Progression Of Portal Hypertension Research Articles

Metabolomics reveals altered metabolites in cirrhotic patients with severe portal hypertension in Tibetan population.

Portal hypertension (PHT) presents a challenging issue of liver cirrhosis. This study aims to identify novel biomarkers for severe PHT (SPHT) and explore the pathophysiological mechanisms underlying PHT progression. Twenty-three Tibetan cirrhotic patients who underwent hepatic venous pressure gradient (HVPG) measurement were included. Eleven patients had an HVPG between 5 mmHg and 15 mmHg (MPHT), while 12 had an HVPG ≥16 mmHg (SPHT). Peripheral sera were analyzed using liquid chromatograph-mass spectrometer for metabolomic assessment. An additional 14 patients were recruited for validation of metabolites. Seven hundred forty-five metabolites were detected and significant differences in metabolomics between MPHT and SPHT patients were observed. Employing a threshold of p < 0.05 and a variable importance in projection score >1, 153 differential metabolites were identified. A significant number of these metabolites were lipids and lipid-like molecules. Pisumionoside and N-decanoylglycine (N-DG) exhibited the highest area under the curve (AUC) values (0.947 and 0.9091, respectively). Additional differential metabolites with AUC >0.8 included 6-(4-ethyl-2-methoxyphenoxy)-3,4,5-trihydroxyoxane-2-carboxylic acid, sphinganine 1-phosphate, 4-hydroxytriazolam, 4,5-dihydroorotic acid, 6-hydroxy-1H-indole-3-acetamide, 7alpha-(thiomethyl)spironolactone, 6-deoxohomodolichosterone, glutaminylisoleucine, taurocholic acid 3-sulfate, and Phe Ser. Enzyme-linked immunosorbent assay further confirmed elevated levels of sphinganine 1-phosphate, N-DG, and serotonin in SPHT patients. Significant disruptions in linoleic acid, amino acid, sphingolipid metabolisms, and the citrate cycle were observed in SPHT patients. Pisumionoside and N-DG are identified as promising biomarkers for SPHT. The progression of PHT may be associated with disturbances in lipid, linoleic acid, and amino acid metabolisms, as well as alterations in the citrate cycle.

Analysis of Factors Influencing Prognosis and Assessment of 60 Cases of Decompensated Cirrhotic Patients with Portal Hypertension.

To investigate the risk factors for the development of portal hypertension in patients with decompensated cirrhosis and analyze their prognosis. Patients with decompensated cirrhosis who were admitted to our hospital and Qu fu People's Hospital from June 2022 to June 2023 were included in this study. Among them, there were 45 male and 15 female patients, with a median age of 56 (range: 35-77) years. A comparative analysis was performed between Group A (hepatic venous pressure gradient, HVPG <16 mmHg) and Group B (HVPG ≥16 mmHg) patients, along with various clinical outcomes. Multivariate analysis was conducted to explore the risk factors influencing the occurrence of portal hypertension and adverse prognosis in patients with cirrhosis. In Group A patients with portal hypertension, we observed lower levels of aspartate aminotransferase, laminin, serum hyaluronic acid, type III procollagen N-terminal peptide, total bile acids, and cholylglycine acid compared to Group B. On the other hand, levels of alanine aminotransferase, white blood cells, and serum albumin were higher in Group A than in Group B. These differences between the groups were statistically significant (P < 0.05). Multivariate analysis of the aforementioned risk factors indicated that low white blood cell count, high cholylglycine acid levels, and high serum hyaluronic acid levels were identified as independent risk factors for the occurrence of difficult-to-control complications in decompensated portal hypertension among patients with liver cirrhosis (P < 0.05). Liver cirrhosis patients with portal hypertension and multiple risk factors like low white blood cell count and high liver transaminase levels should be cautious regarding the progression of portal hypertension when combined with splenomegaly, liver fibrosis, and bile stasis, as it often indicates a poor prognosis.

Case report: Oxaliplatin-induced idiopathic non-cirrhotic portal hypertension: a case report and literature review

Oxaliplatin has become a widely used agent in neoadjuvant chemotherapy for gastrointestinal tract tumors and is an integral part of the therapeutic approach for managing colorectal cancer recurrences and metastases, resulting in a more favorable prognosis for patients. Nevertheless, oxaliplatin can give rise to idiopathic non-cirrhotic portal hypertension (INCPH). The emergence of INCPH can disrupt tumor chemotherapy and incite persistent adverse reactions in later stages, significantly complicating clinical management. Consequently, we have presented a case report of INCPH induced by oxaliplatin chemotherapy with the aim of advancing the diagnosis and treatment of this condition, with a particular focus on the clinical manifestations. This study has ascertained that the condition is primarily attributed to complications related to portal hypertension, such as gastrointestinal bleeding, splenomegaly, and hypersplenism. The pathological features primarily involve hepatic sinus dilation and congestion, portal obstruction, absence, stenosis, shunting, localized venous and perisinusoidal fibrosis, as well as hepatocellular atrophy. Treatment primarily concentrates on strategies typically employed for cirrhosis. Endoscopic ligation, sclerotherapy, and non-selective beta-blockers (NSBBs) can be selected to prevent and treat variceal hemorrhage. Transjugular intrahepatic portosystemic shunt (TIPS) and liver transplantation can also be chosen for severe cases. Notably, despite the timely discontinuation of oxaliplatin, most patients continue to experience disease progression, ultimately resulting in a poor prognosis due to either tumor advancement or the ongoing progression of portal hypertension. This emphasizes the importance for physicians to be aware of and consider the risk of INCPH when prescribing oxaliplatin.

Transient elastography and von Willebrand factor as predictors of portal hypertension and decompensation in children

Von Willebrand factor antigen (vWFAg), a protein measured to test the level of vWF released from the vascular endothelium has gained much attention as a marker for portal hypertension (PHT) severity. The objectives of this study were to investigate the use of vWFAg as a biomarker along with liver and spleen stiffness measurements by transient elastography as potential predictors of clinically significant varices (CSV), variceal bleeding (VB) and decompensation in children with PHT. This observational prospective cohort study included 117 children (median age 10 [IQR 6-14] years) who underwent oesophagogastroduodenoscopy between January'2012 to November'2021 and a validation group of 33 children who underwent the same procedure between December'2021 to March'2023. Measurements of vWFAg and glycoprotein Ib binding activity of VWF (GPIbR) were available in 97 patients in the study group and in all patients in the validation group.Results: vWFAg and GPIbR were significantly higher in children with CSV (223 IU/dl and 166 IU/dl; p= 0.015 and p= 0.04, respectively) and VB (218 IU/dl and 174 IU/dl; p= 0.077 and p= 0.03, respectively) than in those without CSV or VB, respectively. Ninety-six patients had liver and spleen stiffness measurements. Spleen stiffness was significantly higher in patients with CSV compared to those without CSV (p= 0.003). In a chronic liver disease subgroup, a predictive scoring tool based on vWFAg, GPIbR, platelet count, and spleen/liver stiffness measurements could predict CSV with an AUROC of 0.76 (p= 0.04). This study suggests the predictive value of vWF for CSV and VB increases when combined with spleen stiffness, with AUROCs of 0.88 and 0.82, respectively. Hence, a combination of biomarkers could assist clinicians in diagnosing CSV, preventing unnecessary invasive procedures. Surveillance endoscopies in children with portal hypertension (PHT) have their own risks and non-invasive markers, such as von Willebrand factor antigen, glycoprotein Ib binding activity of VWF (GPIbR), and transient elastography could be used to predict clinically significant varices, variceal bleeding and disease compensation in children with PHT. Such non-invasive markers for PHT and varices are lacking in the paediatric population. The results show that von Willebrand factor and GPIbR along with transient elastography can be used to formulate a scoring system which can be used as a clinical tool by paediatric hepatologists to monitor the progression of PHT and risk of bleeding, and hence to stratify the performance of invasive endoscopic procedures under general anaesthesia. However, there is a need to validate the scoring system in children with portal vein thrombosis and for hepatic decompensation in a multi-centre registry in the future.

The use of endoscopic band ligation in the primary prevention of bleeding in patients with ascites listed in the liver transplantation waiting list

Background. Saving lives and preventing patients from dropping out of the waiting list for liver transplantation due to the progression of portal hypertension and the development of complications is an urgent task of transplantology in conditions of a donor organ shortage, which causes long waiting times for this operation. Aim. To study the efficacy of endoscopic band ligation versus no intervention in the primary prevention of upper gastrointestinal bleeding and assess the impact on survival of patients with ascites listed in the liver transplantation waiting list. Material and methods. A retrospective comparative study was conducted in patients with decompensated liver diseases with severe ascites and varicose veins, without a history of bleeding, when included in the waiting list for liver transplantation. Primary prevention of bleeding from varices was carried out in patients by means of endoscopic ligation of varicose veins (n=92, group 1); this intervention was not performed in other patients (n=89, group 2). Results. The compared groups were comparable in demographics, clinical parameters, MELD and Child-TurcottePugh scores, or the incidence of severe ascites. The study groups of patients did not have significant differences in the numbers of medium-size and large varices. The incidence of bleeding was significantly lower in the group of patients with endoscopic band ligation as a method of primary prevention than in the group of patients without this intervention (23.9% and 78.7%, respectively, p=0.0001). Patient survival was significantly higher in the group of patients who underwent endoscopic band ligation than in the group of patients without interventions, which was established using the Kaplan-Meier method (Log Rank=0.0001). Conclusion. Primary prevention of bleeding from the upper digestive tract through endoscopic band ligation is an effective method of saving lives and preventing patients with ascites from dropping out of the liver transplantation waiting list in conditions of a donor organ shortageб which causes a long waiting period for surgery.

SAT-559 - Progression of portal hypertension in PBC: doppler ultrasound velocity as a non-invasive assessment

SAT-559 - Progression of portal hypertension in PBC: doppler ultrasound velocity as a non-invasive assessment

Prediction of esophageal varices and risk of bleeding in liver cirrhosis by aspartate aminotransferase to-platelet ratio index and fibrosis-4 index

Background: Liver cirrhosis is the end-stage for chronic liver disease. During the course of cirrhosis repeated endoscopy is recommended. As this intervention is expensive and often poorly accepted by patients who may refuse further follow up, there is a need for non-invasive methods to predicts the progression of portal hypertension as well as the presence and size of esophageal varices. This study was aimed to assess the value of aspartate aminotransferase (AST)-to-platelet ratio index (APRI) and fibrosis-4 index (FIB-4) for predicting esophageal varices in cirrhotic patients. Objectives of the study were: prediction of esophageal varices and risk of bleeding in liver cirrhosis by APRI, and prediction of esophageal varices and risk of bleeding in liver cirrhosis by FIB-4. Methods: It was a single centre, observational study in 100 patients of chronic liver disease. Patients were included in the study after applying inclusion and exclusion criteria. Complete blood count (CBC), liver function test (LFT), kidney function test (KFT), SE, viral marker, ultrasonography (USG) whole abdomen, and upper gastrointestinal endoscopy (UGIE) was done for all patients. Child-Pugh-Turcotte (CTP) score was calculated for every patient. Results: The APRI and FIB-4 shows moderate diagnostic accuracy in predicting the presence of esophageal varices and variceal bleed. Conclusions: In conclusion, the APRI and FIB-4 shows moderate diagnostic accuracy in predicting the presence of esophageal varices and variceal bleed. They help in starting prophylactic therapy earlier to prevent the bleeding and other complications of varices. Although endoscopy remains the primary modality for diagnosis of esophageal varices but these non-invasive parameters can also play an effective role in conjunction with endoscopy in predicting the presence of esophageal varices.

Progression of Portal Hypertension in Acute Cellular Rejection After Liver Transplantation.

This study was designed to investigate the frequency of computed tomography features indicating progression of portal hypertension and their clinical relevance in patients who experienced acute cellular rejection after liver transplantation. This retrospective study included 141 patients with pathologically diagnosed acute cellular rejection following liver transplant. Patients were divided into early and late rejection groups according to the time of diagnosis. Two radiologists analyzed the interval changes in spleen size and variceal engorgement on computed tomography images obtained at the times of surgery and biopsy. Aggravation of splenomegaly and variceal engorgement were considered computed tomography features associated with the progression of portal hypertension. Clinical outcomes, including responses to treatment and graft survival, were compared between patients with and without these features. The frequency of progression of portal hypertension was 31.9% and did not differ significantly in patients who experienced early (30.8% [28/91]) and late (34.0% [17/50]) rejection (P = .694). In the late rejection group, computed tomography features indicating progression of portal hypertension were significantly associated with poor response to treatment (P = .033). Graft survival in both the early and late rejection groups did not differ significantly in patients with and without progression of portal hypertension. Computed tomography features suggesting the progression of portal hypertension were encountered in about one-third of patients who experienced acute cellular rejection after liver transplant. Progression of portal hypertension was significantly related to poor response to treatment in the late rejection group.

UPLC-MS/MS-Based Serum Metabolomics Signature as Biomarkers of Esophagogastric Variceal Bleeding in Patients With Cirrhosis.

Background: Esophagogastric variceal bleeding (EVB) is a common and ominous complication of cirrhosis and represents the degree of portal hypertension progression and cirrhosis decompensation, desiderating the investigation into sensitive and specific markers for early detection and prediction. The purpose of this study is to characterize unique metabolites in serum of cirrhotic EVB patients and identify potential noninvasive biomarkers for detecting and assessing risk of variceal bleeding and cirrhosis progression through metabolomics-based approaches and explore possible pathophysiological mechanisms. Methods: We used ultra-performance liquid chromatography coupled to tandem mass spectrometry (UPLC-MS/MS) to profile serum metabolomes. In one discovery cohort (n = 26, 13 cases of EVB), univariate and multivariate statistical analyses were performed to demonstrate separation between the two groups and identify differentially expressed metabolites. Potential biomarkers were screened by Boruta and logistic regression analyses, further evaluated by receiver operating characteristic analysis, and tested in two validation cohorts (n = 34, 17 cases and n = 10, 5 cases). Results: Bioinformatics analyses demonstrated that EVB patients possessed distinct metabolic phenotypes compared with nEVB controls, characterized by seven elevated and six downregulated metabolites, indicating that EVB-related metabolic disturbance might be associated with vitamin metabolism and fatty acid metabolism. Eight potential biomarkers were selected among which citrulline and alpha-aminobutyric acid with moderate AUC values, tested in the validation cohorts, were identified as specific biomarkers of EVB. Conclusion: Our metabolomic study provides an overview of serum metabolic profiles in EVB patients, highlighting the potential utility of UPLC-MS/MS-based serum fingerprint as a feasible avenue for early detection of EVB.

Two cases of rapid progression of esophageal varices after atezolizumab-bevacizumab treatment for hepatocellular carcinoma.

We report two cases of rapid progression of esophageal varices after atezolizumab-bevacizumab treatment for hepatocellular carcinoma (HCC). Case 1: a man in his 60s with hepatitis C-related liver cirrhosis after viral eradication by direct acting antiviral. He was diagnosed with HCC 8years previously. He had undergone surgical resection 4 times, radio-frequency ablation (RFA) several times, and transcatheter arterial chemoembolization (TACE). However, HCC progressed and could not be controlled by locoregional treatment. Systemic chemotherapy was, therefore, selected. Atezolizumab-bevacizumab was administered after lenvatinib and sorafenib failure. Before starting treatment, his liver function was preserved (Child-Pugh score 5 and class A). His alpha fetoprotein and des-gamma-carboxyprothrombin levels were 3.6ng/mL and 443 mAU/mL, respectively. Esophagogastroduodenoscopy showed no remarkable esophageal varices before atezolizumab-bevacizumab treatment. Nine months after the initiation of atezolizumab-bevacizumab, the patient was admitted for hematemesis from esophageal varices. The disease control of HCC was classified as stable disease (SD) for the liver and lung metastases, and partial response for the lymph node metastases. Neither AST nor ALT was markedly elevated in the clinical course. Endoscopic variceal ligation (EVL) for the spurting point of large esophageal varices with red wale signs was able to successfully achieve hemostasis. Atezolizumab-bevacizumab was stopped and additional EVL eradicated the esophageal varices. However, the post-banding ulcer was prolonged in comparison to usual cases. Case 2: a man in his 60s with hepatitis C-related liver cirrhosis after viral eradication by direct acting antiviral therapy. He was diagnosed with HCC 6years previously. He had received RFA 2 times and TACE 7 times. Atezolizumab-bevacizumab was administered after lenvatinib failure. The disease control of HCC was classified as SD; however, the esophageal varices ruptured after 15 courses of atezolizumab-bevacizumab. Neither AST nor ALT were markedly elevated in the clinical course. The esophageal varices of these patients did not require treatment before atezolizumab-bevacizumab; however, they rapidly worsened and ruptured during atezolizumab-bevacizumab treatment. Although rare, similar cases with rapid progression of portal hypertension after atezolizumab-bevacizumab have been reported. We should pay attention to the worsening of esophageal varices during atezolizumab-bevacizumab treatment and poor wound healing after EVL.

Diagnosis and Management of Esophageal and Gastric Variceal Bleeding: Focused on 2019 KASL Clinical Practice Guidelines for Liver Cirrhosis

Varices are a frequent complication of liver cirrhosis and a major cause of mortality in patients with liver cirrhosis. Patients with decompensated cirrhosis complications have a poor prognosis and require careful management. Portal hypertension is the most common complication of liver cirrhosis, which is the key determinant for varices development. Increased intrahepatic vascular resistance to portal flow leads to the development of portal hypertension. Collateral vessels develop at the communication site between the systemic and portal circulation with the progression of portal hypertension. Varices are the representative collaterals, develop gradually with the progression of portal hypertension and may eventually rupture. Variceal bleeding is a major consequence of portal hypertension and causes the death of cirrhotic patients. The present paper reviews the latest knowledge regarding the diagnosis and management of esophageal and gastric variceal bleeding.

The Role of Perfusion Computed Tomography of the Liver in the Assessment of Hemodynamics in Patients with Compensated Cirrhosis of the Liver and the Presence of Type 2 Diabetes Mellitus. Pilot Study

Currently the relationship between liver diseases and glucose metabolism disorders is being studied. To characterize the negative impact of the mechanisms of insulin resistance on the liver parenchyma altered due to cirrhosis, we can use CT-perfusion of the liver — a method that allows us to assess hemodynamic disorders in the liver tissue. During the pilot study, it was found that the values of arterial perfusion and hepatic perfusion index in patients with compensated cirrhosis of the liver in the presence of type 2 diabetes mellitus were statistically significantly higher than in the absence of this pathology (p = 0,007 and p = 0,009 respectively). The values of portal and total perfusion in patients with compensated cirrhosis of the liver in the presence of type 2 diabetes mellitus were significantly lower than in the absence of this pathology (p &lt; 0,001 and p = 0,007 respectively). CT-perfusion of the liver can be used in patients with compensated cirrhosis and the presence of type 2 diabetes mellitus in the anamnesis as a non-invasive method of instrumental diagnosis of hemodynamic changes, including in assessing the progression of portal hypertension and the subsequent detection of concomitant complications.

Laparoscopic splenectomy and proximal splenorenal shunt for portal hypertension due to portal vein thrombosis in a patient with protein S deficiency

Portal vein thrombosis (PVT) is a rare condition in the general population that develops serious complications if left untreated for long time. We present a case of a 29-year-old woman who developed PVT due to protein S deficiency versus neonatal funiculitis. Over time, the patient developed upper gastrointestinal bleeding due to esophageal varices and hypersplenism with splenic sequestration that caused minor bleeding episodes. Laparoscopic splenectomy and proximal splenorenal shunt with distal pancreatectomy due to aneurysmal dilatations of the splenic artery were successfully performed to avoid mayor progression of portal hypertension. Patient was discharged with indefinite anticoagulation and after surgery platelets raised 3 3 ectomy and proximal splenorenal shunt for portal hypertension due to portal vein ombosis is an adequate surgery procedure which should be applied in these medical cases.

Portal hypertension in primary biliary cholangitis: prevalence, natural history and histological correlates

The histopathological mechanisms underlying portal hypertension in primary biliary cholangitis (PBC) are poorly understood, as is its natural history. We have therefore determined the prevalence, severity and progression of portal hypertension in PBC and investigated whether its presence is related to specific histological lesions. Hepatic venous pressure gradient (HVPG) was measured in 86 patients, with 186 assessments over up to 7 years of follow-up and the results correlated with a semiquantitative grading of 8 histological features and nodular regenerative hyperplasia (NRH). Portal hypertension (HVPG >5 mmHg) was present in 88% of all assessments (86% at baseline), and in 45% of patients at baseline was >12 mmHg (high-risk portal hypertension). The rise in portal pressure occurs early in the disease, since 45% of patients with normal serum bilirubin had a raised HVPG, as did 72% of patients with early (Ludwig stages 1 and 2) disease. After baseline, there was a small increase in HVPG over the next 5 years in most patients. In patients with precirrhotic PBC, 82% had portal hypertension and in 34% this was >12 mmHg. Portal pressure correlated significantly with a semiquantitative grading of cholestasis, interface hepatitis and portal tract and sinusoidal fibrosis. NRH was present in only 20% of wedge biopsies. Portal hypertension commences in the early stages of PBC, long preceding both rises in serum bilirubin and the development of cirrhosis. Around 34% of precirrhotic PBC patients have 'high-risk' portal hypertension, which is associated with lesions in the portal tracts and sinusoids rather than with NRH.

S2555 Longstanding Hepatosplenomegaly in an Undiagnosed Sarcoidosis Patient

INTRODUCTION: Sarcoidosis, a multisystem granulomatous disease, typically affects the lungs and lymph nodes. Although there is hepatic involvement in approximately 66% of cases, the liver is rarely the cause of symptoms.We present a case of longstanding sarcoidosis in a young patient whose delayed diagnosis likely resulted in worsened portal hypertension and severe pancytopenia. CASE DESCRIPTION/METHODS: In 2015, a 25 year-old Panamanian woman was referred to Hepatology for elevated liver tests. Initial workup ruled out autoimmune hepatitis and viral hepatitis. She was lost to follow-up until 2017 when she saw a different hepatologist for elevated liver tests. As noted in Table 1, she developed significant cholestasis during that interval. Serologic studies for primary cholestatic liver disease were negative. Imaging showed hepatosplenomegaly but she was again lost to follow-up. In 2019, she presented to the Emergency Department with severe abdominal pain. Labs showed pancytopenia and computed tomography (CT) of the abdomen/pelvis showed hepatosplenomegaly. She was referred to Hematology/Oncology. Bone marrow biopsy was negative. She was again referred to Hepatology. She reported a chronic rash on her lower extremities, but was otherwise asymptomatic. Skin biopsy suggested erythema nodosum. Physical exam was notable for massive splenomegaly, confirmed by CT (Figure 1). Labs revealed pancytopenia and persistent cholestasis. An extensive workup for granulomatous diseases and systemic fungal, viral and mycobacterial infections was completed. Angiotensin converting enzyme (ACE) was markedly elevated (Table 1). Ultimately, liver biopsy was performed. Results confirmed granulomatous hepatitis. (Figure 2). After referral to the Sarcoidosis team, she was noted to have significantly elevated interleukin-2 (IL-2) level, consistent with the diagnosis. DISCUSSION: This case nicely illustrates the natural history of hepatic sarcoidosis. Our patient presented with a normal hematologic profile and mildly elevated liver tests, however she progressed to develop significant cholestasis, portal hypertension and pancytopenia. Earlier recognition and treatment may have hindered progression of portal hypertension. Sarcoidosis should be strongly considered in the diagnostic workup of elevated liver tests, especially in young patients who are at highest risk . In addition to ACE, absolute lymphocyte count and IL-2 level are highly sensitive for sarcoidosis and were also abnormal in our patient.Table 1.: Lab values from 2015-2020. Abbreviations: VCA: Viral Capsid Antigen; EBNA: Epstein-Barr Nuclear AntiigenFigure 1.: CT abdomen and Pelvis showing hepatosplenomegaly.Figure 2.: Liver biopsy pathology showing granulomatous hepatitis.

LIVER TRANSPLANTATION FOR PORTAL VEIN THROMBOSIS: SINGLE CENTER EXPERIENCE

Introduction: Portal vein thrombosis (PVT) is a common complication of liver cirrhosis. The presence of portal thrombosis leads to the progression of portal hypertension and potentially complicate the liver transplantation. The most common classification (Yerdel) is based on the prevalence of thrombosis of the portal system (IV stages). For a long time, severe PVT (III-IV) was considered as a contraindication to liver transplantation due to the complexity of portal revascularisation. However, the current development of vascular surgery suggests a few effective surgical options for these patients. Purpose: Analysis of deceased donor liver transplantation in patients with the presence of PVT. Materials and Methods: The study included the period from January 2016 to February 2020. During this period at the National Medical Research Center of Transplantology and Artificial Organs were performed 241 deceased donor liver transplantation for adult patients. Of these, 25 recipients (10,3%) obtained PVT before transplantation. Fifteen patients had PVT stage I-II, ten patients had severe thrombosis of III and IV stage (six and four respectively). To revascularization of portal flow in the patients with local thrombosis, thrombectomy was performed in 15 cases, in 6 cases (with PVT III stage) an eversion thrombectomy technique was used to remove the thrombus. In four cases (PVT stage IV) were performed various techniques of portal flow bypass. One case was applied by rent portal transposition witch was supplemented by jump-graft between superior mesenteric vein (SMV) and graft’s portal vein (PV). In another case, just a jump-graft technique using donor IVC graft was applied. In two cases, portal supply was carried out from the varicose left gastric vein. When comparing with the control group (n = 216), there were no statistically significant differences in-hospital mortality rates or the length of hospital stay, however, in the group of patients with severe portal vein thrombosis (stages III-IV), early postoperative bleeding was more common. Conclusions: Portal vein thrombosis, including severe thrombosis (Yardel III-IV stages) is not a contraindication for liver transplantation. In a high-volume centers, the presence of PVT is not impact on the results of transplantation.

TIPSS for variceal bleeding in patients with idiopathic non‐cirrhotic portal hypertension: comparison with patients who have cirrhosis

In patients with idiopathic non-cirrhotic portal hypertension (INCPH), the usual recommended strategy for management of variceal bleeding is the same as that in cirrhosis. However, this policy has been challenged by the different natural history between INCPH and cirrhosis. To compare outcomes after transjugular intrahepatic portosystemic shunt (TIPSS) between INCPH and cirrhotic patients admitted for variceal bleeding. Between March 2001 and September 2015, 76 consecutive patients with biopsy-proven INCPH undergoing TIPSS for variceal bleeding in a tertiary-care centre were included. 76 patients with cirrhotic portal hypertension receiving TIPSS for variceal bleeding, and matched for age, sex, Child-Pugh class, stent type and index year of TIPSS creation served as controls. Patients with INCPH, compared to those with cirrhosis, had significantly lower mortality (11% vs 36% at 5years, adjusted HR, 0.37; 95% CI 0.15-0.87, P=0.022), overt hepatic encephalopathy (16% vs 33% at 5years, adjusted HR, 0.35; 95% CI 0.16-0.75, P=0.007) and hepatic impairment, despite similar rates of further bleeding (33% vs 32% at 5years, adjusted HR, 0.72; 95% CI 0.36-1.44, P=0.358), and shunt dysfunction (35% vs 36% at 5years, adjusted HR, 0.84; 95% CI 0.41-1.72, P=0.627). These findings were consistent across different relevant subgroups. Patients with INCPH treated with TIPSS for variceal bleeding had similar progression of portal hypertension (further bleeding and shunt dysfunction) but fewer complications of liver disease (overt hepatic encephalopathy and hepatic insufficiency) and lower mortality rate compared with cirrhotic patients with comparable liver function.

Validation of Baveno VI Criteria for Screening and Surveillance of Esophageal Varices in Patients With Compensated Cirrhosis and a Sustained Response to Antiviral Therapy

Management of patients with cirrhosis includes endoscopic screening and surveillance to detect esophageal varices (EV) and prevent bleeding. However, the Baveno VI guidelines recommend avoiding endoscopies for patients with liver stiffness measurements below 20 kPa and platelet counts above 150,000 (favorable Baveno VI status) and endoscopic assessment of patients with higher levels of liver stiffness and platelet counts (unfavorable Baveno VI status). We aimed to validate the Baveno VI guidelines, evaluating outcomes of patients in the ANRS-CO12 CirVir cohort with compensated cirrhosis associated with hepatitis B virus (HBV) or hepatitis C virus (HCV) infection, with or without a sustained response to antiviral therapy. We performed an ancillary study using data from 891 patients in the ANRS CO12 CirVir cohort, treated at 35 centers in France, with HCV or HBV infection and biopsy-proven cirrhosis, Child-Pugh A scores, no previous complications, and no hepatocellular carcinoma who underwent an endoscopic procedure and had interpretable liver stiffness measurements and platelet counts. Progression of portal hypertension (PHT) was defined as the onset of varices needing treatment (VNT) or PHT-related bleeding. An sustained response to antiviral therapy was defined as undetectable level of HCV RNA by polymerase chain reaction assay (<50 IU/mL) 12 weeks after the end of treatment (SVR) or an undetectable level of HBV DNA. The primary aims were to validate the Baveno VI guidelines for screening and surveillance of EV in patients with compensated cirrhosis and to study the effects of an SVR on the progression of PHT. A total of 200 patients achieved an SVR (22.4%) (94 patients with HCV infection, 98 patients with HBV infection, and 8 patients with both); 80 of these patients had favorable Baveno VI status and none had VNT. Progression of PHT was studied in 548 patients; during a follow-up period of 61.2 months (interquartile range, 39.5-80.6 months), 105 of these patients (19.1%) had progression of PHT. Lack of an SVR and grade 1 EV were independently associated with progression of PHT. At the time of PHT progression, all patients had unfavorable Baveno VI status. Achieving favorable Baveno VI status after an SVR was associated with the absence of PHT progression. Favorable Baveno VI status and SVR were independently associated with survival. In an analysis of data from a large cohort of patients with HBV- or HCV-associated cirrhosis in France, we validated the Baveno VI guidelines on screening and surveillance of PHT, even for patients who achieved a sustained response to antiviral therapy.

The possibilities of interventional radiology before and after orthotopic liver transplantation

Presented the case of a combined approach preparation of 47 years old patient with primary biliary cirrhosis for orthotopic liver transplantation (OLT) and arterial flow insufficiency correction after surgery. The patient was under waiting list for OLT due liver cirrhosis progression. The patient underwent Intraportal infusion of autologous bone marrow mononuclear cells (MNC) which is allowed temporary stabilized the cirrhotic transformation. The transjugular intrahepatic portosystemic shunt (TIPS) procedure performed due to portal hypertension progression with episodes of bleeding from the esophageal and gastric varices, that allowed to receive organ donor and OLT. At 6 months after OLT the patient had clinical signs of a jaundice caused by splenic artery steal syndrome which was corrected by endovascular intervention: splenic artery trunk embolization.

Screening and Surveillance of Varices in Patients With Cirrhosis

Gastro-esophageal varices (GEV) and variceal hemorrhage (VH) are clinical milestones in the natural history of cirrhosis, as they are closely related to the severity of portal hypertension and define specific stages in disease progression. Variceal hemorrhage is a life-threatening complication of cirrhosis and is one of the clinical complications that defines cirrhosis decompensation. The goal of screening and surveillance of varices is to identify patients with GEV at a high risk of bleeding, so that prevention strategies can be implemented. There have been significant updates in the management of GEV over the last years, particularly in the use of non-invasive methods to assess the degree of portal hypertension and the likelihood of having GEV. This paper is focused on esophageal varices with or without extension along the lesser curvature (type 1 or GOV1), as special considerations are required for the management of cardiofundal varices (GOV2 - esophageal varices extending into the fundus, or IGV1 - isolated gastric varices in the fundus) or isolated gastric varices type 2 (IGV2 – gastric varices elsewhere in the stomach, not in the fundus).