Portal Vein Thrombosis In Patients Research Articles

Clinical characteristics and predictors of benign portal vein thrombosis in patients with liver cirrhosis: A retrospective single-center study.

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 in Liver Cirrhosis. Part 1: Epidemiology, Pathogenesis, Clinic, Diag-nosis, Impact on Prognosis

Portal vein thrombosis is the most common thrombotic complication in patients with liver cirrhosis, especially in cases of severe forms. The pathogenesis is multifactorial in nature, it determined by a change in the balance between the coagulation and anticoagulation systems. Thrombosis is often asymptomatic and is accidentally detected, although it can be complicated by varicose bleeding, intestinal ischemia, and portal biliopathy. Ultrasound Doppler examination is a screening method, as an alternative, computed tomography and magnetic resonance imaging are used. The review highlights data on epidemiology, risk factors, clinical features, and diagnosis of portal vein thrombosis in patients with liver cirrhosis. The data on the effect of portal vein thrombosis on the progression of liver cirrhosis and the survival of patients, including after liver transplantation, are presented.

Metabolic dysfunction-associated steatotic liver disease related cirrhosis and incidence of portal vein thrombosis.

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.

Platelet Activation is Upregulated in Cirrhotic Patients with Portal Vein Thrombosis.

Platelet plays a key role in thrombosis formation, especially that the alteration of platelet function may influence the thrombosis development. This study aimed to investigate platelet function alterations in the formation of portal vein thrombosis (PVT) in cirrhosis. Cirrhotic patients admitted to The First Affiliated Hospital of Soochow University between October 2021 and April 2023 were recruited and divided into PVT and non-PVT groups according to radiological results. Clinical parameters and prognosis were also collected and assessed to identify potential risk factors. Flow cytometry was used to detect the expression of CD62p, CD63, monocyte-platelet aggregates (MPAs), neutrophil-platelet aggregates (NPAs), and von Willebrand factor antigen (vWF-Ag) to evaluate platelet activation and adhesion function. A total of 145 subjects were enrolled in our study including 60 cirrhotic PVT patients, 60 cirrhotic non-PVT patients, and 25 healthy volunteers. Multivariate analysis suggested that esophageal gastric varices, splenectomy, and D-dimer were independent risk factors for PVT pathogenesis in cirrhosis. The vWF-Ag expression level was reduced in the PVT group compared with the non-PVT group (p = 0.046) but was not an independent risk factor for PVT formation pathogenesis. The expression of CD41+CD62p+ and CD41+CD63+ platelets in the PVT group was significantly elevated compared with that in the non-PVT group (p < 0.05). There were no significant differences in MPAs and NPAs between the two cirrhotic groups. Subgroup analysis showed that the mean fluorescence intensity (MFI) of CD62p and CD63 was associated with portal hypertension-related complications (p = 0.008, p < 0.001), and CD63 MFI was significantly associated with thrombosis burden (p = 0.019). CD41+CD62p+ and CD41+CD63+ platelets as well as MPAs and NPAs were highly expressed in the splenectomy group compared with those in the nonsplenectomy group in cirrhotic patients (p < 0.05). Positive correlations were found between CD62p MFI and CD63 MFI, MPAs and NPAs (r = 0.642, p < 0.001; r = 0.378, p = 0.003; r = 0.430, p < 0.001). In addition, platelet counts were also correlated with MPAs (r = 0.556, p < 0.001) and NPAs (r = 0.467, p < 0.001). Cirrhotic patients with PVT had higher mortality and were more likely to experience portal hypertension-related complications in the prognostic analysis (p < 0.05). Highly activated platelet function exists in patients with cirrhosis, and platelet activation was elevated during PVT formation, suggesting that activated platelets may participate in the formation of PVT in patients with cirrhosis.

Systemic Thrombolysis of Acute Portal Venous System Thrombosis in Patients with Liver Cirrhosis: A Pilot Study

Background The prevalence of Portal Vein Thrombosis (PVT) is highly variable at different stages of liver disease: in compensated patients 10%, in decompensated patients 17%, in acute decompensated cirrhosis 9%, and in post-liver transplantation patients 2-26%. Aim The aim of the study was to assess the efficacy and safety of systemic thrombolysis in acute portal vein thrombosis in patients with liver cirrhosis. Methods A total of 10 compensated cirrhotic patients with acute portal vein thrombosis were examined by abdominal ultrasonography with color Doppler and Contrast-enhanced computerized tomography. Continuous intravenous infusion of recombinant tissue plasminogen activator(r-tPA.) and Low molecular weight heparin (LMWH) was used to treat all patients for a maximum of 7 days. Patients were followed up for improvement of clinical symptoms and radiological by abdominal ultrasound with color Doppler and contrast-enhanced computerized tomography. Results The regimen of therapy was found to be well-tolerated by all the patients. At the end of the seven days, six patients (60%) had full recanalization of the portal vein, while three had partial recanalization (30%) and no recanalization in only one patient (10%). Conclusion The preliminary data indicate that systemic thrombolytic therapy combined with low molecular weight heparin for the treatment of PVT appears to be safe and effective over a few days with no clinically significant side effects.

Predictive model for non-malignant portal vein thrombosis associated with cirrhosis based on inflammatory biomarkers.

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.

Portal Vein Thrombosis in Patients with Cirrhosis

Portal Vein Thrombosis in Patients with Cirrhosis

Statin use in cirrhosis and its association with incidence of portal vein thrombosis.

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 180days 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±12.3years, 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.

P239 Characteristics and outcomes of portal vein thrombosis in patients with Inflammatory Bowel Disease in Korea

Abstract Background Portal vein thrombosis (PVT) is known to occur frequently in patients with inflammatory bowel disease (IBD), particularly when compounded by factors such as abdominal infection, IBD flares, or intra-abdominal surgery. However, PVT can lead to diverse complications, causing acute issues like intestinal ischemia or necrosis and long-term problems such as portal hypertension, varices, and ascites. Nevertheless, there is a significant shortage of research regarding the characteristics and prognosis of PVT in the context of IBD. Particularly, with the rising prevalence of IBD patients in Asia, the authors conducted an evaluation of clinical presentation and prognosis of PVT in IBD patients at a large tertiary hospital in South Korea. Methods This study is a retrospective study conducted at a single tertiary center in South Korea. It examined patients aged 18 and above diagnosed with inflammatory bowel disease (IBD) who had confirmed portal vein thrombosis (PVT) between June 1, 1989, and December 15, 2021. The study focused on investigating patient characteristics, PVT characteristics, treatment methods, and outcomes. The diagnosis and resolution of PVT were confirmed using enhanced CT imaging. Results A total of 78 patients met the inclusion criteria for this study. Only 21% (16/78) received oral anticoagulants, yet nearly all patients (96%; 75/78) achieved Complete Radiologic Resolution (CRR). When comparing baseline characteristics between the anticoagulation use group and the non-use group, a trend was observed with a higher utilization of anticoagulants in cases where the main portal vein was involved rather than only the left or right portal vein (p-value 0.006). However, when conducting multivariable analysis, no factors significantly influenced CRR, especially anticoagulant use and surgery status. Conclusion PVT concomitant with IBD demonstrated favorable outcomes regardless of anticoagulation use.

Portal vein thrombosis in patients with liver cirrhosis

Background/Aim. Portal vein thrombosis (PVT) in patients with liver cirrhosis (LC) has a prevalence of 0.6- 26%. It is most commonly discovered incidentally as part of the evaluation of LC or in the context of acute decompensation of LC due to portal hypertension. The aim of the study was to determine the prevalence of PVT in patients with LC in relation to the severity of the disease and individual elements of portal hypertension. Methods. A total of 326 patients treated for LC decompensation were included in a retrospective study. Standard laboratory analyses, abdominal ultrasonography and/or computed tomography, and esophagogastroduodenoscopy were performed. Results. The diameter of the portal vein (PV) differed between patients without esophageal varices (12.2 mm) and those with large varices (13.6 mm), p = 0.026. PVT was identified in 6.1% of patients with LC. The patients were classified according to the Child-Pugh scoring system, which has the A, B, and C categories used to assess the severity of liver disease. PVT was present in 3.0% of patients in class C and 12.0% in class B, while none of the patients in class A had PVT (p = 0.005). PVT was present in 4.4% of patients with small varices and 16.7% with large varices (p &lt; 0.001). There was no difference in the presence of PVT between the groups of patients with and without variceal bleeding nor between groups with different degrees of ascites. A fatal outcome occurred in 29.4% of patients, but there was no difference between patients with and without PVT. Conclusion. PVT is present in more advanced stages of LC and predominantly in patients with large esophageal varices. There was no higher prevalence of PVT observed with the occurrence of variceal bleeding or with the death outcome in patients with LC.

Relationship between Neutrophil/Lymphocyte Ratio (NLR), Platelet/Lymphocyte Ratio (PLR) and Thrombosis in Patients with Portal Vein Thrombosis (PVT) without Acquired Risk Factor for Thrombosis.

Inflammation occurring after vascular endothelial damage plays a role in thrombus formation. Changes in various blood parameters that develop after the inflammatory condition can be used as a marker to predict thrombus. This study aimed to investigate the relationship between the neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), and portal vein thrombosis (PVT). After applying the exclusion and inclusion criteria to the patients diagnosed with PVT and followed up in our center between January 2006 and May 2018, a total of 38 patients without acquired risk factors for the development of PVT and 52 healthy controls were included in the study. Clinical features and NLR and PLR at diagnosis were evaluated. NLR and PLR values were detected to be significantly higher in patients diagnosed with PVT compared to the control group (P < 0.001 for NLR, P < 0.001 for PLR). Findings were as follows: In acute PVT patients for NLR = 3.645 (area under the receiver operating characteristic (AUROC) 0.886, sensitivity 69.2%, specificity 96.2%, P < 0.001), for PLR = 196.24 (AUROC 0.754, sensitivity 53.2%, specificity 96.2%, P = 0.005), while in chronic PVT patients, for NLR = 3.645 (AUROC 0.744, sensitivity 40%, specificity 96.2%, P = 0.001), and for PLR = 195.93 (AUROC 0.715, sensitivity 44%, specificity 96.2%, P = 0.002). NLR and PLR were associated with the diagnosis of PVT. In PVT patients, NLR and PLR values were observed to be significantly higher than the control group. In our study, the relationship between NLR and PLR in patients with noncirrhotic, nonmalignant PVT without acquired risk factors for thrombosis was shown for the first time.

A nomogram model to predict the portal vein thrombosis risk after surgery in patients with pancreatic cancer.

Portal vein thrombosis (PVT) is a common postoperative complication in patients with pancreatic cancer (PC), significantly affecting their quality of life and long-term prognosis. Our aim is to establish a new nomogram to predict the risk of PVT after PC surgery. We collected data from 416 patients who underwent PC surgery at our hospital between January 2011 and June 2022. This includes 87 patients with PVT and 329 patients without PVT. The patients were randomly divided into a training group and a validation group at a ratio of 7:3. We constructed a nomogram model using the outcomes from both univariate and multivariate logistic regression analyses conducted on the training group. The nomogram's predictive capacity was assessed using calibration curve, receiver operating characteristic (ROC) curve, and decision curve analysis (DCA). In the study, the prevalence of PVT was 20.9%. Age, albumin, vein reconstruction and preoperative D-dimer were independent related factors. The model achieved a C-index of 0.810 (95% confidence interval: 0.752-0.867), demonstrating excellent discrimination and calibration performance. The area under the ROC curve of the nomogram was 0.829 (95% CI: 0.750-0.909) in the validation group. DCA confirmed that the nomogram model was clinically useful when the incidence of PVT in patients was 5%-60%. We have established a high-performance nomogram for predicting the risk of PVT in patients undergoing PC surgery. This will assist clinical doctors in identifying individuals at high risk of PVT and taking appropriate preventive measures.

Role of contrast-enhanced ultrasound for differentiation of benign vs. malignant portal vein thrombosis in hepatocellular carcinoma - Asystematic review a meta-analysis.

Patients with cirrhosis and hepatocellular carcinoma (HCC) can develop both benign and malignant portal vein thrombosis (PVT). Characterising the nature of PVT is important for planning an optimal therapeutic strategy. In the absence of typical findings or contraindications to computed tomography (CT) or magnetic resonance imaging (MRI), contrast-enhanced ultrasound (CEUS) could help in this differentiation. The present meta-analysis aimed to evaluate the performance of CEUS for characterising PVT in patients with HCC. Electronic databases of PubMed, Embase and Scopus were searched from inception to 31 December 2022 for studies analysing the role of CEUS in the differentiation of benign and malignant PVT in HCC. Using the bivariate random effect model, pooled sensitivity and specificity were calculated, and the summary receiver operating characteristic (sROC) curve was plotted. A total of 12 studies with data from 712 patients were included in the meta-analysis. The pooled sensitivity and specificity of CEUS for the diagnosis of tumour in vein were 97.0% (95% CI: 93.0-98.7) and 96.8% (95% CI: 92.1-98.7), respectively, without significant heterogeneity. A sROC curve was plotted, and the area under the receiver operating characteristic was 0.99 (95% CI: 0.98-1.00). Despite the presence of publication bias, sensitivity analysis did not show any change in sensitivity and specificity. Our meta-analysis summarises the accuracy data from 12 studies, including >700 subjects. Contrast-enhanced ultrasound had excellent diagnostic accuracy with pooled sensitivity and specificity of 97.5% (95% CI: 93.5-99.1) and 98.2% (95% CI: 91.5-99.6), respectively, without any significant heterogeneity. Additionally, the pooled positive LR, negative LR and DOR were 54.6 (95% CI: 11.1-25.6), 0.02 (0.01-0.07) and 2186.8 (318.3-15022.2), respectively. A positive result increases the pretest probability of malignant PVT from 50% to 98%, whereas a negative result decreases it from 50% to 2%. Most of the studies included in our meta-analysis used identical techniques and 6-12-month follow-up scans to check for thrombus progression or regression. Our analysis showed no significant heterogeneity in the studies, and area under receiver operating characteristic curve (AUROC) with 95% CI was 1.00 (95% CI: 0.99-1.00). This critical meta-analysis thus propels CEUS to the forefront for differentiating benign from tumoural PVT and suggests routinely using CEUS in patients presenting with HCC and evidence of thrombus on greyscale ultrasound. Contrast-enhanced ultrasound is an effective diagnostic modality differentiation of benign and malignant PVT in patients with HCC and can be an alternative modality to CT or MRI. Further studies are required to study the role of CEUS as initial diagnostic modality for the characterisation of PVT in HCC.

Prevalence of portal vein thrombosis in non-alcoholic fatty liver disease: a meta-analysis of observational studies.

Portal vein thrombosis (PVT) is a common complication of cirrhosis as a result of portal hypertension and modification in the hemostatic balance. Accumulating evidence now suggests that patients with non-alcoholic fatty liver disease (NAFLD), especially those with advanced forms, have an increased risk of PVT. Hence, we performed a meta-analysis of observational studies to estimate the overall prevalence of PVT in patients with NAFLD and its advanced forms compared with patients with advanced liver diseases from other etiologies.We systematically searched PubMed, Scopus and Web of Science databases from the inception date to December 30th 2022, using predefined keywords, to identify observational studies. Meta-analysis was performed using random-effects modeling.We included five observational studies for a total of 225,571 patients. Of these, 26,840 (11.9%) patients had NAFLD, whereas the PVT prevalence was 8.5% (n = 2,280). When compared with patients with advanced liver diseases from other etiologies, patients with NAFLD and its advanced forms had a higher risk of prevalent PVT (OR 1.34, 100% CI 1.07-1.67 p < 0,01). The between-study heterogeneity was substantial (I2 = 88%).This meta-analysis suggests that compared with patients with advanced liver diseases from other etiologies, patient with NAFLD and its advanced forms had a higher risk of prevalent PVT. Further research is required to understand the complex link between NAFLD/NASH and PVT development.

Portal Vein Thrombosis in Patients With Cirrhosis of the Liver: Prevalence and Risk Factors.

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.

Predicting de-novo portal vein thrombosis after HCV eradication: A long-term competing risk analysis in the ongoing PITER cohort.

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 38.3months (IQR: 25.1-48.7months) after the end of treatment (EOT), among 1609 SVR patients, 32 (2.0%) developed de novo PVT. Aplatelet count ≤120,000/μL, albumin levels ≤3.5mg/dL, bilirubin >1.1mg/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.

Risk factors and construction of a nomogram model for cirrhotic portal vein thrombosis combined with esophagogastric variceal bleeding

Objective: To investigate the risk factors and construct a nomogram model for predicting the occurrence of cirrhotic portal vein thrombosis in patients combined with esophagogastric variceal bleeding (EVB). Methods: Clinical data on 416 cirrhotic PVT cases was collected from the First Hospital of Lanzhou University between January 2016 and January 2022. A total of 385 cases were included after excluding 31 cases for retrospective analysis. They were divided into an esophagogastric variceal bleeding group and a non-esophagogastric variceal bleeding group based on the clinical diagnosis. The esophagogastric variceal group was then further divided into an EVB group and a non-bleeding group. All patients underwent gastroscopy, serology, and imaging examinations. The risk factors of PVT combined with EVB were identified by univariate analysis using SPSS 26. The prediction model of cirrhotic PVT in patients combined with EVB was constructed by R 4.0.4. The prediction efficiency and clinical benefits of the model were evaluated by the C-index, area under the receiver operating characteristic curve, calibration plots, and decision curve. The measurement data were examined by a t-test or Mann-Whitney U test. The counting data were tested using the χ(2) test or the Fisher exact probability method. Results: There were statistically significant differences in the etiology, Child-Pugh grade,erythrocyte count, hematocrit, globulin, and serum lipids between the esophageal and non-esophageal varices groups (P < 0.05). There were statistically significant differences in etiology, erythrocyte count, hemoglobin, hematocrit, neutrophil percentage, total protein, globulin, albumin/globulin, urea, high-density lipoprotein cholesterol, calcium, and neutrophil lymphocyte ratio (NLR) between the EVB and non-bleeding groups (P < 0.05). Multivariate logistic regression analysis showed that etiology (OR = 3.287, 95% CI: 1.497 ~ 7.214), hematocrit (OR = 0.897, 95% CI: 0.853 ~ 0.943), and high-density lipoprotein cholesterol (OR = 0.229, 95% CI: 0.071 ~ 0.737) were independent risk factors for cirrhotic PVT patients combined with EVB. The constructed normogram model predicted the probability of bleeding in patients. The nomogram model had shown good consistency and differentiation (AUC = 0.820, 95% CI: 0.707 ~ 0.843), as verified by 10-fold cross-validation (C-index = 0.799) and the Hosmer-Lemeshow goodness of fit test (P = 0.915). The calibration plot and the decision curve suggested that the prediction model had good stability and clinical practicability. Conclusion: The risk factors for EVB occurrence include etiology, erythrocyte, hemoglobin, hematocrit, percentage of neutrophils, total protein, globulin, albumin/globulin, urea, high-density lipoprotein cholesterol, calcium, and NLR in patients with cirrhotic liver. The constructed prediction model has good predictive value, and it can provide a reference for medical personnel to screen patients with high bleeding risk for targeted treatment.

The Role of Contrast-Enhanced Ultrasound (CEUS) in the Detection of Neoplastic Portal Vein Thrombosis in Patients with Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is the principal primary liver cancer and one of the most frequent malignant tumors worldwide in patients with chronic liver disease. When diagnosed at an advanced stage, it is often associated with portal vein tumor thrombosis (PVTT), which heavily affects patients' prognosis. Imaging evaluation is crucial in PVTT detection and staging; computed tomography and magnetic resonance are the principal diagnostic tools. Contrast-enhanced ultrasound (CEUS) is a non-invasive and easily repeatable method that can also be used in patients with impaired renal function. It represents an important means for the identification of PVTT, particularly differentiating neoplastic and non-neoplastic thrombosis through the analysis of ultrasound enhancement characteristics of the thrombosis (arterial hyperenhancement and portal washout), thus allowing more refined disease staging, appropriate treatment planning, and response evaluation, along with prognosis assessment.

Causes for the absence of thrombocytopenia in patients with liver cirrhosis and portal vein thrombosis: A case-control study

Background: Complications of liver cirrhosis (LC), such as thrombocytopenia and portal vein thrombosis (PVT), have similar pathophysiology. However, the association between PVT and platelet count in LC patients is contradictory.&#x0D; Aim: To assess factors affecting the platelet count in patients with LC and PVT.&#x0D; Materials and methods: This was a retrospective case-control study. The cases were 114 patients with LC of various etiologies and newly diagnosed PVT unrelated to invasive hepatocellular carcinoma. From the database of LC patients without PVT, 228 controls were randomly selected with stratification by gender, age and etiology of cirrhosis. The patients from both groups were divided into subgroups with thrombocytopenia ( 150 × 109/L) and without thrombocytopenia (≥ 150 × 109/L). We analyzed the LC etiology, portal hypertension severity (ascites, hepatic encephalopathy, gastroesophageal varices and associated bleedings, the spleen length, and portal vein diameter), laboratory parameters (white blood cell counts, neutrophils, lymphocytes, hemoglobin levels, total protein, albumin, total bilirubin, fibrinogen, neutrophil-to-lymphocyte ratio, and prothrombin); also, the rates of newly diagnosed malignant tumors was assessed. The statistical analysis included calculation of odds ratios (OR) and 95% confidence intervals (CI), logistic regression models with assessment of the model accuracy, and the area under the ROC curve (AUC).&#x0D; Results: There were no differences in the severity of thrombocytopenia between the case and control groups: thrombocytopenia was severe in 15.8% (18 patients) vs 13.6% (31 patients, p = 0.586); moderate, in 41.2% (47 patients) vs 46.1% (105 patients, p = 0.398) and mild, in 31.6% (36 patients) vs 24.5% (56 patients, p = 0.168). The proportion of the patients without thrombocytopenia was 11.4% (13 patients) in the case group and 15.8% (36 patients) in the control group, with the between-group difference being non-significant (p = 0.276). In the subgroups of patients without thrombocytopenia (both in the cases and in the controls), the proportion alcoholic etiology of LC, white blood cells counts, neutrophils, lymphocytes, and fibrinogen concentrations were significantly higher (p 0.05) than in those with thrombocytopenia. The model based on the outcome "absence of thrombocytopenia" included white blood cells counts, hemoglobin and albumin levels, the presence of newly diagnosed malignant tumors in the case group (model accuracy 90.4%, AUC 0.873), and neutrophil counts and spleen length in the control group (model accuracy 86.4%, AUC 0.855). In the patients with PVT and platelet counts of ≥ 150 × 109/L, the OR for all newly diagnosed malignant tumors was 26.3 (95% CI 7.37–93.97, р 0.0001), for newly diagnosed hepatocellular carcinoma without portal vein invasion 17.42 (95% CI 4.84–62.65, р 0.0001).&#x0D; Conclusion: In LC patients, the prevalence and severity of thrombocytopenia are not different depending on the PVT presence or absence. The absence of thrombocytopenia in PVT patients is associated with a higher risk of malignant tumors identification, primarily that of hepatocellular carcinoma.

Prothrombotic states in portal vein thrombosis and Budd-Chiari syndrome in India: A systematic review and meta-analysis.

Both Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT) have been linked to various prothrombotic (PT) conditions. The PT profile in Asians is different from the west and there are no nationwide epidemiological surveys from India. Hence, the present meta-analysis was aimed at analyzing the prevalence of acquired and hereditary thrombophilia among Indian patients with non-cirrhotic PVT and BCS. A comprehensive literature search of Embase, Medline and Scopus was conducted from January 2000 to February 2022 for studies evaluating the prevalence of various PT conditions in Indian patients with PVT and BCS. Pooled prevalence rates across studies were expressed with summative statistics. Thirty-five studies with 1005 PVT patients and 1391 BCS patients were included in the meta-analysis. At least one PT condition was seen in 46.2% (28.7-63.7) of the PVT patients and 44.9% (37.3-60.7) of the BCS patients. Multiple PT conditions were seen in 13.0% (4.2-21.8) of the PVT patients and 7.9% (3.5-12.4) of the BCS patients. Among PVT patients, hyperhomocysteinemia was the commonest prothrombotic condition (21.6%) followed by protein C (PC) deficiency (10.7%), Janus kinase 2(JAK-2) mutation (8.5%) and antiphospholipid antibodies (APLA) (7.5%). Among patients with BCS, PC deficiency was the commonest prothrombotic condition (10.6%) followed by methylenetetrahydrofolate reductase (MTHFR) mutation (9.8%), APLA (9.7%) and JAK-2 mutation (9.1%). The PT profile in Indian patients with abdominal vein thrombosis is different from that of the western data with a lower prevalence of PT conditions in patients with BCS.