotic patients admitted due to AEVH.

Concepts regarding the status of the coagulation process in cirrhosis are rapidly changing. Instead of a disease defined by excessive bleeding risk, recent studies have shown cirrhosis to be associated with a fragile state of rebalanced hemostasis, easily swayed in either direction, thrombosis, or bleeding. These findings, combined with the ever-growing population of patients with cirrhosis with an indication for anticoagulation (AC) and the emergence of the non-alcoholic fatty liver disease epidemic, have prompted a reexamination of the use of AC in patients with cirrhosis, either as a treatment for a concurrent thrombotic disorder or even as a possible therapeutic option that could influence the natural course of the disease and its complications. In recent years, a significant number of studies have been formulated to evaluate these possibilities. These studies evaluated, among others, the efficacy and safety of AC in thrombotic disorders or thrombotic complications of cirrhosis, its effect on survival, and the class of anticoagulants which is more suitable for patients with cirrhosis, depending on disease severity. This review examines recent studies investigating the use of AC in patients with cirrhosis and attempts to provide a simple guide for clinicians regarding the use of AC in patients with cirrhosis and its potential risks and benefits.

The expression splanchnic vein thrombosis encompasses Budd-Chiari syndrome and portal vein thrombosis. These disorders have common characteristics: they are both rare diseases which can cause portal hypertension and its complications. Budd-Chiari syndrome and portal vein thrombosis in the absence of underlying liver disease share many risk factors, among which myeloproliferative neoplasms represent the most common; a rapid comprehensive work-up for risk factors of thrombosis is needed in these patients. Long-term anticoagulation is indicated in most patients. Portal vein thrombosis can also develop in patients with cirrhosis and in those with porto-sinusoidal vascular liver disease. The presence and nature of underlying liver disease impacts the management of portal vein thrombosis. Indications for anticoagulation in patients with cirrhosis are growing, while transjugular intrahepatic portosystemic shunt is now a second-line option. Due to the rarity of these diseases, studies yielding high-grade evidence are scarce. However, collaborative studies have provided new insight into the management of these patients. This article focuses on the causes, diagnosis, and management of patients with Budd-Chiari syndrome, portal vein thrombosis without underlying liver disease, or cirrhosis with non-malignant portal vein thrombosis.

Portal vein thrombosis (PVT) and acute variceal bleeding (AVB) are frequent complications of cirrhosis. The efficacy, safety, and timing of anticoagulant treatment in cirrhotic patients with PVT and AVB are contentious issues. We aimed to establish the safety and efficacy of initiating nadroparin calcium-warfarin sequential (NWS) anticoagulation therapy early after esophageal variceal band ligation within PVT patients having cirrhosis and AVB. Cirrhotic patients having AVB and PVT who underwent EVL were included and randomly allocated to either the NWS therapy group (1-month nadroparin calcium by subcutaneous injection following 5-month warfarin through oral administration, n = 43) or the control group (without any anticoagulation therapy, n = 43). The primary endpoint was the rate of PVT recanalization. Secondary endpoints included major bleeding events mainly referring to variceal rebleeding (5-day failure, 14-day, 4-week, 6-week, and 6-month rebleeding rates) and mortality after EVL. The overall recanalization (complete and partial) rate in the NWS therapy group was significantly higher than that in the control group (67.4% vs. 39.5%, P = 0.009). Low Child-Pugh score (P = 0.039, OR: 0.692, 95% CI 0.488-0.982), D-dimer < 2.00 ug/mL (P = 0.030, OR: 3.600, 95% CI 1.134-11.430), and NWS anticoagulation therapy (P = 0.002, OR: 4.189, 95% CI 1.660-10.568) were the predictors of PVT recanalization through univariate analysis of binary logistic regression. NWS anticoagulation therapy (P = 0.003, OR: 4.506, 95% CI 1.687-12.037) was the independent factor of recanalization through multivariate analysis. Nobody bled except for variceal rebleeding. Five-day failure and 14-day rebleeding were zero. There were no significantly different in 4-week (2.3% vs. 4.7%, P = 1.000), 6-week (4.7% vs. 9.3%, P = 0.672) and 6-month rebleeding (18.6% vs. 20.9%, P = 0.787) between the two groups. There was no mortality during six months follow-up. Low serum albumin (P = 0.011, OR: 0.844, 95% CI 0.741-0.962), high MELD score (P = 0.003, OR: 1.564, 95% CI 1.167-2.097) and Child-Pugh score (P = 0.006, OR: 1.950, 95% CI 1.206-3.155) were predictors of rebleeding by univariate analysis of binary logistic regression analysis. The Child-Pugh score (7 [6-8] vs. 6 [5-7], P = 0.003) and albumin levels (33.93 ± 5.30 vs. 37.28 ± 4.32, P = 0.002) were improved in the NWS therapy group at six months. In PVT patients with cirrhosis and AVB, starting NWS anticoagulation therapy early after EVL was safe and effective. It has the potential to raise albumin levels and improve liver function.

the incidence of acute-on-chronic liver disease (AoCLD) is increasing.

to investigate the clinical features and risk factors of AoCLD and construct an effective prognostic nomogram model for older patients with AoCLD.

data from 3,970 patients included in the CATCH-LIFE study were used, including 2,600 and 1,370 patients in the training and validation sets, respectively. Multivariate Cox regression analyses were performed to identify predictive risk factors in older individuals, and an easy-to-use nomogram was established. Performance was assessed using area under the curve, calibration plots and decision curve analysis (DCA).

of the 3,949 patients with AoCLD, 809 were older with a higher proportion of autoimmune-related abnormalities, hepatitis C viral infection and schistosomiasis. In the older patient group, the incidence of cirrhosis, hepatic encephalopathy (HE), infection, ascites and gastrointestinal bleeding; neutrophil-to-lymphocyte ratio (NLR), aspartate-to-alanine transaminase ratio (AST/ALT), creatinine and blood urea nitrogen levels were higher, whereas incidence of acute-on-chronic liver failure, white blood cell, platelet and haemoglobin levels; albumin, total bilirubin (TB), AST and ALT levels; international normalised ratio (INR), estimated glomerular filtration rate and blood potassium levels were lower than in the younger group. The final nomogram was developed based on the multivariate Cox analysis in training cohort using six risk factors: ascites, HE grades, NLR, TB, INR and AST/ALT. Liver transplantation-free mortality predictions were comparable between the training and validation sets. DCA showed higher net benefit for the nomograph than the treat-all or treat-none strategies, with wider threshold probabilities ranges.

our analysis will assist clinical predictions and prognoses in older patients with AoCLD.

Portal vein thrombosis (PVT) is an increasingly recognized complication of cirrhosis and possibly associated with mortality. This study aims to evaluate provoking factors for PVT, then establish a concise and efficient nomogram for predicting PVT presence among admitted cirrhotic patients.

All cirrhotic patients admitted in Hunan Provincial People's Hospital between January 2010 and September 2020 were retrospectively reviewed, the clinical and laboratory data were collected. Multivariate logistic regression analysis and the least absolute shrinkage and selection operator regression method were used for screening the independent predictors and constructing the nomogram. The calibration curve was plotted to evaluate the consistent degree between observed outcomes and predicted probabilities. The area under the receiver operating characteristics curve was used to assess the discriminant performance. The decision curve analysis (DCA) was carried out to evaluate the benefits of nomogram.

A total of 4,479 patients with cirrhosis were enrolled and 281 patients were identified with PVT. Smoking history, splenomegaly, esophagogastric varices, surgical history, red blood cell transfusion, and D-dimer were independent risk factors for PVT in cirrhosis. A nomogram was established with a good discrimination capacity and predictive efficiency with an the area under the curve (AUC) of 0.704 (95% CI: 0.664-0.745) in the training set and 0.685 (95% CI: 0.615-0.754) in the validation set. DCA suggested the net benefit of nomogram had a superior risk threshold probability.

A concise and efficient nomogram was established with good performance, which may aid clinical decision making and guide best treatment measures.

Portal vein thrombosis (PVT) is a common complication in cirrhotic patients and will aggravate portal hypertension, thus leading to a series of severe complications. The aim of this study was to develop a nomogram based on a simple and effective model to predict PVT in cirrhotic patients.

Clinical data of 656 cirrhotic patients with or without PVT in the First Affiliated Hospital of Soochow University and The Third Affiliated Hospital of Nantong University from January 2017 to March 2022 were retrospectively collected, and all patients were divided into training, internal and external validation cohorts. SPSS and R software were used to identify the independent risk factors and construct a predictive model. We evaluated the predictive value of the model by receiver operating characteristic (ROC) curve, calibration curve, and decision curve analyses. The feasibility of the model was further validated in the internal and external cohorts. All enrolled patients were followed up to construct the survival curves and calculate the incidence of complications.

The predictors of PVT included serum albumin, D-dimer, portal vein diameter, splenectomy, and esophageal and gastric varices. Based on the clinical and imaging findings, the final model served as a potential tool for predicting PVT in cirrhotic patients, with an AUC of 0.806 (0.766 in the internal validation cohort and 0.845 in the external validation cohort). The decision curve analysis revealed that the model had a high level of concordance between different medical centers. There was a significant difference between the PVT and non-PVT groups in survival analyses, with p values of 0.0477 and 0.0319 in the training and internal validation groups, respectively, along with p value of 0.0002 in the external validation group according to log-rank test; meanwhile, the median survival times of the PVT group were 54, 43, and 40 months, respectively. The incidence of recurrent esophageal and gastric variceal bleeding (EGVB) during the follow-up showed significant differences among the three cohorts (p = 0.009, 0.048, and 0.001 in the training, internal validation, and external validation cohorts, respectively).

The nomogram based on our model provides a simple and convenient method for predicting PVT in cirrhotic patients. Cirrhotic patients with PVT had a shorter survival time and were prone to recurrent EGVB compared with those in the non-PVT group.

The association between thrombolytic therapy and the outcome in patients with portal vein thrombosis (PVT) remains controversial. This study aimed to evaluate the outcome in patients with PVT who received antithrombin III-based therapy.

This study was a retrospective, multicenter study to investigate the liver-related events and the survival rates in 240 patients with PVT who received the therapy.

The patients comprised 151 men and 89 women, with a median age of 69 years. The rate of favorable response, defined as maximum area of PVT changed to ≤75%, was 67.5% (162/240). The cumulative rates of liver-related events at 1, 2, and 3 years were 38.2%, 53.9%, and 68.5%, respectively. The multivariate analysis showed that viable hepatocellular carcinoma, absence of maintenance therapy, non-responder, and PVT progression were significantly associated with liver-related events. The PVT progression was observed in 23.3% (56/240). The multivariate analysis identified older age, absence of maintenance therapy, and non-responder as independent factors associated with PVT progression. The multivariate analysis revealed that younger age, no hepatocellular carcinoma, presence of maintenance therapy, and lower Model for End-stage Liver Disease-Sodium score significantly contributed to 3-year survival. Of the 240 patients, 13 (8.9%) prematurely discontinued treatment due to any adverse events.

This study suggests that maintenance therapy, favorable response, and absence of PVT progression may suppress or control liver-related events in antithrombin III-based therapy for patients with PVT. Specifically, maintenance therapy could suppress not only liver-related events, but also PVT progression and improve the prognosis.

The accuracy of model for end-stage liver disease (MELD) and MELD with sodium (MELD-Na) scores in reflecting the clinical outcomes of patients with cirrhosis and portal vein thrombosis (PVT) remains unclear. This study aimed to evaluate the performance of scores in predicting 90-day mortality in patients with cirrhosis and PVT.

Post hoc analysis was performed in two prospective cohorts (NCT02457637 and NCT03641872). The correlation between the MELD/MELD-Na score and 90-day liver transplantation (LT)-free mortality was investigated in patients with cirrhosis with and without PVT.

In this study, 2826 patients with cirrhosis were included, and 255 (9.02%) had PVT. The cumulative incidence of 90-day LT-free mortality did not significantly differ between patients with and without PVT (log-rank P = 0.0854). MELD [area under the receiver operating curve (AUROC), 0.649 vs. 0.842; P = 0.0036] and MELD-Na scores (AUROC, 0.691 vs. 0.851; P = 0.0108) were compared in patients with and without PVT, regarding the prediction of 90-day LT-free mortality. In MELD < 15 and MELD-Na < 20 subgroups, patients with PVT had a higher 90-day LT-free mortality than those without PVT (7.91% vs. 2.64%, log-rank P = 0.0011; 7.14% vs. 3.43%, log-rank P = 0.0223), whereas in MELD ≥ 15 and MELD-Na ≥ 20 subgroups, no significant difference was observed between patients with and without PVT.

The performance of MELD and MELD-Na scores in predicting 90-day LT-free mortality of patients with cirrhosis was compromised by PVT. MELD < 15 or MELD-Na < 20 may underestimate the 90-day LT-free mortality in patients with PVT.