Computed tomography perfusion in liver and spleen for hepatitis B virus-related portal hypertension:A correlation study with hepatic venous pressure gradient

BACKGROUND Hepatic venous pressure gradient(HVPG)is the gold standard for diagnosis of portal hypertension(PH).However,its use can be limited because it is an invasive procedure.Therefore,it is necessary to explore a non-invasive method to assess PH.AIM To investigate the correlation of computed tomography(CT)perfusion of the liver with HVPG and Child-Pugh score in hepatitis B virus(HBV)-related PH.METHODS Twenty-eight patients(4 female,24 male)with gastroesophageal variceal bleeding induced by HBV-related PH were recruited in our study.All patients received CT perfusion of the liver before transjugular intrahepatic portosystemic stent-shunt(TIPS)therapy.Quantitative parameters of CT perfusion of the liver,including liver blood flow(LBF),liver blood volume(LBV),hepatic artery fraction,splenic blood flow and splenic blood volume were measured.HVPG was recorded during TIPS therapy.Correlation of liver perfusion with Child-Pugh score and HVPG were analyzed,and the receiver operating characteristic curve was analyzed.Based on HVPG(>12 mmHg vs≤12 mmHg),patients were divided into moderate and severe groups,and all parameters were compared.RESULTS Based on HVPG,18 patients were classified into the moderate group and 10 patients were classified into the severe group.The Child-Pugh score,HVPG,LBF and LBV were significantly higher in the moderate group compared to the severe group(all P<0.05).LBF and LBV were negatively associated with HVPG(r=-0.473,P<0.05 and r=-0.503,P<0.01,respectively),whereas splenic blood flow was positively associated with hepatic artery fraction(r=0.434,P<0.05).LBV was negatively correlated with Child-Pugh score.Child-Pugh score was not related to HVPG.Using a cutoff value of 17.85 mL/min/100 g for LBV,the sensitivity and specificity of HVPG≥12 mmHg for diagnosis were 80%and 89%,respectively.CONCLUSION LBV and LBF were negatively correlated with HVPG and Child-Pugh scores.CT perfusion imaging is a potential non-invasive quantitative predictor for PH in HBV-related liver cirrhosis.

Spontaneous rupture of splenic hamartoma in a patient with hepatitis C virus-related cirrhosis and portal hypertension:A case report and review of the literature

Spontaneous rupture is a rare complication of splenic hamartoma. A review of the literature revealed only four such cases. To the best of our knowledge, this is the first report of spontaneous rupture of splenic hamartoma associated with liver cirrhosis and portal hypertension. A 53-year-old woman, who was followed up for aortic dissection and hepatitis C virus （HCV）-related liver cirrhosis, was referred with sudden left chest and shoulder pain. An abdominal ultrasound showed intraabdominal bleeding, and computed tomography indicated rupture of a splenic tumor. Emergent splenectomy was carried out. The postoperative course was uneventful, and the patient was discharged on the 13th postoperative day. Pathology revealed the tumor to be a ruptured splenic hamartoma. The non-tumorous splenic parenchyma revealed congestive changes. We consider that the presence of liver cirrhosis and portal hypertension are risk factors for spontaneous rupture of the splenic hamartoma.

Laparoscopic splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension

Since the first laparoscopic splenectomy(LS)was reported in 1991,LS has become the gold standard for the removal of normal to moderately enlarged spleens in benign conditions.Compared with open splenectomy,fewer postsurgical complications and better postoperative recovery have been observed,but LS is contraindicated for hypersplenism secondary to liver cirrhosis in many institutions owing to technical difficulties associated with splenomegaly,well-developed collateral circulation,and increased risk of bleeding.With the improvements of laparoscopic technique,the concept is changing.This article aims to give an overview of the latest development in laparoscopic splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension.Despite a lack of randomized controlled trial,the publications obtained have shown that with meticulous surgical techniques and advanced instruments,LS is a technically feasible,safe,and effective procedure for hypersplenism secondary to cirrhosis and portal hypertension and contributes to decreased blood loss,shorter hospital stay,and less impairment of liver function.It is recommended that the dilated short gastric vessels and other enlarged collateral circulation surrounding the spleen be divided with the LigaSure vessel sealing equipment,and the splenic artery and vein be transected en bloc with the application of the endovascular stapler.To support the clinical evidence,further randomized controlled trials about this topic are necessary.

Glycyrrhizinate reduces portal hypertension in isolated perfused rat livers with chronic hepatitis

AIM:To investigate the effects of diammonium glycyrrhizinate(Gly)on portal hypertension(PHT)in isolated portal perfused rat liver(IPPRL)with carbon tetrachloride(CCl4)-induced chronic hepatitis.METHODS:PHT model was replicated with CCl4 in rats for 84 d.Model was identified by measuring the ascetic amounts,hepatic function,portal pressure in vivo,splenic index,and pathological alterations.Inducible nitric oxide synthase(iNOS)in liver was assessed by immunohistochemistry.IPPRLs were performed at d0,d28,d56,and d84.After phenylephrine-induced constriction,Gly was geometrically used to reduce PHT.Gly action was expressed as median effective concentration(EC50)and area under the curve(AUC).Underlying mechanism was exploited by linear correlation between AUC values of Gly and existed iNOS in portal triads.RESULTS:PHT model was confirmed with ascites,splenomegaly,serum biomarkers of hepatic injury,and elevated portal pressure.Pathological findings had shown normal hepatic structure at d0,degenerations at d28,fibrosis at d56,cirrhosis at d84in PHT rats.Pseudo lobule ratios decreased and collagen ratios increased progressively along with PHT development.Gly does dose-dependently reduce PHT in IPPRLs with CCl4-induced chronic hepatitis.Gly potencies were increased gradually along with PHT development,characterized with its EC50at 2.80×10-10,3.03×10-11,3.77×10-11and 4.65×10-11mol/L at d0,d28,d56and d84,respectively.Existed iNOS was located at hepatocyte at d0,stellate cells at d28,stellate cells and macrophages at d56,and macrophages in portal triads at d84.Macrophages infiltrated more into portal triads and expressed more iNOS along with PHT development.AUC values of Gly were positively correlated with existed iNOS levels in portal triads.CONCLUSION:Gly reduces indirectly PHT in IPPRL with CCl4-induced chronic hepatitis.The underlying mechanisms may relate to rescue NO bioavailability from macrophage-derived peroxynitrite in portal triads.

Selection of a TIPS stent for management of portal hypertension in liver cirrhosis: An evidence-based review

Nowadays,transjugular intrahepatic portosystemic shunt(TIPS)has become a mainstay treatment option for the management of portal hypertension-related complications in liver cirrhosis.Accumulated evidence has shown that its indications are being gradually expanded.Notwithstanding,less attention has been paid for the selection of an appropriate stent during a TIPS procedure.Herein,we attempt to review the current evidence regarding the diameter,type,brand,and position of TIPS stents.Several following recommendations may be considered in the clinical practice:(1)a 10-mm stent may be more effective than an 8-mm stent for the management of portal hypertension,and may be superior to a 12-mm stent for the improvement of survival and shunt patency;(2)covered stents are superior to bare stents for reducing the development of shunt dysfunction;(3)if available,Viatorr stent-grafts may be recommended due to a higher rate of shunt patency;and(4)the placement of a TIPS stent in the left portal vein branch may be more reasonable for decreasingthe development of hepatic encephalopathy.However,given relatively low quality of evidence,prospective well-designed studies should be warranted to further confirm these recommendations.

Combined Laparoscopic Splenectomy and Esophagogastric Devascularization versus Open Splenectomy and Esophagogastric Devascularization for Portal Hypertension due to Liver Cirrhosis

This study was conducted to compare the feasibility,safety and effectiveness of the combined-laparoscopic splenectomy and esophagogastric devascularization(C-LSED)with open splenectomy and esophagogastric devascularization surgery(OSED)in patients with portal hypertension due to liver cirrhosis.From February 2014 to June 2018,68 patients with portal hypertension were diagnosed as having serious gastroesophageal varices and/or hypersplenism in our center.Thirty patients underwent C-LSED and 38 patients received OSED.Results and outcomes were compared retrospectively.No patients of C-LSED group required an intraoperative conversion to open surgery.Significantly shorter operating time,less blood loss,lower transfusion rates,shorter postoperative hospital stay,lower rates of complications were found in C-LSED group than in C-LSED group(P<0.05).No death and rebleeding were documented in both groups during the follow-up periods of one year Postoperative endoscopy revealed that varices in the patients of both groups were alleviated significantly from severe to mild,and in a part of cases,the varices disappeared.The final results suggest that the C-LSED technique is superior to open procedure,due to slightly invasive,simplified operative procedure,significantly shorter operating time,less intraoperative bleeding and lower post-operative complication rates.And C-LSED offers comparable long-term effects to open surgery.

Attenuation of portal hypertension by natural taurine in rats with liver cirrhosis

AIM： To investigate the inhibitory effect of natural taurine （NTau） on portal hypertension （PHT） in rats with experimentally-induced liver cirrhosis （LC）. METHODS： Experimentally-induced LC Wistar rats （20 rats/group） were treated with either oral saline or oral NTau for 6 consecutive weeks. Evaluation parameters included portal venous pressure （PVP）, portal venous resistance （PVR）, portal venous flow （PVF）, splanchnic vascular resistance （SVR） and mean arterial pressure （NAP）. Vasoactive substance levels including nitric oxide （NO）, nitric oxide synthase （NOS） and cyclic guanosine monophosphate （cGMP） were also measured. Histological investigation of type Ⅰ and Ⅲ collagen （COL Ⅰ and Ⅲ） and transforming growth factor-β1 （TGF-β1） was also performed. RESULTS： Treatment with NTau （1） significantly decreased PVP, PVR and PVF, and increased MAP and SVP; （2） markedly increased the vascular compliance and reduced the zero-stress of the portal vein; （3） markedly decreased the amount of NO and cGMP and activity of NOS; and （4） improved the pathological status of the liver tissue and reduced the expression of COL Ⅰ, COL Ⅲ and TGF-β1. CONCLUSION： NTau inhibited the LC-induced PHT by improving hyperdynamic circulation, morphology of liver and biomechanical properties of the portal vein in experimentally-induced LC rats.

Contemporary concepts of the medical therapy of portal hypertension under liver cirrhosis

Severe complications of liver cirrhosis are mostly related to portal hypertension. At the base of the pathogenesis of portal hypertension is the increase in hepatic vascular resistance to portal blood flow with subsequent development of hyperdynamic circulation, which, despite of the formation of collateral circulation, promotes progression of portal hypertension. An important role in its pathogenesis is played by the rearrangement of vascular bed and angiogenesis. As a result, strategic directions of the therapy of portal hypertension under liver cirrhosis include selectively decreasing hepatic vascular resistance with preserving or increasing portal blood flow, and correcting hyperdynamic circulation and pathological angiogenesis, while striving to reduce the hepatic venous pressure gradient to less than 12 mm Hg or 20% of the baseline. Over the last years, substantial progress in understanding the pathophysiological mechanisms of hemodynamic disorders under liver cirrhosis has resulted in the development of new drugs for their correction. Although the majority of them have so far been investigated only in animal experiments, as well as at the molecular and cellular level, it might be expected that the introduction of the new methods in clinical practice will increase the efficacy of the conservative approach to the prophylaxis and treatment of portal hypertension complications. The purpose of the review is to describe the known methods of portal hypertension pharmacotherapy and discuss the drugs that may affect the basic pathogenetic mechanisms of its development.

Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives

Developing medicines for hemodynamic disorders that are characteristic of cirrhosis of the liver is a relevant problem in modern hepatology. The increase in hepatic vascular resistance to portal blood flow and subsequent hyperdynamic circulation underlie portal hypertension(PH) and promote its progression, despite the formation of portosystemic collaterals. Angiogenesis and vascular bed restructurization play an important role in PH pathogenesis as well. In this regard, strategic directions in the therapy for PH in cirrhosis include selectively decreasing hepatic vascular resistance while preserving or increasing portal blood flow, and correcting hyperdynamic circulation and pathological angiogenesis. The aim of this review is to describe the mechanisms of angiogenesis in PH and the methods of antiangiogenic therapy. The Pub Med database, the Google Scholar retrieval system, and the reference lists from related articles were used to search for relevant publications. Articles corresponding to the aim of the review were selected for 2000-2017 using the keywords: "liver cirrhosis", "portal hypertension", "pathogenesis", "angiogenesis", and "antiangiogenic therapy". Antiangiogenic therapy for PH was the inclusion criterion. In this review, we have described angiogenesis inhibitors and their mechanism of action in relation to PH. Although most of them were studie donly in animal experiments, this selective therapy for abnormally growing newly formed vessels is pathogenetically reasonable to treat PH and associated complications.

Analysis of the nitric oxide-cyclic guanosine monophosphate pathway in experimental liver cirrhosis suggests phosphodiesterase-5 as potential target to treat portal hypertension

AIM To investigate the potential effect of inhibitors of phosphodiesterase-5(PDE-5) for therapy of portal hypertension in liver cirrhosis.METHODS In the rat model of thioacetamide-induced liver fibrosis/cirrhosis the nitric oxide-cyclic guanosine monophosphate(NO-cGMP) pathway was investigated. Expression and localization of PDE-5, the enzyme that converts vasodilating cGMP into inactive 5'-GMP, was in the focus of the study. Hepatic gene expression of key components of the NO-cGMP pathway was determined by qRT-PCR: Endothelial NO synthase(eNOS), inducible NO synthase(iNOS), soluble guanylate cyclase subunits α1 and β1(sGCa1, sGCb1), and PDE-5. Hepatic PDE-5 protein expression and localization were detected by immunohistochemistry. Serum cGMP concentrations were measured using ELISA. Acute effects of the PDE-5 inhibitor Sildenafil(0.1 mg/kg or 1.0 mg/kg) on portal and systemic hemodynamics were investigated using pressure transducers.RESULTS Hepatic gene expression of eNOS(2.2-fold; P = 0.003), sGCa1(1.7-fold; P = 0.003), sGCb1(3.0-fold; P = 0.003), and PDE-5(11-fold; P = 0.003) was increased in cirrhotic livers compared to healthy livers. Overexpression of PDE-5(7.7-fold; P = 0.006) was less pronounced in fibrotic livers. iNOS expression was only detected in fibrotic and cirrhotic livers. In healthy liver, PDE-5 protein was localized primarily in zone 3 hepatocytes and to a lesser extent in perisinusoidal cells. This zonation was disturbed in cirrhosis: PDE-5 protein expression in perisinusoidal cells was induced approximately 8-fold. In addition, PDE-5-expressing cells were also found in fibrous septa. Serum cGMP concentrations were reduced in rats with cirrhotic livers by approximately 40%. Inhibition of PDE-5 by Sildenafil caused a significant increase in serum cGMP concentrations [+ 64% in healthy rats(P = 0.024), + 85% in cirrhotic rats(P = 0.018)]. Concomitantly, the portal venous pressure was reduced by 19% in rats with liver cirrhosis. CONCLUSION Overexpression and abrogated zonation of PDE-5 likely contribute to the pathogenesis of cirrhotic portal hypertension. PDE-5 inhibition may therefore be a reasonable therapeutic approach for portal hypertension.

Plasma Nogo-A and placental growth factor levels are associated with portal hypertension in patients with liver cirrhosis

BACKGROUND Clinically significant portal hypertension(CSPH) and severe portal hypertension(SPH) increase the risk for decompensation and life-threatening complications in liver cirrhosis. Pathologic angiogenesis might contribute to the formation of these conditions. Placental growth factor(PlGF) and Nogo-A protein are biomarkers of pathological angiogenesis, but data on their role in liver cirrhosis and portal hypertension is scarce.AIM To determine plasma levels of PlGF and Nogo-A in patients with liver cirrhosis,CSPH, SPH and potential to predict portal hypertension.METHODS A cohort of 122 patients with hepatitis C virus and/or alcohol-induced liver cirrhosis with characterized hepatic venous pressure gradient(HVPG) were included in the study. Demographic data, medical history, Child-Turcotte-Pugh and Model of End Stage liver disease score, clinical chemistry, liver stiffnessvalues were recorded on the day of the procedure prior HVPG measurement. The degree of portal hypertension was determined by the invasive HVPG measurement. Nogo-A and PlGF plasma levels were evaluated using enzyme linked immunosorbent assay. The control group consisted of 30 healthy age-and sex-matched individuals.RESULTS Peripheral PlGF levels were higher and Nogo-A levels were lower in patients with liver cirrhosis(23.20 vs 9.85;P < 0.0001 and 2.19 vs 3.12;P = 0.004 respectively). There was a positive linear correlation between peripheral levels of PlGF and HVPG(r = 0.338, P = 0.001) and negative linear correlation between the peripheral Nogo-A levels and HVPG(r =-0.267, P = 0.007). PlGF levels were higher in CSPH and SPH(P = 0.006;P < 0.0001) whereas Nogo-A levels were lower(P = 0.01;P < 0.033). Area under the curve for the diagnosis of CSPH for PlGF was 0.68(P = 0.003) and for Nogo-A-0.67(P = 0.01);for SPH 0.714(P <0.0001) and 0.65(P = 0.014) respectively. PlGF levels were higher and Nogo-A levels were lower in patients with esophageal varices(P < 0.05). PlGF cut-off value of 25 pg/mL distinguished patients with CSPH at 55.7% sensitivity and76.7% specificity;whereas Nogo-A cut-off value of 1.12 ng/mL was highly specific(93.1%) for the diagnosis of CSPH.CONCLUSION Plasma PlGF levels were higher while Nogo-A levels were lower in patients with liver cirrhosis and portal hypertension. Biomarkers showed moderate predictive value in determining CSPH and SPH.

Causes of Peripheral Blood Cytopenias in Patients with Liver Cirrhosis Portal Hypertension and Clinical Significances

Liver cirrhosis portal hypertension patients to reduce the number of blood cells are common in clinical, and often affect the prognosis. This paper discusses cirrhotic portal hypertension patients complicated by the reason of the decrease in the number of peripheral blood cells and what is the clinical significance of these reasons so as to provide theoretical support for the choice of treatment. Splenomegaly and hypersplenism caused should be the main reason for reducing the number of blood cells, but not all, other reasons are alcohol and virus inhibition of bone marrow, liver function impairment, autoimmune damage and loss of blood, etc. If it is a function of the spleen hyperfunction caused by blood cells decreases, blood should rise to normal after splenectomy, or consider other reason or there are other reasons at the same time.

Portal hypertension in patients with nonalcoholic fatty liver disease:Current knowledge and challenges

Portal hypertension(PH)has traditionally been observed as a consequence of significant fibrosis and cirrhosis in advanced non-alcoholic fatty liver disease(NAFLD).However,recent studies have provided evidence that PH may develop in earlier stages of NAFLD,suggesting that there are additional pathogenetic mechanisms at work in addition to liver fibrosis.The early development of PH in NAFLD is associated with hepatocellular lipid accumulation and ballooning,leading to the compression of liver sinusoids.External compression and intraluminal obstacles cause mechanical forces such as strain,shear stress and elevated hydrostatic pressure that in turn activate mechanotransduction pathways,resulting in endothelial dysfunction and the development of fibrosis.The spatial distribution of histological and functional changes in the periportal and perisinusoidal areas of the liver lobule are considered responsible for the pre-sinusoidal component of PH in patients with NAFLD.Thus,current diagnostic methods such as hepatic venous pressure gradient(HVPG)measurement tend to underestimate portal pressure(PP)in NAFLD patients,who might decompensate below the HVPG threshold of 10 mmHg,which is traditionally considered the most relevant indicator of clinically significant portal hypertension(CSPH).This creates further challenges in finding a reliable diagnostic method to stratify the prognostic risk in this population of patients.In theory,the measurement of the portal pressure gradient guided by endoscopic ultrasound might overcome the limitations of HVPG measurement by avoiding the influence of the pre-sinusoidal component,but more investigations are needed to test its clinical utility for this indication.Liver and spleen stiffness measurement in combination with platelet count is currently the best-validated non-invasive approach for diagnosing CSPH and varices needing treatment.Lifestyle change remains the cornerstone of the treatment of PH in NAFLD,together with correcting the components of metabolic syndrome,using nonselective beta blockers,whereas emerging candidate drugs require more robust confirmation from clinical trials.

Impact of hepatitis C oral therapy in portal hypertension

Chronic hepatitis C is a leading cause of morbidity and mortality, mainly related to fibrosis/cirrhosis and portal hypertension. Direct antiviral agents are highly effective and safe and can now cure > 90% of the patients. Sustained viral response (SVR) after interferon-based regimens has been associated with improvement in liver function, fibrosis and portal hypertension in a significant proportion of patients, although a point of no return seems to exist from which viral elimination is no longer capable of preventing portal hypertension progression and liver decompensation. Indeed, although SVR is associated with improvement of hepatic venous pressure gradients and therefore a decreased risk of de novo esophageal varices, several studies show that viral clearance does not eliminate the risk of variceal progression, liver decompensation and death in patients with pre-established portal hypertension. Although evidence about the effects of direct antiviral agents (DAAs) on clinically significant outcomes is still scarce and with short follow-up, DAAs can decrease the burden of the disease if patients are timely treated before significant fibrosis and portal hypertension develops. Studies with longer follow-up are waited to establish the real magnitude of hepatitis C treatment on portal hypertension. Future studies should also focus on predictors of portal hypertension resolution since it can influence management and avoid unnecessary monitoring

Spleen stiffness mirrors changes in portal hypertension after successful interferon-free therapy in chronic-hepatitis C virus patients

AIM To investigate changes in spleen stiffness measurements(SSMs) and other non-invasive tests(NITs) after treatment with direct-acting antivirals(DAAs) and identify predictors of SSM change after sustainedvirological response(SVR). METHODS We retrospectively analysed 146 advanced-chronic liver disease(ACLD) patients treated with DAA with available paired SSM at baseline and SVR24. Liver stiffness(LSM), spleen diameter(SD), platelet count(PLT) and liver stiffness-spleen diameter to platelet ratio score(LSPS) were also investigated. LSM ≥ 21 k Pa was used as a cut-off to rule-in clinically significant portal hypertension(CSPH). SSM reduction > 20% from baseline was defined as significant.RESULTS SSM significantly decreased at SVR24, in both patients with and without CSPH; in 44.8% of cases, SSM reduction was > 20%. LSPS significantly improved in the entire cohort at SVR24; SD and PLT changed significantly only in patients without CSPH. LSM significantly decreased in 65.7% of patients and also in 2/3 patients in whom SSM did not decrease. The independent predictor of decreased SSM was median relative change of LSM. CSPH persisted in 54.4% patients after SVR. Delta LSM and baseline SSM were independent factors associated with CSPH persistence.CONCLUSION SSM and other NITs significantly decrease after SVR, although differently according to the patient's clinical condition. SSM faithfully reflects changes in portal hypertension and could represent a useful NIT for the follow-up of these patients.

Advancing hepatic recompensation:Baveno VII criteria and therapeutic innovations in liver cirrhosis management

The Baveno VII criteria redefine the management of decompensated liver cirrhosis,introducing the concept of hepatic recompensation marking a significant departure from the conventional view of irreversible decline.Central to this concept is addressing the underlying cause of cirrhosis through tailored therapies,including antivirals and lifestyle modifications.Studies on alcohol,hepatitis C virus,and hepatitis B virus-related cirrhosis demonstrate the efficacy of these interventions in improving liver function and patient outcomes.Transjugular intrahepatic portosystemic shunt(TIPS)emerges as a promising intervention,effectively resolving complications of portal hypertension and facilitating recompensation.However,optimal timing and patient selection for TIPS remain unresolved.Despite challenges,TIPS offers renewed hope for hepatic recompensation,marking a significant advancement in cirrhosis management.Further research is needed to refine its implementation and maximize its benefits.In conclusion,TIPS stands as a promising avenue for improving hepatic function and patient outcomes in decompensated liver cirrhosis within the framework of the Baveno VII criteria.

Contemporary concepts of prevention and management of gastroesophageal variceal bleeding in liver cirrhosis patients

This editorial describes the contemporary concepts of prevention and management of gastroesophageal variceal bleeding in liver cirrhosis(LC)patients according to the current guidelines.Gastroesophageal variceal bleeding is the most dangerous complication of portal hypertension in LC patients.Risk stratification and determination of an individual approach to the choice of therapeutic measures aimed at their prevention and management has emerged as one of the top concerns in modern hepatology.According to the current guidelines,in the absence of clinically significant portal hypertension,etiological and nonetiological therapies of LC is advisable for the primary preventing gastroesophageal variceal bleeding,whereas its presence serves as an indication for the administration of non-selectiveβ-blockers,among which carvedilol is the drug of choice.Non-selectiveβ-blockers,as well as endoscopic variceal ligation and transjugular intrahepatic portosystemic shunt can be used to prevent recurrence of gastroesophageal variceal bleeding.Pharmacotherapy with vasoactive drugs(terlipressin,somatostatin,octreotide),endoscopic variceal ligation,endovascular techniques and transjugular intrahepatic portosystemic shunt are recommended for the treatment of acute gastroesophageal variceal bleeding.Objective and accurate risk stratification of gastroesophageal variceal bleeding will allow developing individual strategies for their prevention and management,avoiding the first and further decompensation in LC,which will improve the prognosis and survival of patients suffering from it.

Spleen volume is associated with overt hepatic encephalopathy after transjugular intrahepatic portosystemic shunt in patients with portal hypertension

BACKGROUND Portal shunt and immune status related to the spleen are related to the occurrence of hepatic encephalopathy(HE).It is unknown whether spleen volume before transjugular intrahepatic portosystemic shunt(TIPS)is related to postoperative HE.AIM To investigate the relationship between spleen volume and the occurrence of HE.METHODS This study included 135 patients with liver cirrhosis who underwent TIPS,and liver and spleen volumes were elevated upon computed tomography imaging.The Kaplan-Meier curve was used to compare the difference in the incidence rate of HE among patients with different spleen volumes.Univariate and multivariate Cox regression analyses were performed to identify the factors affecting overt HE(OHE).Restricted cubic spline was used to examine the shapes of the dose-response association between spleen volumes and OHE risk.RESULTS The results showed that 37(27.2%)of 135 patients experienced OHE during a 1-year follow-up period.Compared with preoperative spleen volume(901.30±471.90 cm3),there was a significant decrease in spleen volume after TIPS(697.60±281.0 cm^(3))in OHE patients.As the severity of OHE increased,the spleen volume significantly decreased(P<0.05).Compared with patients with a spleen volume≥782.4 cm^(3),those with a spleen volume<782.4 cm^(3) had a higher incidence of HE(P<0.05).Cox regression analysis showed that spleen volume was an independent risk factor for post-TIPS OHE(hazard ratio=0.494,P<0.05).Restricted cubic spline model showed that with an increasing spleen volume,OHE risk showed an initial increase and then decrease(P<0.05).CONCLUSION Spleen volume is related to the occurrence of OHE after TIPS.Preoperative spleen volume is an independent risk factor for post-TIPS OHE.

Milestones to optimize of transjugular intrahepatic portosystemic shunt technique as a method for the treatment of portal hypertension complications

This editorial describes the milestones to optimize of transjugular intrahepatic portosystemic shunt(TIPS)technique,which have made it one of the main methods for the treatment of portal hypertension complications worldwide.Innovative ideas,subsequent experimental studies and preliminary experience of use in cirrhotic patients contributed to the introduction of TIPS into clinical practice.At the moment,the main achievement in optimize of TIPS technique is progress in the qualitative characteristics of stents.The transition from bare metal stents to extended polytetrafluoroethylene–covered stent grafts made it possible to significantly prevent shunt dysfunction.However,the question of its preferred diameter,which contributes to an optimal reduction of portal pressure without the risk of developing post-TIPS hepatic encephalopathy,remains relevant.Currently,hepatic encephalopathy is one of the most common complications of TIPS,significantly affecting its effectiveness and prognosis.Careful selection of patients based on cognitive indicators,nutritional status,assessment of liver function,etc.,will reduce the incidence of post-TIPS hepatic encephalopathy and improve treatment results.Optimize of TIPS technique has significantly expanded the indications for its use and made it one of the main methods for the treatment of portal hypertension complications.At the same time,there are a number of limitations and unresolved issues that require further randomized controlled trials involving a large cohort of patients.

Hepatic venous pressure gradient: Inaccurately estimates portal venous pressure gradient in alcoholic cirrhosis and portal hypertension

BACKGROUND Portal hypertension(PHT)in patients with alcoholic cirrhosis causes a range of clinical symptoms,including gastroesophageal varices and ascites.The hepatic venous pressure gradient(HVPG),which is easier to measure,has replaced the portal venous pressure gradient(PPG)as the gold standard for diagnosing PHT in clinical practice.Therefore,attention should be paid to the correlation between HVPG and PPG.METHODS Between January 2017 and June 2020,134 patients with alcoholic cirrhosis and PHT who met the inclusion criteria underwent various pressure measurements during transjugular intrahepatic portosystemic shunt procedures.Correlations were assessed using Pearson’s correlation coefficient to estimate the correlation coefficient(r)and determination coefficient(R^(2)).Bland-Altman plots were constructed to further analyze the agreement between the measurements.Disagreements were analyzed using paired t tests,and P values<0.05 were considered statistically significant.RESULTS In this study,the correlation coefficient(r)and determination coefficient(R2)between HVPG and PPG were 0.201 and 0.040,respectively(P=0.020).In the 108 patients with no collateral branch,the average wedged hepatic venous pressure was lower than the average portal venous pressure(30.65±8.17 vs.33.25±6.60 mmHg,P=0.002).Hepatic collaterals were identified in 26 cases with balloon occlusion hepatic venography(19.4%),while the average PPG was significantly higher than the average HVPG(25.94±7.42 mmHg vs 9.86±7.44 mmHg;P<0.001).The differences between HVPG and PPG<5 mmHg in the collateral vs no collateral branch groups were three cases(11.54%)and 44 cases(40.74%),respectively.CONCLUSION In most patients,HVPG cannot accurately represent PPG.The formation of hepatic collaterals is a vital reason for the strong underestimation of HVPG.