Non-malignant Portal Vein Thrombosis Research Articles

Portal vein thrombosis and liver transplantation: management, matching, and outcomes. A retrospective multicenter cohort study.

Besides the increased risk of perioperative morbidity, graft failure, and mortality, the majority of PVT are diagnosed at liver transplantation (LT). Improving preoperative management and patient selection may lead to better short-term and long-term outcomes and reduce the risk of a futile LT. The authors aimed to identify predictors of adverse outcomes after LT in patients with nonmalignant portal vein thrombosis (PVT) and improve donor to recipient matching by analyzing the results of the Italian cohort of LT recipients. Adult patients who underwent LT in Italy between January 2000 and February 2020 diagnosed with PVT pre-LT or at time of LT were considered eligible for inclusion. Based on a survey encompassing all 26 surgeons participating in the study, a binary composite outcome was defined. Patients were classified as having the composite event if at least one of these conditions occurred: operative time more than 600min, estimated blood loss greater than 5000ml, more than 20 ICU days, 90 days mortality, 90 days retransplant. Seven hundred fourteen patients were screened and 698 met the inclusion criteria. The analysis reports the results of 568 patients that fulfilled the criteria to enter the composite outcome analysis.Overall, 156 patients (27.5%) developed the composite outcome. PVT stage 3/4 at transplant and need for any surgical correction of PVT are independent predictors of the composite outcome occurrence. When stratified by PVT grade, overall survival at 1-year ranges from 89.0% with PVT grade 0/1 to 67.4% in patients with PVT grade 3/4 at LT ( P <0.001). Nevertheless, patients with severe PVT can improve their survival when identified risk factors are not present. Potential LT candidates affected by PVT have a benefit from LT that should be adequately balanced on liver function and type of inflow reconstruction needed to mitigate the incidence of adverse events. Nonetheless, the absence of specific risk factors may improve the outcomes even in patients with PVT grades 3-4.

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.

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.

Comparative Efficacy of Anticoagulant Medications in Nonmalignant Portal Vein Thrombosis in Liver Cirrhosis-A Systematic Review and Network Meta-analysis.

Ghazaleh, Sami MD1; Chuang, Justin MD1; Sayeh, Wasef MD1; Iqbal, Amna MD1; Beran, Azizullah MD1; Khader, Yasmin MD1; Burmeister, Cameron MD, MS1; Aziz, Muhammad MD2; Assaly, Ragheb MD1; Nawras, Ali MD2 Author Information

Presence of Hepatocellular Carcinoma Does Not Affect Course and Response to Anticoagulation of Bland Portal Vein Thrombosis in Cirrhotic Patients.

Malignancies are generally considered a risk factor for deep vein thrombosis and may hamper the recanalisation of thrombosed veins. We investigate whether the natural course and response to anticoagulant treatment of bland portal vein thrombosis (PVT) in patients with cirrhosis complicated by hepatocellular carcinoma (HCC) differ from those without HCC. Retrospective study in two hepatology referral centres, in Italy and Romania where patients with a diagnosis of PVT on cirrhosis and follow-up of at least 3 months with repeated imaging were included. A total of 162 patients with PVT and matching inclusion and exclusion criteria were identified: 30 with HCC were compared to 132 without HCC. Etiologies, Child-Pugh Score (7 vs 7) and MELD scores (11 vs 12, p=0.3679) did not differ. Anticoagulation was administered to 43% HCC vs 42% nonHCC. The extension of PVT in the main portal trunk was similar: partial/total involvement was 73.3/6.7% in HCC vs 67.4/6.1% in nonHCC, p=0.760. The remainder had intrahepatic PVT. The recanalization rate was 61.5% and 60.7% in HCC/nonHCC in anticoagulated patients (p=1). Overall PVT recanalisation, including treated and untreated patients, was observed in 30% of HCC vs 37.9% of nonHCC, p=0.530. Major bleeding incidence was almost identical (3.3% vs 3.8%, p=1). Progression of PVT after stopping anticoagulation did not differ (10% vs 15.9%, respectively, HCC/nHCC, p=0.109). The course of bland non-malignant PVT in cirrhosis is not affected by the presence of active HCC. Treatment with anticoagulation in patients with active HCC is safe and as effective as in nonHCC patients, this can potentially allow us to use otherwise contraindicated therapies (ie TACE) if a complete recanalization is achieved with anticoagulation.

[Successful therapy of non-cirrhotic non-malignant portal vein thrombosis (NCNMPT) by interventional therapy using transjugular lysis catheter].

NCNMPT is a rare condition with a prevalence of 0.3%. THERAPY: Patient (69 y) with NCNMPT and small bowel ileus received interventional therapy using transjugular local lysis into the superior mesenteric vein. OUTCOME/DISCUSSION: Successful lysis with complete remission. Improved therapeutic efficacy of interventional versus drug therapy alone.

Conservative short-term treatment of non-cirrhotic non-malignant portal vein thrombosis

Introduction. Portal vein (PV) thrombosis (PVT) is a partial or complete obstruction of blood f low as a result of a thrombus mass in the lumen of PV. In the acute phase, the symptoms such as right upper quadrant pain, nausea, and fever are unspecific. A diversity of subacute and chronic symptoms is associated with complications related to PVT and portal hypertension. Case report. A 50-year-old female was admitted to the hospital due to acute abdominal cramping pain. The pain lasted for 15 to 20 min and was followed by defecation of normal stool and hematochezia on three occasions. The abdominal pain recurred after several hours, again followed by hematochezia and tenesmus every 10 min. After admission, a colonoscopy was performed, and it revealed vulnerable, erythematous mucosa of the colon with contact bleeding from the lienal flexure to the rectosigmoid junction. During the colonoscopy, a biopsy was performed. A computed tomography (CT) scan revealed partial PVT of intrahepatic branches of PV, and thrombosis of the inferior mesenteric vein. After conservative treatment with low molecular weight heparin (LMWH) and other supportive measures, the digestive bleeding ceased, and defecation became normal. During the one-month follow-up, the patient had no complications, and the control CT scan revealed normal PV flow without thrombosis. Conclusion. Although rare, a non-malignant and non-cirrhotic PVT should not be neglected in the differential diagnosis because timely and vigilant therapy with LMWH can lead to complete resolution without serious complications.

Transjugular Intrahepatic Portosystemic Shunt in Chronic Portal Vein Thrombosis-From Routine Recommendations to Demanding Scenarios.

Portal vein thrombosis (PVT), particularly the presence of portal cavernoma, was traditionally considered a relative contraindication for transjugular intrahepatic portosystemic shunting (TIPS) due to the technical difficulties in accessing and maneuvering the portal vein and avoiding the high risk for bleeding periportal collaterals. However, the last decade has seen a surge in the number of studies-mostly case reports and small series of patients-demonstrating that TIPS is not only technically feasible in the vast majority of these patients but also provides effective and long-term control of symptoms associated with portal hypertension in cases refractory to the standard line of therapy. The present article aims to provide a concise but exhaustive overview of the role and the standard and technically difficult TIPS placement scenarios in patients with chronic non-malignant PVT and with and without underlying liver disease. The review is strategically punctuated by exemplary instances from the authors' experience.

Implantation of transjugular intrahepatic portosystemic shunt (TIPS): indication and patient selection.

This review summarizes indications and contraindications for implantation of transjugular intrahepatic portosystemic shunt (TIPS). Further, patient selection strategies are discussed. TIPS implantation is a highly effective treatment for portal hypertension. Main indications are ascites and variceal bleeding in patients with liver cirrhosis. There is growing evidence that early TIPS implantation after variceal bleeding is associated with an improved survival (preemptive TIPS).Preliminary data also suggest that an analogous concept of early TIPS implantation may be beneficial for patients with ascites. Further, well-selected patients with acute or chronic nonmalignant portal vein thrombosis can be effectively treated with TIPS implantation. In contrast, there is generally no recommendation for TIPS implantation in patients with hepatic veno-occlusive disease, noncirrhotic portal hypertension or prior before surgery to avoid complications of portal hypertension. Apart from evidence-based patient selection, the newly developed FIPS score can be an objective component in decision-making. Consideration of well-established indications and contraindications for TIPS implantation as well as concise patient selection criteria are essential for an optimal outcome after TIPS implantation.

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

Background and Aims: Non-malignant portal vein thrombosis (PVT) is one of the complications of liver cirrhosis. The predisposing factors for PVT in cirrhotic patients are not entirely clear. The aim of this study was to identify possible clinical risk factors related to the development of PVT in patients with liver cirrhosis.

ABO blood group does not influence Child-Pugh A cirrhosis outcome: An observational studyfrom CIRRAL and ANRS CO12 CIRVIR cohorts.

Non-O blood group promotes deep vein thrombosis and liver fibrosis in both general population and hepatitis C. We aimed to evaluate the influence of Non-O group on the outcome of Child-Pugh A cirrhotic patients. We used two prospective cohorts of Child-Pugh A cirrhosis due to either alcohol or viral hepatitis. Primary end point was the cumulated incidence of 'Decompensation' at 3years, defined as the occurrence of ascites , hydrothorax, encephalopathy, gastrointestinal bleeding related to portal hypertension, or bilirubin >45μmol/L. Secondary end points were the cumulated incidences of (1) 'Disease Progression' including a « decompensation» or « the occurrence of one or more parameters » among: prothrombin time (PT) <45%, albumin <28g/L, Child-Pugh worsening (B or C vs A or B, C vs B), hepatorenal syndrome, and hepato-pulmonary syndrome, (2) other events such as non-malignant portal vein thrombosis (nmPVT), and (3) overall survival. Patients (n=1789; 59.9% Non-O group; 40.1% group O) were followed during a median of 65.4months. At 3years cumulated incidence of Decompensation was 8.3% in Non-O group and 7.2% in group O (P=.27). Cumulated incidence ofDisease Progressionwas 20.7% in Non-O group and 18.9% in group O (P=.26). Cumulated incidence of nmPVT was 2.7% in Non-O group and 2.8% in group O (P=.05). At 3years overall survival was 92.4% in Non-O group and 93.4% in group O (P=1). Non-O group does not influence disease outcome in Child-Pugh A cirrhotic patients. Clinicals trial number NCT03342170.

Interventional recanalization therapy in patients with non-cirrhotic, non-malignant portal vein thrombosis: comparison between transjugular versus transhepatic access

PurposeTo compare the safety and outcome of transjugular versus percutaneous technique in recanalization of non-cirrhotic, non-malignant portal vein thrombosis.MethodsWe present a retrospective bicentric analysis of 21 patients with non-cirrhotic, non-malignant PVT, who were treated between 2016 and 2021 by interventional recanalization via different access routes (percutaneous [PT] vs. transjugular in transhepatic portosystemic shunt [TIPS] technique). Complication rates with a focus on periprocedural bleeding and patency as well as outcome were compared.ResultsOf the 21 patients treated (median age 48 years, range of 19–78), seven (33%) patients had an underlying prothrombotic condition. While 14 (57%) patients were treated for acute PVT, seven (43%) patients had progressive thrombosis with known chronic PVT. Nine patients underwent initial recanalization via PT access and twelve via TIPS technique. There was no significant difference in complete technical success rate according to initial access route (55.5% in PT group vs. 83.3% in TIPS group, p = 0.331). However, creation of an actual TIPS was associated with higher technical success in restoring portal venous flow (86.6% vs. 33.3%, p = 0.030). 13 (61.9%) patients received thrombolysis. Nine (42.8%) patients experienced hemorrhagic complications. In a multivariate analysis, thrombolysis (p = 0.049) and PT access as the first procedure (p = 0.045) were significant risk factors for bleeding.ConclusionInvasive recanalization of the portal vein in patients with PVT and absence of cirrhosis and malignancy offers a good therapeutic option with high recanalization and patency rates. Bleeding complications result predominantly from a percutaneous access and high amounts of thrombolytics used; therefore, recanalization via TIPS technique should be favored.

A case-control study of ultrasonographic determinants and 2D-Shearwave elastography changes of liver and spleen associated with non-malignant portal vein thrombosis in patients with decompensated cirrhosis

Background and Aim: Portal vein thrombosis (PVT) due to portal flow stasis, complex thrombophilic disorders and factors leading to endothelial dysfunction, is an increasingly recognized complication in patients with cirrhosis. We tried to assess the Ultrasonography of Abdomen(USS) parameters and stiffness of liver and spleen as risk factors associated with non-malignant PVT in decompensated chronic liver disease patients(DCLD). Methods: We prospectively enrolled 502 patients with DCLD(CHILD B/C). All patients underwent detailed clinical evaluation, baseline investigation and ultrasonography. PVT was confirmed by CECT Abdomen in patients with USG evidence of PVT or alteration in portal flow dynamics. Liver and spleen stiffness(in kPa) were assessed by 2D Shear wave elastography (Supersonic Aixplorer). ROC was plotted to derive the best cut-off of parameters for development of PVT. Results: 39 patients were excluded. Of the 463 patients included, 51 had PVT (11%). It was observed that non-malignant PVT group patients had smaller liver size (11.8±1.8 vs 12.4±1.5, p=0.032), higher spleen size (14.9±2.3 vs 13.5±2.2, p<0.01), higher portal vein diameter(PVD, 14.4±3.2 vs 12.2±1.7,p<0.01), lower portal vein velocity(PVV,11.5±3.6 vs 16.7±3.6,p<0.01), higher liver stiffness(61.3±21.7 vs 55.2±17.1,p=0.02), higher splenic stiffness(50.3±15.1 vs 36.7±7.5,p<0.01) as compared to non-PVT group. On plotting ROC; PVV<12.5cm/sec (AUROC 0.86, sensitivity 74%, specificity 88%, NPV 95.9%)), PVD>13.7cm (AUROC 0.75), liver stiffness>66.5 kPa (AUROC 0.72), liver size<11.95cm(AUROC 0.63) were significantly associated with development of non-malignant PVT(p<0.01). On multiple logistic analysis PVD >13.75cm (B=1.21, OR:95%CI 3.36(1.05-10.7), p=0.04), PVV<12.5cm/sec (B= -1.06, OR:95%CI 0.35(0.13-0.09), p=0.03) were significant risk factors for PVT development in DCLD. Conclusion: The association of higher liver stiffness and smaller liver size as markers of extent of cirrhosis, higher splenic size and stiffness as a reflection of severity of portal hypertension, dilated PV and low PVV indicating sluggish portal flow that trigger thrombosis in the spleno-portal axis, were significantly associated with non-malignant PVT in DCLD.

Risk factors associated with non-malignant portal vein thrombosis in patients with decompensated cirrhosis : a case-control study

Backgrounds and Aim: Portal vein thrombosis (PVT) is defined as thrombosis of the portal vein and branches of spleno-portal axis. Incidence of PVT in compensated liver disease is between 0.6-5% and up to 25% in advanced disease. Presence of PVT in decompensated chronic liver disease (DCLD) is associated with significant morbidity and mortality. We evaluated the proportion and risk factors associated with non-malignant PVT in DCLD patients. Methods: 502 patients with DCLD were enrolled over a period of 1.5 years. Patients underwent detailed clinical history and evaluation, baseline investigation and ultrasonography. CECT Abdomen was performed in patients with USG evidence of PVT or alteration in portal flow dynamics. Results: 39 patients were excluded. 51 of the 463 patients included had PVT (11.0%). Duration of cirrhosis >4years(p<0.01), NASH related etiology (p<0.01), prior history of obesity(p<0.01), dyslipidaemia with high serum cholesterol and LDL(p<0.01), clinically evident sarcopenia (p<0.01), first initial decompensation of cirrhosis as upper gastro-intestinal bleed (UGIB), prior UGIB (p=0.002), poorly controlled ascites (p<0.01), 2 history of episodes of SBP(p<0.01), platelet count <66.5x109/L(p=0.002), leucocyte count <5350/cu mm(p<0.01) were significantly associated with PVT group. There was no difference between CHILD B and C status, among the 2 groups. On multiple logistic regression analysis, prior endoscopic variceal ligation, SAAG >1.95 were found as independent risk factors for development of PVT in DCLD patients. Conclusions: Proportion of non-malignant PVT in decompensated cirrhosis was 11%. Presence of poorly controlled ascites, prior history of UGIB, high SAAG, low Platelet count as markers of severity of portal hypertension in cirrhosis are significantly associated with non-malignant PVT in DCLD. Patients with prior history of obesity and dyslipdemia, with NASH related cirrhosis are at high risk for PVT development.

Significance of altered anticoagulant proteins and D-dimer in cirrhotic portal vein thrombosis: relation to the degree of liver dysfunction.

Portal vein thrombosis (PVT) is a well-known consequence of cirrhosis. Its pathophysiology is complex, with possible downstream hepatic decompensation. This study was conducted to describe the changes of protein C (PC), protein S (PS) and D-dimer blood levels associated with PVT formation in cirrhosis and the relation to the degree of liver dysfunction. This was a case-control study that included 50 cirrhotic patients who presented with acute de novo non-malignant PVT and 50 cirrhotic patients without PVT as a control group. The severity of liver disease was classified as per the Child-Turcotte-Pugh (CTP) score. Doppler ultrasonography identified acute portal vein occlusion, and dynamic contrast-enhanced computed tomography confirmed the extent and nature of PVT. Blood PC, PS and D-dimer levels were measured using enzyme-linked immunosorbent assay. PC and PS levels were significantly lower, and the D-dimer level was significantly higher, in cirrhotic patients with PVT compared to the control group. PC and PS levels were significantly decreased in patients with higher CTP score of both groups. The D-dimer level did not vary significantly with the degree of liver dysfunction in patients of either group. PC, PS and D-dimer at the cut-off points of ≤ 77 IU/dl, ≤ 63 IU/dl, and > 300 ng/ml, respectively, significantly suggested PVT occurrence. Alteration of the anticoagulant proteins and D-dimer contributed to PVT formation in cirrhotic patients and could help stratify the degree of liver dysfunction. Blood level of these hemostatic proteins could be incorporated into a probability score for early diagnosis and treatment of PVT in cirrhosis.

Non-malignant portal vein thrombosis in a cohort of cirrhotic patients: Incidence and risk factors.

Non-malignant portal vein thrombosis (PVT) is a complication of liver cirrhosis. The aim of this study was to evaluate the annual incidence of PVT and related risk factors. We retrospectively reviewed clinical, laboratory, and radiological data collected prospectively from September 2016 to September 2017. A follow-up of 36months was performed in a subset of patients to determine the cumulative incidence of PVT and related complications. The study included 567 patients. The incidence of PVT at 12, 24, and 36months was 3.7%, 0.8%, and 1.4%, respectively. Patients with PVT were compared with patients without PVT, and showed differences in albumin (p=0.04), aspartate aminotransferase (p=0.04), hemoglobin (p=0.01), and prothrombin activity (p=0.01). The presence of hydropic decompensation (57.1% vs. 30.1%; p 0.004), gastroesophageal varices (76.2% vs. 39.5%; p=0.05), variceal bleeding (52.4% vs. 22.7%; p<0.001), hepatic encephalopathy (38.1% vs. 9.9%; p=0.01), spontaneous bacterial peritonitis (9.5% vs. 1.7%; p<0.001), and use of beta-blockers (71.4% vs. 27.7%; p<0.001) were significantly associated. In the multivariate analysis, use of beta-blockers and hepatic encephalopathy appeared as risk factors, and high albumin levels a protective factor. The incidence of PVT was 3.7%. Beta-blockers and hepatic encephalopathy were risks factors. High albumin levels were a protective factor.

Treatment of portal vein thrombosis: an updated narrative review.

Portal vein thrombosis (PVT) is the most frequent among the splanchnic vein thrombosis, accounting for 90% of cases. More than half of PVT are provoked by liver cirrhosis, solid cancer or myeloproliferative neoplasms. The remaining cases are non-malignant non-cirrhotic PVT and include either unprovoked events or thrombosis secondary to other less common risk factors (e.g. abdominal surgery, intrabdominal inflammations/infections, or hormonal stimuli). Anticoagulant therapy in patients with acute symptomatic PVT should be started early after diagnosis, if no active bleeding, to obtain greater vessel recanalization and reduce the occurrence of portal-hypertension related complications. Gastroesophageal varices do not represent a contraindication to anticoagulant treatment, as long as adequate measures have been undertaken for the prophylaxis of gastroesophageal bleeding. Different treatment options (unfractionated or low molecular weight heparin, vitamin K antagonists and direct oral anticoagulants [DOACs]) can be considered. In this narrative review we will discuss the treatment of PVT in the three most common scenarios (cirrhosis-associated, cancer-associated and non-malignant non-cirrhotic PVT). We will also discuss the role of the DOACs and summarize recent guidelines on this topic.

Anticoagulation and Transjugular Intrahepatic Portosystemic Shunt for the Management of Portal Vein Thrombosis in Cirrhosis: A Prospective Observational Study.

Current guidelines recommend anticoagulation as the mainstay of portal vein thrombosis (PVT) treatment in cirrhosis. However, because of the heterogeneity of PVT, anticoagulation alone does not always achieve satisfactory results. This study aimed to prospectively evaluate an individualized management algorithm using a wait-and-see strategy (i.e., no treatment), anticoagulation, and transjugular intrahepatic portosystemic shunt (TIPS) to treat PVT in cirrhosis. Between February 2014 and June 2018, 396 consecutive patients with cirrhosis with nonmalignant PVT were prospectively included in a tertiary care center, of which 48 patients (12.1%) were untreated, 63 patients (15.9%) underwent anticoagulation, 88 patients (22.2%) underwent TIPS, and 197 patients (49.8%) received TIPS plus post-TIPS anticoagulation. The decision of treatment option mainly depends on the stage of liver disease (symptomatic portal hypertension or not) and degree and extension of thrombus. During a median 31.7 months of follow-up period, 312 patients (81.3%) achieved partial (n = 25) or complete (n = 287) recanalization, with 9 (3.1%) having rethrombosis, 64 patients (16.2%) developed major bleeding (anticoagulation-related bleeding in 7 [1.8%]), 88 patients (22.2%) developed overt hepatic encephalopathy, and 100 patients (25.3%) died. In multivariate competing risk regression models, TIPS and anticoagulation were associated with a higher probability of recanalization. Long-term anticoagulation using enoxaparin or rivaroxaban rather than warfarin was associated with a decreased risk of rethrombosis and an improved survival, without increasing the risk of bleeding. However, the presence of complete superior mesenteric vein thrombosis was associated with a lower recanalization rate, increased risk of major bleeding, and poor prognosis. In patients with cirrhosis with PVT, the individualized treatment algorithm achieves a high-probability recanalization, with low rates of portal hypertensive complications and adverse events.

Predictors of insufficient recanalization and portal hypertensive complications after treatment of non-cirrhotic, non-malignant portal vein thrombosis – a population-based study

Objectives In acute portal vein thrombosis (PVT), a six-month anticoagulation treatment achieves complete recanalization in only 35%–45% of patients, but the predictors of poor treatment responses are unclear. We examined treatment outcomes in PVT and aimed to identify predictors of incomplete recanalization and portal hypertensive complications. Materials and methods This retrospective study comprised patients diagnosed with PVT between 2006 and 2015. Key exclusion criteria were liver cirrhosis, malignancy, and age <18. Results The final cohort comprised 145 patients, of whom 132 (92%) were primarily treated with anticoagulation. The 5-year cumulative incidence of complete recanalization was 42% and of portal hypertensive complications, 31%. Independent predictors of insufficient recanalization were sub-acute or chronic thrombosis (hazard ratio (HR) 3.1, 95% CI 1.6–5.8), while acute pancreatitis was a protective factor (HR 0.3, 95% CI 0.2 − 0.7). Independent predictors of incident portal hypertensive complications were as cites at baseline (HR 3.3, 95% CI 1.7–6.7), sub-acute or chronic thrombosis (HR 2.9, 95% CI 1.6–5.3), extension of thrombosis to the splenic or mesenteric vein (HR 2.6, 95% CI 1.2–5.7), myeloproliferative disease (HR 3.0, 95% CI 1.4–6.5), and anemia (HR 2.1, 95% 1.1–3.9), while acute pancreatitis was a protective factor (HR 0.1, 95% CI 0.03–0.5). Conclusions Etiology and age of thrombosis are associated with treatment responses in PVT. The presence of ascites at baseline, etiology, and extent of thrombosis, a non-acute thrombosis and anemia, are associated with the risk of portal hypertensive complications. Etiology and extent of thrombosis should be taken into account when determining the treatment (method) for PVT.

Portal Thrombosis in Cirrhosis: Role of Thrombophilic Disorders.

In patients with liver cirrhosis the contribution of inherited and acquired prothrombotic disorders in the development of non-malignant portal vein thrombosis (PVT) is inconclusive. The purpose of this retrospective study was to examine the prevalence of thrombophilia in this setting at our center from January 2012 to November 2019. Tests included gene mutational analysis for Factor V Leiden, prothrombin G20210A, JAK2 (V617F), Calreticulin (CARL), in addition to activated protein C resistance, antithrombin III, protein C and S levels, and antiphospholipid antibodies. We included 77 patients, six of whom (7.8%) had a thrombophilic disorder: antiphospholipid syndrome in four patients, prothrombin gene mutation in one and factor V Leiden mutation in one. This latter patient had also been diagnosed with polycythemia vera years before PVT development. Complete thrombosis of the main portal vein and re-thrombosis after stopping anticoagulation were more frequent in patients with thrombophilia, but the rates of recanalization under anticoagulant therapy were similar among groups. No other difference was accounted between groups. The low prevalence of acquired and inherited thrombophilia found in patients with cirrhosis and PVT support testing for these disorders on an individual basis and avoiding universal screening to reduce costs and unwarranted testing.