Cirrhotic Portal Hypertension Research Articles

Pregnancy with Non-cirrhotic Portal Hypertension: A Case Report

Pregnancy with non cirrhotic portal hypertension is an uncommon condition. Due to physiological changes in pregnancy, the patients with portal hypertension may exaggerate and produce life threatening complicationslike variceal haemorrhage and increased incidents of adverse maternal and fetal outcomes. Pregnancy also predisposes the patient to develop hepatic decompensation. So, management of such cases requires a multi-disciplinary approach. In this case report,21-year-old primigravida presented with known case of non cirrhotic portal hypertension at her 33 weeks of pregnancy with huge splenomegaly and history of hematemesis.The pregnancy ran uneventfully, and she underwent elective LSCS at 38+ weeks and gave birth of a live female baby, weighing 3kg was delivered. Post operative recovery was uneventful. The patient was discharged on the 4th post operative day. We want to focus upon different aspects of pregnancy with portal hypertensionto prevent complications and manage the case. J Rang Med Col. March 2024; Vol. 9, No. 1: 86-88

Hepatic Cirrhosis with Esophageal Varices: A Case Report

Background: In adults, portal hypertension is generally caused by hepatic cirrhosis, whereas in children it is more commonly caused by extrahepatic abnormalities with normal liver function. Portal hypertension causes hemodynamic abnormalities. Gastrointestinal bleeding is the most severe clinical manifestation of portal hypertension in both children and adults. Pathogenetically, increased pressure in the portal vein can be caused by increased vascular resistance and increased portal blood flow. The site of obstruction can be prehepatic (portal vein obstruction), intrahepatic (presinusoidal: eg congenital hepatic fibrosis; para sinusoidal: cirrhosis, hepatotoxic drug therapy, vitamin A hepatotoxicity; post sinusoidal: venocclusive disease) and/or post hepatic (Budd-Chiari syndrome, constrictive pericarditis). Case presentation: The study reports the results of observations of a case of a boy, FAA, aged 12 years and 2 months who came to the emergency room at Dr. M. Djamil General Hospital Padang with the main complaint of hematemesis and splenomegaly from physical examination. Non cirrhotic portal fibrosis is a cause that is not uncommon in the population in the early second decade of life. Some children with non-cirrhotic portal fibrosis as adults can end up with end stage liver disease. Conclusion: Patients with noncirrhotic or cirrhotic portal hypertension can be assessed using the Child Pugh instrument as an instrument that is still used to determine the survival rate if patients with portal hypertension.

Pathophysiology and therapeutic options for cirrhotic portal hypertension.

Portal hypertension represents the primary non-neoplastic complication of liver cirrhosis and has life-threatening consequences, such as oesophageal variceal bleeding, ascites, and hepatic encephalopathy. Portal hypertension occurs due to increased resistance of the cirrhotic liver vasculature to portal blood flow and is further aggravated by the hyperdynamic circulatory syndrome. Existing knowledge indicates that the profibrogenic phenotype acquired by sinusoidal cells is the initial factor leading to increased hepatic vascular tone and fibrosis, which cause increased vascular resistance and portal hypertension. Data also suggest that the phenotype of hepatic cells could be further impaired due to the altered mechanical properties of the cirrhotic liver itself, creating a deleterious cycle that worsens portal hypertension in the advanced stages of liver disease. In this Review, we discuss recent discoveries in the pathophysiology and treatment of cirrhotic portal hypertension, a condition with few pharmacological treatment options.

Obliteration of portal venules contributes to portal hypertension in biliary cirrhosis.

The effects of the obliteration of portal venules (OPV) in cirrhotic portal hypertension are poorly understood. To investigate its contribution to portal hypertension in biliary cirrhosis and its underlying mechanism,we evaluated OPV using two-dimensional (2D) histopathology in liver explants from patients with biliary atresia (BA, n = 63), primary biliary cholangitis (PBC, n = 18), and hepatitis B-related cirrhosis (Hep-B-cirrhosis, n = 35). Then, three-dimensional (3D) OPV was measured by X-ray phase-contrast CT in two parallel models in rats following bile duct ligation (BDL) or carbon tetrachloride (CCl4) administration, representing biliary cirrhosis and post-necrotic cirrhosis, respectively. The portal pressure was also measured in the two models. Finally, the effects of proliferative bile ducts on OPV were investigated. We found that OPV was significantly more frequent in patients with biliary cirrhosis, including BA (78.57 ± 16.45%) and PBC (60.00 ± 17.15%), than that in Hep-B-cirrhotic patients (29.43 ± 14.94%, p < 0.001). OPV occurred earlier, evidenced by the paired liver biopsy at a Kasai procedure (KP), and was irreversible even after a successful KP in the patients with BA. OPV was also significantly more frequent in the BDL models than in the CCl4 models, as shown by 2D and 3D quantitative analysis. Portal pressure was significantly higher in the BDL model than that in the CCl4 model. With the proliferation of bile ducts, portal venules were compressed and irreversibly occluded, contributing to the earlier and higher portal pressure in biliary cirrhosis. OPV, as a pre-sinusoidal component, plays a key role in the pathogenesis of portal hypertension in biliary cirrhosis. The proliferated bile ducts and ductules gradually take up the 'territory' originally attributed to portal venules and compress the portal venules, which may lead to OPV in biliary cirrhosis. © 2024 The Pathological Society of Great Britain and Ireland.

Anaesthetic management of a case of non-cirrhotic portal hypertension with severe thrombocytopenia for elective cesarean section

Pregnancy with non-cirrhotic portal hypertension usually presents with portal hypertension due to Physiological hemodynamic changes associated with pregnancy, thereby putting the mother at risk of potentially dangerous complications like variceal bleeding and splenic aneurysmal rupture. Management of such cases requires a multidisciplinary approach involving obstetricians, gastroenterologist and, anesthesiologist Here through the case report of a 36-year-old primigravida with Non Cirrhotic portal hypertension with at 37 weeks gestational age in labor. We intend to focus upon different aspects of anesthetic management of pregnancy with portal hypertension and its complications.

Analysis of transjugular intrahepatic portosystemic shunt by hemodynamic simulation.

Transjugular intrahepatic portosystemic shunt (TIPS), which artificially creates a portocaval shunt to reduce portal venous pressure, has gradually become the primary treatment for portal hypertension (PH). However, there is no prefect shunting scheme in TIPS to balance the occurrence of postoperative complications and effective haemostasis. To construct cirrhotic PH models and compare different shunting schemes in TIPS. Three cases of cirrhotic PH with different liver volumes were selected for enhanced computed tomography scanning. The models for different shunting schemes were created using Mimics software, and following FLUENT calculation, all the models were imported into the software computational fluid dynamic-post for processing. In each shunting scheme, the differences in portal vein pressure, hepatic blood perfusion and blood flow from the superior mesenteric vein in the shunt tract were compared. The coefficient G was adapted to evaluate the advantages and disadvantages. (1)Concerning the precise location of the shunt tract, the wider the diameter of the shunt tract, the lower the pressure of the portal vein and the lesser the hepatic blood perfusion. Meanwhile, the pressure drop objective was not achieved with the 6 mm-diameter shunting scheme. (2)The 8 mm-diameter shunting scheme through the left portal vein (LPV) had the highest coefficient G. The 8 mm-diameter shunting scheme through the LPV may demonstrate a superior effect and prognosis in TIPS procedures.

Physiological and Pathological Significance of Chloride Channels.

Cl- influx and efflux through Cl- channels play a role in regulating the homeostasis of biological functions. Therefore, the hyperfunction or dysfunction of Cl- channels elicits pathological mechanisms. The Cl- channel superfamily includes voltage-gated Cl- (ClC) channels, Ca2+-activated Cl- channels (ClCa; TMEM16A/TMEM16B), cystic fibrosis transmembrane conductance regulator channels, and ligand-gated Cl- channels. These channels are ubiquitously expressed to regulate ion homeostasis, muscle tonus, membrane excitability, cell volume, survival, neurotransmission, and transepithelial transport. The activation or inhibition of Cl- channels changes the membrane potential, thereby affecting cytosolic Ca2+ signals. An elevation in cytosolic [Ca2+] triggers physiological and pathological responses in most cells. However, the roles of Cl- channels have not yet been examined as extensively as cation (Na+, Ca2+, and K+) channels. We recently reported the functional expression of: (i) TMEM16A/ClCa channels in portal vein and pulmonary arterial smooth muscle cells (PASMC), pinealocytes, and brain capillary endothelial cells; (ii) TMEM16B/ClCa channels in pinealocytes; (iii) ClC-3 channels in PASMC and chondrocytes; and (iv) ClC-7 channels in chondrocytes. We also showed that the down-regulation of TMEM16A and ClC-7 channel expression was associated with cirrhotic portal hypertension and osteoarthritis, respectively, whereas the enhanced expression of TMEM16A and ClC-3 channels was involved in the pathogenesis of cerebral ischemia and pulmonary arterial hypertension, respectively. Further investigations on the physiological/pathological functions of Cl- channels will provide insights into biological functions and contribute to the screening of novel target(s) of drug discovery for associated diseases.

Novel Preoperative Type IV Collagen to Predict the Risk of Hepatocellular Carcinoma in Patients with Hepatitis B Virus-Related Cirrhotic Portal Hypertension After Laparoscopic Splenectomy and Azygoportal Disconnection.

Although laparoscopic splenectomy and azygoportal disconnection (LSD) can significantly decrease portal vein pressure and even the incidence of hepatocellular carcinoma (HCC) in patients with cirrhotic portal hypertension (CPH), postoperative HCC inevitably occurs in certain patients. The purpose of this study was to seek a novel preoperative non-invasive predictive indicator to predict the occurrence of postoperative HCC. From April 2012 to April 2022, we collected clinical data of 178 hepatitis B virus (HBV)-related CPH patients. Based on inverse treatment probability weighting, candidate variables for predicting postoperative HCC were determined by means analysis. Then, a novel preoperative non-invasive prediction indicator (ie, type IV collagen-alpha fetoprotein-fibrosis-4 score [IVAF-FIB-4]) was established based on candidate variables, and its predictive ability was explored. Postoperative HCC occurred in 9 (5.1%) patients. Correlation analyses showed that the IVAF-FIB-4 had a significant positive correlation with HCC (r = 0.835, P < 0.001). IVAF-FIB-4 showed a high accuracy (the area under the receiver operating characteristic curve: 0.939, 95% confidence interval [CI]: 0.818-1.000; sensitivity: 88.9%; specificity: 93.5%). At the end of follow-up, the incidence density of HCC in patients with IVAF-FIB-4 (1) was significant higher than that in patients with IVAF-FIB-4 (0) (138.1/1000 vs 1.1/1000 person-years; rate ratio: 130.475, 95% CI: 16.318-1043.227). In logistic regression, IVAF-FIB-4 was an independent risk factor for HCC (odds ratio: 668.000, 95% CI: 53.895-8279.541; P < 0.001). IVAF-FIB-4 is a novel preoperative noninvasive predictive indicator for predicting postoperative HCC in HBV-related CPH patients after LSD, with satisfactory predictive ability.

Cediranib ameliorates portal hypertensive syndrome via inhibition of VEGFR-2 signaling in cirrhotic rats

Portal hypertension (PHT) is a syndrome caused by systemic and portal hemodynamic disturbances with the progression of cirrhosis. However, the exact mechanisms regulating angiogenesis-related responses in PHT remain unclear. Cediranib is a potent inhibitor of vascular endothelial growth factor receptor (VEGFR) tyrosine kinases, exhibiting a greater affinity for VEGFR-2. Liver cirrhosis was induced by common bile duct ligation (BDL) in Sprague–Dawley rats. Sham-operated rats were controls. BDL and sham rats were randomly allocated to receive Cediranib or vehicle after BDL. On the 28th day, portal hypertension related parameters were surveyed. Cediranib treatment could significantly reduce the portal pressure (PP) in BDL rats, while it did not affect the mean arterial pressure (MAP) in sham groups and BDL groups. Cediranib treatment could significantly affect the stroke volume (SV), cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR), superior mesenteric artery (SMA) flow and SMA resistance in BDL groups and BDL with Cediranib groups. Cediranib treatment could improve the mesenteric vascular remodeling and contractility. Cediranib treatment significantly reduced mesenteric vascular density. And phospho-VEGFR-2 was significantly downregulated by Cediranib. On the other hand, phospho-endothelial Nitric Oxide Synthases (phospho-eNOS) expressions were upregulated. Cediranib not only improved splanchnic hemodynamics, extrahepatic vascular remodeling and vasodilation, but also alleviated intrahepatic fibrosis and collagen deposition significantly. Cediranib treatment could reduce intrahepatic angiogenesis between BDL-vehicle and BDL-Cediranib rats. In conclusion, Cediranib could improve extrahepatic hyperdynamic circulation by inhibiting extrahepatic angiogenesis through inhibition of the VEGFR-2 signaling pathway, portal collateral circulation formation, as well as eNOS-mediated vasodilatation and vascular remodeling, and at the same time, Cediranib improved intrahepatic fibrogenesis and angiogenesis, which together alleviate cirrhotic PHT syndrome.

Consensus on clinical application of hepatic venous pressure gradient in China (2023 edition)

Hepatic venous pressure gradient (HVPG) is considered the gold standard for diagnosing clinically significant portal hypertension (CSPH). To further standardize the application of HVPG measurement, the Chinese Portal Hypertension Alliance (CHESS) and the Minimally Invasive Interventional Collaboration Group of the Chinese Society of Gastroenterology have updated the "Consensus on clinical application of hepatic venous pressure gradient in China (2023 edition)". This consensus provides 10 recommendations, with the aim of effectively promoting standardized measurement and the regulated application of HVPG in the field of cirrhotic portal hypertension in China.

Preliminary exploration of a multidisciplinary management model for cirrhotic portal hypertension

Preliminary exploration of a multidisciplinary management model for cirrhotic portal hypertension

Endoscopic variceal ligation in primary and secondary prevention of variceal bleeding: a retrospective study in Digestive Endoscopy Unit, University Hospital Joseph Raseta Befelatanana, Antananarivo, Madagascar

IntroductionEndoscopic variceal ligation (EVL) is a crucial procedure for the primary and secondary prevention of variceal bleeding. The objective of this study was to evaluate the efficacy and tolerability of EVL in the prevention of variceal bleeding.MethodsThis was a retrospective, single-center study over 8 years, from January 2013 to December 2020, including all patients who came for EVL in primary or secondary prevention.ResultsFifty-seven patients (male/female: 39/18) were included. The mean age of the patients was 40.02 ± 12.32 years (range: 19–68). Portal hypertension was secondary to cirrhosis in 13 patients (22.8%) and to a non-cirrhotic cause in 44 patients (77.2%). EVL was indicated for primary and secondary prevention in 5.3% and 94.7%, respectively. All patients had received propranolol with a mean daily dose of 108.07 ± 38.52 mg (extremes: 80–160). Eradication of varices was achieved in 33 patients (57.9%) with an average of 3.06 ± 0.70 sessions (extremes: 1–5) and an average duration of 10.12 ± 6.21 months (extremes: 1–24). Ten patients (17.5%) had variceal bleeding, and one patient (1.8%) died. There was no significant difference between patients with cirrhotic and non-cirrhotic portal hypertension in terms of varices eradication, variceal bleeding, and mortality. Gender (HR: 37.18; CI: 0.14–18.4; p = 0.009) and the number of previous bleeds (HR: 1.34; CI: 1.01–1.80; p = 0.041) were independent predictors of variceal bleeding during EVL. Dysphagia (73.7%) and retrosternal pain (78.9%) were the main adverse events after ligation.ConclusionEVL is an efficient technique to eradicate varices. Its tolerance is good with post-ligation signs that are rapidly regressive.

A Narrative Review on Non-Cirrohotic Portal Hypertension: Not All Portal Hypertensions Mean Cirrhosis.

Non-cirrhotic portal hypertension (NCPH), also known as idiopathic non-cirrhotic portal hypertension (INCPH) and porto-sinusoidal vascular disorder (PSVD), is a rare disease characterized by intrahepatic portal hypertension (IPH) in the absence of cirrhosis. The precise etiopathogenesis of IPH is an area of ongoing research. NCPH diagnosis is challenging, as there are no specific tests available to confirm the disease, and a high-quality liver biopsy, detailed clinical information, and an expert pathologist are necessary for diagnosis. Currently, the treatment of NCPH relies on the prevention of complications related to portal hypertension, following current guidelines of cirrhotic portal hypertension. No treatment has been studied that aimed to modify the natural history of the disease; however, transjugular intrahepatic porto-systemic shunt (TIPS) placement, shunt and liver transplantation are considerable symptomatic options. In this review, we discuss the heterogeneity of NCPH as well as its etiopathogenesis, clinical presentation and management issues. Starting from the assumption that portal hypertension does not always mean cirrhosis, cooperative studies are probably needed to clarify the issues of etiology and the possible genetic background of this rare disease. This knowledge might lead to better treatment and perhaps better prevention.

Guidelines for the Management of Esophagogastric Variceal Bleeding in Cirrhotic Portal Hypertension.

To standardize the diagnosis, treatment, and management of esophagogastric variceal bleeding (EVB) in patients with cirrhotic portal hypertension, the Chinese Society of Hepatology, the Chinese Society of Gastroenterology, and the Chinese Society of Digestive Endoscopy of the Chinese Medical Association brought together relevant experts, reviewed the latest national and international progress in clinical research on EVB in cirrhotic portal hypertension, and followed evidence-based medicine to update the Guidelines on the Management of EVB in Cirrhotic Portal Hypertension. The guidelines provide recommendations for the diagnosis, treatment, and management of EVB in cirrhotic portal hypertension and with the aim to improve the level of clinical treatment of EVB in patients with cirrhotic portal hypertension.

The decreased risk of hepatocellular carcinoma in hepatitis B virus-related cirrhotic portal hypertension patients after laparoscopic splenectomy and azygoportal disconnection.

Posthepatitic cirrhosis is one of the leading risk factors for hepatocellular carcinoma (HCC) worldwide, among which hepatitis B cirrhosis is the dominant one. This study explored whether laparoscopic splenectomy and azygoportal disconnection (LSD) can reduce the risk of HCC among patients with hepatitis B virus (HBV)-related cirrhotic portal hypertension (CPH). A total of 383 patients with HBV-related CPH diagnosed as gastroesophageal variceal bleeding and secondary hypersplenism were identified in our hepatobiliary pancreatic center between April 2012 and April 2022, and conducted an 11-year retrospective follow-up. We used inverse probability of treatment weighting (IPTW) to correct for potential confounders, weighted Kaplan-Meier curves, and logistic regression to estimate survival and risk differences. Patients were divided into two groups based on treatment method: LSD (n = 230) and endoscopic therapy (ET; n = 153) groups. Whether it was processed through IPTW or not, LSD group showed a higher survival benefit than ET group according to Kaplan-Meier analysis (P < 0.001). The incidence density of HCC was higher in the ET group compared to LSD group at the end of follow-up [32.1/1000 vs 8.0/1000 person-years; Rate ratio: 3.998, 95% confidence intervals (CI) 1.928-8.293]. Additionally, in logistic regression analyses weighted by IPTW, LSD was an independent protective predictor of HCC incidence compared to ET (odds ratio 0.516, 95% CI 0.343-0.776; P = 0.002). Considering the ability of LSD to improve postoperative survival and prevent HCC in HBV-related CPH patients with gastroesophageal variceal bleeding and secondary hypersplenism, it is worth promoting in the context of the shortage of liver donors.

Outcomes of Transjugular Intrahepatic Portosystemic Shunt and Gastric Coronary Vein Embolization for Variceal Bleeding in Cirrhotic Portal Hypertension.

Purpose: To evaluate the efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) combined with gastric coronary vein embolization (GCVE) for cirrhotic portal hypertensive variceal bleeding and compare outcomes of first-line with second-line treatment, coil with glue, and single-covered with double stents.Methods: Fifteen patients received TIPS plus GCVE as the first-line treatment for secondary prophylaxis of variceal bleeding, and 45 received it as second-line treatment. Preoperative and postoperative quantitative variables were compared using a paired t test. The incidence of survival rate, re-bleeding, hepatic encephalopathy, and shunt dysfunction were analyzed using the Kaplan-Meier method.Results: The portal venous pressure was significantly decreased from 39.0 ± 5.0 mm Hg to 22.5 ± 4.4 mm Hg (P≤0.001) after TIPS treatment. After 1, 3, 6, 12, 18, and 24 months re-bleeding rates were 1.6%, 3.3%, 6.6%, 13.3%, 0%, and 0%, respectively. Shunt dysfunction rates were 5%, 0%, 10%, 16.6%, 1.6%, and 5%, respectively. Hepatic encephalopathy rates were 3.3%, 1.6%, 3.3%, 6.6%, 0%, and 0%, respectively. And survival rates were 100%, 100%, 100%, 96.6%, 93.3%, and 88.3% respectively. In comparative analysis, statistically significant differences were seen in re-bleeding between the first-line and second-line treatment groups (26.6% vs 24.4%, log-rank P=0.012), and survival rates between single-covered and double stent (3.7% vs 16.1%, log-rang (P=0.043).Conclusion: The results suggest that TIPS combined with GCVE is effective and safer in the treatment of cirrhotic portal hypertensive variceal bleeding. The use of TIP plus GCVE as first-line treatment, may be preferable for high-risk re-bleeding, and more than 25 mm Hg portal venous pressure with repeated variceal bleeding. However, the sample size was small. Therefore, large, randomized, controlled, multidisciplinary center studies are needed for further evaluation.

Comparison of prevention and treatment of portal vein thrombosis between proximal splenic vein ligation followed by postoperative transcatheter anticoagulant therapy and systemic anticoagulant therapy in patients with cirrhotic portal hypertension

AbstractAimsSplenectomy combined with pericardial devascularization is one of the important methods to treat hypersplenism, gastrointestinal bleeding, and other complications caused by liver cirrhosis; however, it is accompanied by a high risk of portal vein thrombosis (PVT). This study aimed to explore the preventive and therapeutic effects of proximal splenic vein ligation (PSVL) with postoperative transcatheter anticoagulant therapy (TCAT) on PVT.MethodsThis study retrospectively selected 143 patients with liver cirrhosis and portal hypertension, who received splenectomy combined with pericardial devascularization from June 30, 2018 to June 30, 2021. According to computed tomography photography, within 1 week before the operation, the patients were divided into a prevention group (without preoperative PVT, n = 112) and a treatment group (preoperative PVT, n = 31). Then, each group was subdivided based on the treatment and prevention measures into PSVL + TCAT (n = 70) and systemic anticoagulant therapy (SAT) subgroups (n = 73). The preventive and therapeutic effects of PSVL followed by TCAT on PVT were analyzed.ResultsThe operation time in the PSVL + TCAT subgroups was longer than that in the SAT subgroups (185 ± 76 min vs. 161 ± 55 min; p &lt; 0.01). There was no difference between the two subgroups in terms of operative bleeding (345 ± 82 mL vs. 336 ± 65 mL; p &gt; 0.50). There was no operative death, and all patients recovered uneventfully. In the prevention group, procedure‐related complications occurred in two patients in the PSVL + TCAT subgroup (3.7% [2/54]), including one patient with slight pancreatitis and one patient with chylous leakage, owing to mobilization of the pancreas. The PVT incidence in the prevention group was significantly different between the two subgroups at postoperative 7th day, 3rd month, and 6th month (PSVL + TCAT: 0%, 11.1%, and 5.6% vs. SAT: 39.7%, 31.0%, and 20.7%, respectively; all p &lt; 0.05). In the treatment group, the thrombus regression rate at postoperative 7th day and disappearance rates at the 3rd month and the 6th month of the PSVL + TCAT subgroup were significantly higher than those in the SAT subgroup after anticoagulant and thrombolysis therapy (PSVL + TCAT: 75.0%, 68.8%, and 87.5% vs. SAT: 20.0%, 26.7%, and 40.0%; all p &lt; 0.05).ConclusionsPSVL + TCAT reduces the risk of PVT after splenectomy and is safe and effective in treating PVT during surgery for portal hypertension.

Chinese expert consensus on the diagnosis of cirrhotic portal hypertension by ultrasound elastography (2023 version)

The population with cirrhosis in China is about 7 million, and portal hypertension is an important factor affecting the prognosis of these patients. The severity of portal hypertension determines the occurrence and development of liver related complications, such as ascites, variceal bleeding, and hepatic encephalopathy. In recent years, ultrasound elastography technology has been rapidly developed and widely applied in the field of liver diseases. Transient elastography, point shear wave elastography, and two-dimensional shear-wave elastography are all of great value for non-invasive evaluation of portal hypertension. However, there is currently no unified operating standard and reference threshold for evaluating cirrhotic portal hypertension using ultrasound elastography. Therefore, Ultrasonic Medicine Branch of the Chinese Medical Association and Chinese Portal Hypertension Alliance (CHESS) initialed and convened domestic experts from multiple disciplines, including ultrasound medicine, hepatology, gastroenterology, to form a consensus based on the latest domestic and international guidelines, medical evidence, and Chinese clinical practice. The aim is to standardize the examination process of different ultrasound elastography techniques, and standardize the application of liver stiffness and spleen stiffness in compensated advanced chronic liver disease, clinically significant portal hypertension, avoidance of endoscopic screening, risk stratification of portal hypertension, and personalized clinical management.

Correlation between hepatic venous pressure gradient and portal pressure gradient in patients with autoimmune cirrhotic portal hypertension and collateral branches of the hepatic venous.

To assess the correlation and agreement between hepatic venous pressure gradient (HVPG) and portal pressure gradient (PPG) in patients with autoimmune liver diseases (ALD) and portal hypertension (PHT), and to investigate the extent to which hepatic vein collateralization affects the accuracy of this assessment. Ninety-eight patients with ALD between 2017 and 2021 who underwent transjugular intrahepatic portosystemic shunt (TIPS) with conventional and innovative 15 ml pressurized contrast were selected to measure wedged hepatic venous pressure (WHVP) and portal venous pressure (PVP) and to calculate the HVPG and PPG. Pearson's correlation was used for correlation analysis between the two groups. Bland-Altman plots were plotted to estimate the agreement between paired pressures. The r values of PPG and HVPG in the early, middle, late, and portal venous visualization were 0.404, 0.789, 0.807, and 0.830, respectively, and the R2 values were 0.163, 0.622, 0.651, and 0.690, respectively. The P-value for the r and R2 values in the early group was 0.015, and the P-values in the remaining groups were less than 0.001. Bland-Altman plots showed that patients in the portal venous visualization group had the narrowest 95% limits of agreement (LoA). The mean value of the difference was close to the zero-scale line. In patients with ALD, the correlation between the HVPG and PPG was good, and the later the collateral development, the better the correlation. Hepatic vein collateral was an essential factor in underestimating WHVP and HVPG, and the earlier the collateral appeared, the more obvious the underestimation. This article is protected by copyright. All rights reserved.

PREDICTIVE FACTORS OF MORBIDITY ASSOCIATED WITH ESOPHAGEAL VARICEAL BLEEDING IN CHILDREN WITH PORTAL HYPERTENSION.

•Most data on the natural history of portal hypertension come from studies in adults. •The morbidity rate of upper gastrointestinal bleeding in children with portal hypertension tend to be underestimated. •This study showed the relevance of morbidity rates after variceal hemorrhage in pediatric patients, especially those with cirrhosis. •Patients with hemodynamic instability requiring blood transfusion or expansion on admission are at increased risk of complications secondary to upper gastrointestinal bleeding and should be closely monitored. Background - Most data on the natural history of portal hypertension come from studies in adults. The morbidity rate of upper gastrointestinal bleeding (UGIB) in children with portal hypertension has not been systematically characterized. Objective - To describe the morbidity and mortality of UGIB in pediatric patients with portal hypertension and identify predictive factors for the occurrence of its main complications. Methods - This retrospective study included pediatric patients with cirrhotic portal hypertension or with extrahepatic portal vein obstruction (EHPVO). Mortality and UGIB complications within a period of up to 6 weeks of the bleeding were investigated. To determine the predictive factors of morbidity, a multivariate analysis was performed using logistic regression; all results were considered significant at P<0.05. Results - A total of 86 patients (51.2% with EHPVO and 48.8% with cirrhosis) had 174 bleeding events. Ascites was the most common complication (43.1% of all cases), being more prevalent in patients with cirrhosis (P<0.001). Cirrhosis was a predictor of the occurrence of any morbidity (OR 20.3). The need for blood transfusion was predictor of at least one complication (OR 5.8), ascites (OR 7.2) and infections (OR 3.8) in the general group and at least one complication (OR 11.3) and ascites (OR 5.8) in cirrhotic patients. The need for expansion was a predictor of any morbidity (OR 4.6) and infections (OR 3.9) in the general group, in addition to being predictor of infection in cirrhotic patients (OR 5.4). There were no deaths from UGIB in the six weeks post-bleeding. Conclusion - The study showed the relevance of morbidity after UGIB in pediatric patients with portal hypertension, especially in those with cirrhosis. The patients with hemodynamic instability requiring blood transfusion or expansion on admission are at increased risk of complications related to upper gastrointestinal bleeding and should be closely monitored.