Development Of Portal Vein Thrombosis Research Articles

Predictive value of hepatic venous pressure gradient in cirrhotic portal vein thrombosis development

Background & AimsThere 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. MethodsThe 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. ResultsEighty-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%. ConclusionsIn 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.

The Molecular Mechanisms of Portal Vein Thrombosis in Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) represents the sixth most diagnosed cancer worldwide and is the second leading cause of cancer-related death in the world. The association of HCC and portal vein thrombosis (PVT) represents an advanced stage of the tumor. PVT has a prevalence of about 25–50% in HCC, determining poor prognosis and a remarkable reduction in therapeutic perspectives in these patients, leading to severe complications such as ascites, metastasis, an increase in portal hypertension and potentially fatal gastrointestinal bleeding. The aim of this review is to evaluate the molecular mechanisms that are at the basis of PVT development, trying to evaluate possible strategies in the early detection of patients at high risk of PVT.

Effect of factor VIII and FVIII/PC ratio on portal vein thrombosis in liver cirrhosis: a systematic review and meta‑analysis

BackgroundTo 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.MethodsThe 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.ResultsThe 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%).ConclusionIn 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.

GSDMD-Dependent Neutrophil Extracellular Traps Mediate Portal Vein Thrombosis and Associated Fibrosis in Cirrhosis.

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.

Carvedilol to prevent decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by liver stiffness: study protocol for a randomied, double-blind, placebo-controlled, multicentre trial in China

IntroductionPatients with clinically significant portal hypertension (CSPH) are recommended to be treated with non-selective beta-blockers (ie, carvedilol) to prevent the first hepatic decompensation event by the renewing Baveno VII consensus....

Neutrophil extracellular traps formation may be involved in the association of propranolol with the development of portal vein thrombosis

Background & aimsNonselective 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. Materials and methodsSerum 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. ResultsSerum 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. ConclusionOur study provides a clue to the potential impact of NETs formation on the association of NSBBs with the development of PVT.

Bacterial infections as a risk factor for non-neoplastic portal vein thrombosis development in cirrhotic patients.

Portal vein thrombosis (PVT) and sepsis are common complications in patients with liver cirrhosis. Factors that lead to PVT are not completely understood. This study aimed to investigate the possible association between bacterial infections and the development of PVT in cirrhotic patients. 202 consecutive cirrhotic patients without previous infections, followed at the Liver Unit in Verona Hospital, were enrolled from 2017 to 2021 (median follow-up 3.3 years). During the follow-up period, PVT was diagnosed by ultrasound, CT and/or MRI, and episodes of bacterial infections requiring hospitalization were recorded. Malignant PVT was an exclusion criterion. Of the 202 patients enrolled (68.3% males, mean age 63.8±11 years), 22 (10.8%) developed PVT during the follow up. In patients with PVT, the prevalence of previous bacterial infections was significantly higher compared to patients without PVT (63.6% vs 31.1%; p=0.02). Cox regression analysis revealed that a history of bacterial infection was the only variable that demonstrated a significant association with the risk of de novo PVT occurrence (HR 4.04, 95% CI: 1.68-9.65). in patients with liver cirrhosis bacterial infections are a predisposing factor for the following development of PVT. Further studies are needed to confirm this evidence.

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.

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.

Potential contribution of the gut microbiota to the development of portal vein thrombosis in liver cirrhosis.

Portal vein thrombosis (PVT) is a serious complication of liver cirrhosis (LC) and is closely related to gut homeostasis. The study aimed to investigate the composition of gut microbiota and its putative role in PVT development in LC. 33 patients with LC admitted between January 2022 and December 2022 were enrolled in this study. Based on imaging findings, they were categorized into LC without PVT (n = 21) and LC with PVT (n = 12) groups. Fecal samples were collected from each participant and underwent 16S rDNA sequencing. D-Dimer and platelet elevations were the main clinical features of LC with PVT. The alpha and beta diversity of the gut microbiota in LC with PVT group was found to be significantly higher compared to the control group. The structure of the gut microbiota was significantly different between the two groups. Based on LEfSe data, the genera Akkermansia, Eubacterium hallii group, Fusicatenibacter, and Anaerostipes were enriched in the LC with PVT, while Enterococcus, Weissella, Bacteroides, and Subdoligranulum were enriched in those of the LC subjects. Changes in microbiota structure result in significant differences in gut microbiota metabolism between the two groups. Altered levels of the microbiota genera were shown to be correlated with coagulation factor parameters. In animal experiments, the addition of Bacteroides reversed the CCl4-induced PVT. Liver cirrhosis with PVT led to a disorder in the gut microbiota, which was characterized by an increase in pathogenic bacteria and a decrease in beneficial bacteria. Furthermore, modulating the gut microbiota, especially Bacteroides, may be a promising therapeutic approach to reduce the progression of PVT in LC.

Understanding the pathogenesis of portal vein thrombosis in liver cirrhosis: We are still on the way.

Portal vein thrombosis (PVT) is a common complication of liver cirrhosis. In this issue of the Journal of Clinical Ultrasound: Sonography and other Imaging Techniques, a systematic review and meta‐analysis by Giri et al assessed the role of portal system hemodynamics for predicting the presence and development of PVT in liver cirrhosis.

Risk Factors of Portal Vein Thrombosis in Patients with Different Child-Pugh Classes Liver Cirrhosis

Aim: to evaluate the frequency of portal vein thrombosis (PVT) and build predictive models of the development of PVT for patients with liver cirrhosis (LC) of A and B/C classes by Child-Pugh.Materials and methods. Research design is a case-control. The Case group included 130 patients with newly diagnosed PVT not caused by invasive hepatocellular carcinoma (HCC); 29 patients were assigned to class A, 101 patients were assigned to class B/C. From the database of cirrhotic patients without PVT 60 Controls for class A and 205 for B/C were selected using sratified randomization by sex, age and etiology of cirrhosis. The Mann-Whitney U-test and Pearson's chi-squared test were used to compare the groups. Odds ratios (OR) and 95 % confidence intervals (95 % CI) were calculated. Logistic regression models are constructed with the separation of the sample into training and test (0.7; 0.3). The operational characteristics of the models were calculated on the test sample; ROC analysis was carried out, the area under the ROC curve (AUC) was calculated.Results. The overall frequency of PVT was 4.1 % (95 % CI 2.7-5.8 %) in class A and 10.4 % (95 % CI 8.5-12.5 %) class B/C. Patients with class A and B/C PVT differed from the corresponding controls by more severe portal hypertension: the frequency of bleeding / number of interventions on varices compared with the control were 41/45 % vs. 7/8 % (p &lt; 0.001) for class A and 25.7/30.7 % vs. 16.1/16.1 % (p &lt; 0.05) for class B/C, ascites frequency was 24 % vs. 8 % (p &lt; 0.05) for class A and 89.1 % vs. 68.3 % (p &lt; 0.001) for class B/C. The cutoff by the portal vein diameter was the same for both classes — 13.4 mm; the spleen length was similar and amounted 17.5 mm for class A, 17.1 mm for class B/C. Patients with PVT differed from the corresponding controls by neutrophil-to-lymphocyte ratio: class A 2.33 (1.82; 3.61) vs. 1.76 (1.37; 2.20), p &lt; 0.01, class B/C 2.49 (1.93; 3.34) vs. 2.15 (1.49; 3.26), p &lt; 0.05. Patients of class B/C had a higher incidence of newly diagnosed malignant tumors - 23.8% (primarily HCC that does not invade the portal vein), compared with control and cases of class A - 6.3 % and 3 % (p &lt; 0.05), respectively. The best model for class A included variceal bleeding, ascites, portal vein diameter, absolute number of neutrophils, for class B — ascites, spleen length, portal vein diameter, malignant tumors / local factors; sensitivity, specificity, accuracy and AUC were 79.3 %, 90 %, 86.5 %, 0.897 and 73.3 %, 68.3 %, 69.9 %, 0.789, respectively.Conclusion. Independently of the Child-Pugh class of LC, the main risk factor for PVT is severe portal hypertension.

Increased Factor VIII Activity Is Predictive of the Occurrence of Portal Vein Thrombosis in Cirrhosis.

The aim of this study was to identify the role of factor VIII (FVIII) in portal vein thrombosis (PVT) occurrence in cirrhotic patients with gastroesophageal variceal bleeding. A total of 453 cirrhotic patients with gastroesophageal varices were enrolled. Computed tomography was performed at baseline and patients were divided into PVT and non-PVT groups (n = 131 vs. 322). Individuals without PVT at baseline were followed up for the development of PVT. Time-dependent receiver operating characteristic analysis of FVIII for PVT development was performed. The Kaplan-Meier methodology was used to analyze the predictive ability of FVIII for PVT incidence at 1 year. FVIII activity (177.00 vs. 153.70, p = 0.001) was significantly increased in the PVT group compared with the non-PVT group in cirrhotic patients with gastroesophageal varices. FVIII activity was positively correlated with the severity of PVT (161.50 vs. 171.07 vs. 187.05%, p = 0.001). Furthermore, FVIII activity (hazard ratio [HR]: 3.48, 95% confidence interval [CI]: 1.14-10.68, p = 0.029 in model 1; HR: 3.29, 95% CI: 1.03-10.51, p = 0.045 in model 2) was an independent risk factor of 1-year PVT development in patients without PVT at baseline, which was confirmed by two separate Cox regression analysis and competing risk models. Patients with elevated FVIII activity exhibit a higher incidence of PVT in the non-PVT group at 1 year (15.17 vs. 3.16%, p < 0.001). The predictive value of FVIII remains significant in individuals who have never received splenectomy (14.76 vs. 3.04%, p = 0.002). Elevated FVIII activity was potentially associated with the occurrence and the severity of PVT. It might be helpful to identify cirrhotic patients at risk of PVT.

Thrombophilia in portal vein thrombosis: Extent at presentation and treatment options

Background: Non-hepatocellular carcinoma-related portal vein thrombosis (PVT) frequently occurs in cirrhotic patients; its prevalence correlates to disease severity and impacts mortality. PVT development has been attributed to compromised hepatic synthetic function and hemodynamic portal vein factors in cirrhotic patients. Whether thrombophilia is a contributor remains unclear. Furthermore, the potential impact of thrombophilia on treatment outcomes has not been studied. We aimed to describe the prevalence, presentation, and treatment outcomes of cirrhotic patients with thrombophilia at our institution.

A novel potential mechanism for the development of portal vein thrombosis in cirrhosis based on portal hemodynamics

BackgroundMarked changes in hemodynamics have been suggested to be a potential contributing factor to portal vein thrombosis (PVT) development. This study investigated the effect of portal hemodynamics based on the anatomical structure of the portal venous system on PVT development.MethodsThe morphological features of portal venous system in patients with PVT and those without PVT subgroups were compared. In addition, idealized PV models were established to numerically evaluate the effect of the variation in the angulation of superior mesenteric vein (SMV) and splenic vein (SV) on the hemodynamics of portal venous system.ResultsThe angle α (angulation of SMV and SV) in patients with PVT was lower than that in patients without PVT (p < 0.0001), which was the only independent risk factor (odds ratio (OR), 0.90 (95% CI 0.84–0.95); p < 0.0001) for the presence of PVT. With the change in angle α, the flow pattern of blood flow changed greatly, especially the helical flow. When α = 80°, helical flow only appeared at the local PV near the intersection of SMV and SV. When α = 120°, most regions were occupied by the helical flow. In addition, the h2 gradually increased with increasing α, when α = 80°, h2 = 12.6 m/s2; when α = 120°, h2 = 29.3 m/s2.ConclusionsThe angulation of SV and SMV was closely associated with PVT development. Helical flow changed following the varying angulation of SV and SMV. Therefore, angulation of SV and SMV may help to identify high-risk cohorts for future PVT development earlier.

Increased platelet ratio in patients with decompensated cirrhosis indicates a higher risk of portal vein thrombosis.

Patients with decompensated cirrhosis are at risk of portal vein thrombosis (PVT). We prospectively investigated whether alterations of platelet aggregation can predict PVT in decompensated cirrhosis. At baseline, all patients underwent whole-blood aggregometry (Multiplate®) to assess ADP-induced platelet aggregation. Aggregometry results were expressed as the ratio between platelet aggregation and platelet count (PLT ratio). Then, patients with cirrhosis were prospectively followed for 1year for PVT development. One-hundred and twenty-eight patients with decompensated cirrhosis were included (Child-Pugh A/B/C 12/39/49%). The cumulative incidence of PVT was 14%. On multivariate analysis, the PLT ratio (OR 4.5, 95% CI 2.63-7.67; p < .0001) and Child-Pugh C versus A/B (OR 4.1, 95% CI 1.18-14.80; p=.03) were independently associated with PVT. The discriminative ability of the PLT ratio was higher than Child-Pugh (AUC 0.92 vs 0.70, p < .0001). A PLT ratio > 0.75 had 83% sensitivity and 84% specificity for PVT. In conclusion, the PLT ratio by Multiplate® seems a promising thrombotic biomarker in decompensated cirrhosis.

The portal vein in patients with cirrhosis is not an excessively inflammatory or hypercoagulable vascular bed, a prospective cohort study

BackgroundA hypercoagulable state is not associated with development of portal vein thrombosis in cirrhosis, as we previously demonstrated. However, some groups demonstrated elevated levels of inflammatory markers and activation of hemostasis in the portal vein (PV) compared to posthepatic veins, but because the liver is involved in clearance of these markers, we hypothesize that interpretation of these data is not straightforward. AimTo determine whether the PV has particular proinflammatory/hypercoagulable characteristics by comparing plasma sampled in the PV, hepatic vein (HV), and the systemic circulation. MethodsPlasma samples from 51 cirrhotic patients with portal hypertension undergoing transjugular intrahepatic portosystemic shunt placement, were taken from the PV, HV, and jugular vein (JV). Markers of inflammation (lipopolysaccharide, tumor necrosis factor‐α, interleukin‐6, thiobarbituric acid‐reactive substances), neutrophil‐extracellular‐traps (cfDNA, MPO‐DNA), endothelial damage (von Willebrand factor [VWF]), and hemostasis were determined and compared among the three vascular beds. ResultsMarkers of inflammation were slightly, but significantly higher in the PV than in the HV and systemic circulation. VWF and markers of hemostasis were modestly elevated in the PV. Levels of multiple markers were lower in the HV compared with the PV and systemic circulation. Higher model for end‐stage liver disease score was associated with a more prothrombotic state in all three sample sites. ConclusionIn contrast to published studies, we did not detect a clear proinflammatory or prothrombotic environment in the PV of cirrhotic patients. Many markers are lowest in the HV, indicating that the low levels of these markers in the HV, at least in part, reflect clearance of those markers in the liver.

Bacterial infections as a predisposing factor for the development of portal vein thrombosis in cirrhotic patients: a prospective study

Bacterial infections as a predisposing factor for the development of portal vein thrombosis in cirrhotic patients: a prospective study

Perioperative Coagulation Changes in Total Pancreatectomy and Islet Autotransplantation.

Thrombotic complications after total pancreatectomy with islet autotransplantation (TPIAT) are common. However, the systemic changes to coagulation in the perioperative period have not been well studied. Our objective was to evaluate the derangements in coagulation in the perioperative period for this procedure. This was a prospective observational study of patients undergoing elective TPIAT for chronic pancreatitis. Multiple methods of evaluating coagulation, including 2 viscoelastic assays and standard laboratory assays were obtained at defined intraoperative and postoperative intervals. Fifteen patients were enrolled. Laboratory values demonstrated initial intraoperative hypercoagulability before significant systemic anticoagulation after islet infusion with heparin. Hypercoagulability is again seen at postoperative days 3 and 7. Subgroup analysis did not identify any major coagulation parameters associated with portal vein thrombosis formation. Apart from the immediate period after islet cell and heparin infusion, patients undergoing TPIAT are generally hypercoagulable leading to a high rate of thrombotic complications. Portal vein thrombosis development had minimal association with systemic derangements in coagulation as it is likely driven by localized inflammation at the time of islet cell infusion. This study may provide the groundwork for future studies to identify improvements in thrombotic complications.