Spleen Stiffness Measurement Research Articles

Spleen Stiffness-Based Algorithms Are Superior to Baveno VI Criteria to Rule Out Varices Needing Treatment in Patients With Advanced Chronic Liver Disease.

The Baveno VI criteria have set the stage for noninvasive assessment of compensated advanced chronic liver disease (ACLD). The algorithm combining liver stiffness measurement (LSM, <20 kPa) and platelet count (>150,000/μL) safely avoids screening endoscopy for varices needing treatment (VNT) but identifies only a relatively low number of patients. We aimed to evaluate the value of spleen stiffness measurement (SSM) using spleen-dedicated elastography in ruling out VNT. In this real-life multicenter retrospective derivation-validation cohort, all consecutive patients with ACLD (defined by LSM ≥10 kPa) with available upper endoscopy, laboratory results, spleen diameter, LSM, and SSM measured with spleen-dedicated transient elastography were included. VNT were defined as medium-to-large varices or small varices with red spots. In the derivation cohort (n = 201, 11.9% VNT), SSM demonstrated excellent capability at identifying VNT (area under the receiver operating characteristic curve [AUROC] 0.88), outperforming LSM (AUROC 0.77, P = 0.03) and platelets (AUROC 0.73, P = 0.002). In comparison with Baveno VI criteria (33.8% spared endoscopies), the sequential Baveno VI plus SSM and a novel spleen size and stiffness model were able to increase the number of patients avoiding endoscopy (66.2% and 71.1%, respectively) without missing more than 5% of VNT. These findings were confirmed in an external validation cohort of patients with more advanced liver disease (n = 176, 34.7% VNT) in which the number of spared endoscopies tripled (27.3% and 31.3% for SSM-based algorithms) compared with Baveno VI criteria (8.5%). Spleen stiffness-based algorithms are superior to Baveno VI criteria in ruling out VNT in patients with ACLD and double the number of patients avoiding screening endoscopy.

Emerging role of Spleen Stiffness Measurement in prediction of clinically significant portal hypertension: a single center experience

Emerging role of Spleen Stiffness Measurement in prediction of clinically significant portal hypertension: a single center experience

Prospective 5-Year Follow-up Study of Spleen Stiffness Measurement with a Spleen-Dedicated Module (SSM@100Hz) for Predicting Hepatic Decompensation in cACLD: Competitive Risk Analysis

Prospective 5-Year Follow-up Study of Spleen Stiffness Measurement with a Spleen-Dedicated Module (SSM@100Hz) for Predicting Hepatic Decompensation in cACLD: Competitive Risk Analysis

Accuracy of a dedicated 100 Hz vibration-controlled spleen stiffness measurement for the detection of esophageal varices in naïve patients with compensated advanced chronic liver disease: interim results from a multicentric cohort

Accuracy of a dedicated 100 Hz vibration-controlled spleen stiffness measurement for the detection of esophageal varices in naïve patients with compensated advanced chronic liver disease: interim results from a multicentric cohort

Competitive Risk Analysis of Spleen Stiffness Measurement with a Spleen-Dedicated Module (SSM@100Hz) for Predicting de-novo HCC Occurrence in cACLD Patients: A Prospective 5-Year Follow-up Study

Competitive Risk Analysis of Spleen Stiffness Measurement with a Spleen-Dedicated Module (SSM@100Hz) for Predicting de-novo HCC Occurrence in cACLD Patients: A Prospective 5-Year Follow-up Study

Spleen stiffness measurement improves non-invasive prediction of clinically significant portal hypertension in primary biliary cholangitis

Spleen stiffness measurement improves non-invasive prediction of clinically significant portal hypertension in primary biliary cholangitis

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 intra-luminal 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.

Assessing the Severity of Portal Hypertension: Is Liver or Spleen Stiffness Measurement an Alternative to the Gold Standard, Hepatic Vein or Porto-Systemic Pressure Gradient?

Introduction: Liver stiffness measurement (LSM) and spleen stiffness measurement (SSM) are increased in patients with cirrhosis and portal hypertension (PH). However, increased SSM values are associated with presence of esophageal varices. Currently, the gold standard for risk stratification in patients with compensated advanced chronic liver disease (cACLD) is by measurement of portal pressure through assessment of hepatic vein or porto-systemic pressure gradient (HVPG and PSPG). However, these procedures are invasive, and either LSM or SSM may be a non-invasive alternative.&#x0D; Aim: We aimed to investigate the relationship between LSM or SSM and HVPG/PSPG and examined the diagnostic accuracy for identification of clinically significant PH (≥10 mm Hg) or severe PH (≥12 mm Hg).&#x0D; Methods: A retrospective study (IRB Protocol #19230) allowed us to identify patients who had who undergone portal pressure measurements (HVPG or PSPG). A total of 36 patients also had SSM values. Of these, 29 patients carried a hepatic cause of PH, while the remaining had pre-hepatic (n=4) and post-hepatic (n=3) etiology.&#x0D; Results: The median age was 58 years (range: 25-71) with 52% male and 83% with cirrhosis. The median LSM and SSM were 35.7 kPa (range:7.4-75.0, normal ≤7.0 kPa) and 43.8 kPa (range: 20.7-100, normal ≤ 21.0 kPa). Both LSM (r = 0.42, P-value = 0.02) and SSM (r = 0.45, P-value: 0.01) correlated significantly with HVPG/PSPG. The diagnostic accuracy for both LSM and SSM for clinically significant PH was good for LSM (AUROC 0.76, 95% CI:0.58-0.94) and excellent for SSM (AUROC: 0.81, 95% CI:0.65-0.98). The diagnostic accuracy of LSM and SSM was lower for severe PH [AUROC 0.71 (P-value = 0.06) and 0.67 (P-value = 0.1) for LSM and SSM, respectively].&#x0D; Conclusion: Both LSM and SSM correlate with portal pressure measurements and provide diagnostic accuracy to identify patients with clinically significant, but not severe, PH.

Evaluation of Noninvasive Tools for Predicting Esophageal Varices in Patients With Cirrhosis at Tygerberg Hospital, Cape Town.

Background: In patients with cirrhosis, esophageal variceal hemorrhage (EVH) is a devastating consequence of portal hypertension (PH). Upper endoscopy is considered the gold standard for the detection and diagnosis of esophageal varices (EVs), despite being invasive and costly. This study was aimed at identifying and evaluating the diagnostic accuracy of noninvasive tools in predicting EVs in patients with compensated cirrhosis. Methods: This cross-sectional study included 50 patients with compensated cirrhosis at the Tygerberg Hospital Gastroenterology Clinic in Cape Town between November 2022 and May 2023. We collected clinical, anthropometric, and laboratory data from patients' physical and electronic charts. All patients underwent an abdominal ultrasound, vibration-controlled transient elastography (VCTE) to assess liver and splenic stiffness, and upper endoscopy. In this comparative study, we evaluated the diagnostic accuracy of different noninvasive tools in detecting EVs in patients with compensated cirrhosis. Results: Of the 50 patients included in the study, 30 (60%) were female and 20 (40%) were male. The patients' age ranged from 18 to 83, with a mean age of 46.6 years. Cirrhosis was mainly due to alcohol use (n = 11, 22%), hepatitis B virus (HBV) infection (n = 11, 22%), and autoimmune hepatitis (n = 10, 20%). The patients included in the study were divided into two subgroups: with (n = 34, 68%) or without (n = 16, 32%) EVs. Statistically significant differences were detected between groups in platelet count (PC), liver stiffness measurement (LSM), spleen stiffness measurement (SSM), portal vein diameter (PVD), bipolar spleen diameter (SBD), aspartate aminotransferase-to-platelet ratio index (APRI), fibrosis-4 index (FIB-4), platelet/bipolar spleen diameter ratio (PSR), liver stiffness-spleen size-platelet ratio (LSPS), liver stiffness-spleen stiffness-platelet ratio score (LS3PS), and spleen stiffness-spleen size-platelet ratio score (SSPS) (p < 0.001). The highest diagnostic precision was observed with SSM (96%), SSPS (96%), LS3PS (94%), LSPS (94%), PSR (94%), and PC (92%). SBD (88%), LSM (86%), APRI (82%), and FIB-4 (82%) had the lowest diagnostic accuracy. Conclusion: SSM and SSPS have the highest diagnostic accuracy for predicting the presence of EVs in patients with compensated cirrhosis. LSPS, LS3PS, and PSR come second at 94%. We recommend SSM and SSPS in institutions with transient elastography equipped with the software necessary to measure splenic stiffness. We introduce and propose LS3PS as a novel composite score for predicting the presence of EVs in patients with compensated cirrhosis. Large-sample-size studies are needed to validate these prediction scores and to allow direct comparison with Baveno VII. These prediction tools can help clinicians avoid unnecessary endoscopic procedures in patients with compensated cirrhosis, especially in developing countries with limited resources such as South Africa.

Spleen-dedicated stiffness measurement performed well to rule out high-risk varices in HBV-related hepatocellular carcinoma: Screening for high-risk varices in HCC.

Esophagogastroduodenoscopy (EGD) is required to screen for high-risk varices (HRV) in patients with hepatocellular carcinoma (HCC), especially since overall survival rates have dramatically improved with new systemic therapies. To assess the Baveno VI and Baveno VII algorithms' ability to rule out HRV in hepatitis B virus (HBV)-related HCC METHODS: We prospectively enrolled consecutive patients with HBV related, compensated cirrhosis and newly diagnosed HCC who underwent liver stiffness measurement, spleen stiffness measurement (SSM) using a 100-Hz shear wave frequency, and EGD. From September 2021 to August 2023, we enrolled 219 patients with HCC, with 107 (48.9%) Barcelona Clinic Liver Cancer (BCLC) A, 28 (12.8%) BCLC B and 84 (38.3%) BCLC C, respectively. HRV prevalence was 28.8% (63/219). Baveno VI criteria safely (HRV missing rate, 3.2%) avoided 27.4% unnecessary EGDs, while the Baveno VII algorithm avoided 49.3% with HRV missing rate at 7.9% (5/63). The SSM ≤40 kPa avoided 47.5% of EGDs safely (HRV missing rate, 4.8%), significantly better than the Baveno VI criteria (p < 0.001) and comparable to the Baveno VII algorithm (p = 0.390). The SSM ≤40 kPa safely avoided EGDs in patient subgroups within Milan criteria, with portal vein tumour thrombosis or BCLC B/C or candidates for systemic therapy. We validated that the SSM ≤40 kPa using a 100-Hz probe could safely eliminate more unnecessary EGDs than the Baveno VI criteria in patients with HBV-related HCC. However, the efficacy of the Baveno VII algorithm in patients with HCC requires further investigation.

Variability of transient elastography-based spleen stiffness performed at 100 Hz

BackgroundSpleen stiffness measurement (SSM) performed by transient elastography at 100 Hz is a novel technology for the evaluation of portal hypertension in advanced chronic liver disease, but technical aspects are lacking. We aimed to evaluate the intraexamination variability of SSM and to determine the best transient elastography protocol for obtaining robust measurements to be used in clinical practice.MethodsWe analyzed 253 SSM exams with up to 20 scans for each examination, performed between April 2021 and June 2022. All SSM results were evaluated according to different protocols by dividing data into groups of n measurements (from 2 to 19). Considering as reference the median SSM values across all the 20 measurements, we calculated the distribution of the absolute deviations of each protocol from the reference median. This analysis was repeated 1,000 times by resampling the data. Distributions were also stratified by etiology (chronic liver disease versus clinically significant portal hypertension) and different SSM ranges: < 25 kPa, 25–75, and > 75 kPa.ResultsOverall, we observed that the spleen stiffness exam had less variability if it exceeded 12 measurements, i.e., absolute deviations ≤ 5 kPa at 95% confidence. For exams with higher SSM values (> 75 kPa), as seen in clinically significant portal hypertension, at least 15 measurements are highly recommendable.ConclusionsFifteen scans per examination should be considered for each SSM exam performed at 100 Hz to achieve a low intraexamination variability within a reasonable time in clinical practice.Relevance statementPerforming at least 15 scans per examination is recommended for 100 Hz SSM in order to achieve a low intraexamination variability, in particular for values > 75 kPa compatible with clinically significant portal hypertension.Key points• Spleen stiffness measurement by transient elastography is used for stratification in patients with portal hypertension.• At 100 Hz, this method may have intraexamination variability.• A minimum of 15 scans per examination achieves a low intraexamination variability.Graphical

Evaluation of liver and spleen stiffness measurement with shear wave elastography in brucellosis.

Human brucellosis, which is endemic in the eastern region of Turkey, infects the reticulo-endothelial system. Acute brucellosis may cause hepatomegaly or splenomegaly. The main purpose of this study was to investigate the effectiveness of the point shear wave elastography (pSWE) method in identifying and detecting liver and spleen stiffness in acute brucellosis. This case-control study included 40 patients with acute brusellosis and 60 healthy individuals as a control group. The demographic data, abdominal ultrasonography (USG) and pSWE results of the patient and control groups were evaluated. Statistical and ROC analyses were performed. The liver pSWE value was 3.8395 ± 1.171kPa in the patient group and 1.6619 ± 0.495kPa in the control group. The spleen pSWE value was 3.2431 ± 1.803kPa in the patient group and 1.3793 ± 0.622kPa in the control group. The mean liver and spleen pSWE values were statistically significantly higher in the patient group than in the control group (p < 0.001). Cut-off values were determined as 2.524 for the liver pSWE and 1.62667 for the spleen pSWE. From the AUC values (0.959, 0.903), the diagnostic performance of liver and spleen pSWE values were seen to be excellent in distinguishing between patient and control groups. The study results showed that liver and spleen stiffness were high in acute brucellosis patients and had predictive significance above certain cut-off values. It can be considered that pSWE, which evaluates liver and spleen stiffness in acute brucellosis, may provide diagnostic benefit as a reliable, non-invasive technique.

Performance of Spleen Stiffness, Liver Stifness, and their Combination for Predicting Esophageal among Patient with HBV-Related Cirrhosis

Background: Liver cirrhosis in Indonesia still become a burden disease, and the etiology is mostly from the hepatitis B virus. Esophageal varices (EV) is the most common complication of portal hypertension in liver cirrhosis. Due to many reasons, esophagogastroduodenoscopy is still not fully suitable for routine surveillance in daily practice. Hence, studies that work in the search for the best non-invasive test are still important for predicting EV.Method: A total of 71 patients with liver cirrhosis due to hepatitis B who had undergone endoscopy, spleen stiffness measurement (SSM), and liver stiffness measurement (LSM), between January–April 2023 were enrolled. Diagnostic applicability was assessed by the area under the receiver-operator curve (AUC) to measure and compare the performance of each measurement and combination for predicting EV and to obtain the corresponding optimal prediction value.Results: This study was participated by 71 subjects with liver cirrhosis. The prevalence of Child-Pugh A was 74.6% (53 patients), Child-Pugh B 22.5% (16 patients), and 2.8% (2 patients) with Child-Pugh C. Among these patients, the proportion of EV was 71.8%. This study showed that SSM with a cut-off of 38.8 kPa had AUC 0.867 (95% CI: 0.774–0.960) (sensitivity 78.4%, specificity 80%) and LSM with a cut-off of 10.55 kPa had AUC 0.822 (95% CI: 0.701–0.943) (sensitivity 88.2%, specificity 65%).Conclusion: Spleen stiffness and liver stiffness measurements have a good performance for predicting EV in patients with liver cirrhosis caused by hepatitis B.

A surveillance for advanced liver disease and characterization of hyperechogenic lesions after Fontan surgery in a prospective cohort of cases with congenital univentricular heart

Abstract Background The congenital univentricular heart (UH) is a rare disease corrected with the palliative Fontan’s intervention, that restores the survival of most child and young patients up to adultwood. Unlikely, these patients develop a series of complications, among all, the Fontan associated liver disease (FALD), that causes the occurrence of liver cirrhosis and hepatocellular carcinoma (HCC), that negatively impacts the life expectancy in the majority of cases. Purpose Our primary aim was to identify the presence of severe FALD in our patients by liver fibrosis and portal hypertension scores (FORNS, liver and spleen-platelet score or LSPS and SSPS), and by liver (LS) and spleen (SS) stiffness measurement in relation to time since Fontan, and secondarly to characterize all the abdominal-US hyperechogenic lesions (US-HL) according to the LI-RADS (LR) CT/MRI categories. Method One-hundred-46 outpatients (83 m/63 f, aged 25,2±11.0 yrs) born with UH corrected with Fontan circuit have been recruited prospectively from 2019 to 2023 (FUmean 24.5±15.1 mos). Each patient underwent a complete clinical history and instrumental examination, by imaging obtained with US, CT and MRI, a specific lab-test profile, and the LS and SS evaluation by transient elastography (VCTE, Fibroscan). ROC curves were built to select the scores cut-off proved to be the most accurate to diagnose and grade FALD. Based on the presence of US-HL found in 43 cases (29,5%), we grouped: 23 cases with LR-1 or 2 (benign), 15 with LR-3 (suspect) and 5 with LR-4 or 5 (malign). Results Features for definition of failing-Fontan appeared in 17.5%, 47.5% and 80% of cases with &amp;lt;15; 15-25 or &amp;gt;25yrs since Fontan surgery, respectively (p&amp;lt;0.01). All the scores used (FORNS with cut-off ≥4, LSPS ≥1.4, SSPS ≥2.3, LS ≥20.2 and SS ≥30.7) showed high sensitivity and specificity, improving FALD diagnostic accuracy and staging (all p&amp;lt;0.001). Moreover by identification of selective criteria related to advanced liver disease and portal hypertension, we applied a novel risk-score for failing-Fontan, that predicted a low-moderate risk profile (HR 0.30;CI 0.18-0.52) in 72 patients and a high risk profile (HR 3,29,CI 1.93-5.60) in 74 (51%). During FU, 13 patients (8.9%) died, 5 received OHT (3.4%) and 5 had HCC occurrence (3.4%). Finally, cases with US-HL stratified by classes LR-3-4-5 (20 cases, 46.5%) appeared significantly associated with a more advanced FALD (16/4, 75% vs. 68/58, 46%; p=0,004) and a longer time since Fontan (26.3±9.4 vs. 19.8±10.8; p=0,025). Conclusion The novel risk score proposed may help to predict the development of cirrhosis in high risk patients and focussed on the need for surveillance by imaging methods to characterized the US-HL, that appeared at risk of malignity (nodule size &amp;gt;20mm and/or presence of wash-out into portal-hepatocellular phase or into LR ≥3 classes).

Relationship Between Spleen Pathologic Changes and Spleen Stiffness in Portal Hypertension Rat Model

The aim of the study described here was to explore the influence of splenic pathology and hemodynamic parameters on spleen stiffness in portal hypertension (PH). A Sprague‒Dawley rat model of PH (n=34) induced by CCl4 was established, and 9 normal rats were used as controls. All animals underwent a routine ultrasound examination, spleen stiffness measurement (SSM), liver stiffness measurement (LSM), portal vein pressure (PVP) measurement and histopathologic assessment. The diagnostic performance of SSM and LSM in PH was evaluated. SSMs were compared among the groups at different pathologic and hemodynamic levels. Multiple linear regression was used to analyze the factors affecting SSM. SSM had excellent diagnostic efficacy for PH (area under the receiver operating characteristic curve [AUC]=0.900) and was superior to LSM (AUC=0.794). In a rat model of PH, pathologic changes such as splenic sinus widening, thickening of the splenic capsule and an increase in collagen fibers were observed in the spleen. There were significant differences in SSM at different splenic capsule thicknesses and splenic sinus widths (all p values <0.05), but there were no significant differences in the SSM at different levels of the splenic collagen fiber area and red pulp area (all p values >0.05). In addition, there were significant differences in SSM at different levels of portal vein diameter, blood flow and congestion index (all p values <0.05). Multiple linear regression analysis revealed that PVP, portal vein congestion index and splenic capsule thickness were significantly associated with SSM. SSM is a good non-invasive way to assess PH. PVP, splenic capsule thickness and portal vein congestion index are responsible for spleen stiffness but not the proliferation of splenic fibrous tissue.

Spleen stiffness measurement predicts decompensation and rules out high-risk oesophageal varices in primary biliary cholangitis

Primary biliary cholangitis (PBC) may lead to portal hypertension (PH). Spleen stiffness measurement (SSM) by vibration-controlled transient elastography accurately predicts PH. We aimed to assess SSM role in stratifying the risk of liver decompensation in PBC. In this monocentric, prospective, cross-sectional study, we included 114 patients with PBC who underwent liver stiffness measurement (LSM) and SSM. In total, 78 and 33 patients underwent two and three sequential vibration-controlled transient elastography examinations, respectively (longitudinal study). Screening for high-risk oesophageal varices by oesophagogastroduodenoscopy was performed according to guidelines and proposed to all patients with SSM >40kPa. Among the 114 patients, 20 (17%) had LSM ≥10kPa, whereas 17 (15%) had SSM >40kPa. None of the patients with SSM ≤40kPa had high-risk oesophageal varices, compared with three of 14 patients with SSM >40kPa (21%; three refused endoscopy); any-size oesophageal varices were found in nine of 14 patients (64%). During a median follow-up of 15 months (IQR 10-31 months), five (4%) patients developed liver decompensation. The probability of liver decompensation was significantly higher among patients with both LSM ≥10kPa and SSM >40kPa: 41% at 24 months vs. 0% in other patient groups (i.e. LSM <10kPa and SSM ≤40kPa, or LSM ≥10kPa and SSM ≤40kPa, or LSM <10kPa and SSM >40kPa) (p <0.0001). Among the 78 patients undergoing longitudinal evaluation, four of nine patients (44%) with SSM increase during follow-up experienced liver decompensation, whereas none of those with stable LSM and SSM had liver decompensation. Both LSM and SSM predict liver decompensation in patients with PBC. SSM ≤40kPa rules out high-risk oesophageal varices and might be used in combination with LSM to improve the prediction of PH-related complications. Spleen stiffness measurement by vibration-controlled transient elastography accurately predicts portal hypertension in patients with chronic viral hepatitis. The present study is the first to demonstrate that in primary biliary cholangitis the combination of liver stiffness and spleen stiffness measurement can significantly improve risk stratification by predicting liver decompensation. Moreover, when spleen stiffness is combined with liver stiffness measurement and platelet count, it aids in identifying individuals with a low probability of having high-risk oesophageal varices, thereby allowing the avoidance of unnecessary endoscopy examinations. Further validation of our results in larger cohorts of patients with primary biliary cholangitis is needed to implement spleen stiffness measurement in clinical practice.

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.

Spleen Thickness Plus Platelets Can Effectively and Safely Screen for High-Risk Varices in Cirrhosis Patients.

Currently, most primary hospitals cannot routinely perform liver stiffness measurements (LSMs) and spleen stiffness measurements (SSMs), which are recommended by guidelines to exclude high-risk varices (HRVs). We tried to find more convenient indicators for HRV screening. We enrolled 213 cirrhosis patients as the training cohort (TC) and 65 primary biliary cirrhosis patients as the validation cohort (VC). We included indicators such as SSM by two-dimensional shear wave elastography, LSM by transient elastography, and other imaging and laboratory tests. Variable analysis revealed SSM, platelets (PLT), and spleen thickness (ST) as independent risk indicators for HRV. In TC, ST+PLT (ST < 42.2 mm and PLT > 113.5 × 109/L) could avoid 35.7% of the esophagogastroduodenoscopies (EGDs), with a 2.4% missed HRV rate. Although the proportion of EGDs spared by ST+PLT was less than SSM+PLT (SSM < 29.89 kPa + PLT > 113.5 × 109/L) (35.7% vs. 44.1%), it was higher than that of the Baveno VI criteria (B6) (35.7% vs. 28.2%). We did not validate SSM+PLT in VC considering our aims. ST+PLT safely spared 24.6% of EGDs in VC, identical to B6. Conclusions: The ability of ST+PLT to exclude HRVs was superior to B6 but slightly inferior to SSM+PLT. When SSM cannot be routinely performed, ST+PLT provides an extra option for patients to exclude HRVs as a more convenient model.

The non-invasive evaluation of liver involvement in patients with cystic fibrosis: A prospective study.

Porto-sinusoidal vascular disease (PSVD) has been described as the prominent pathology in liver explants of patients with cystic fibrosis (CF), but data outside the transplant setting are lacking. We aimed to investigate the prevalence of portal hypertension (PH) in CF-associated liver disease (CFLD) and develop an algorithm to classify liver involvement in CF patients. This is a cross-sectional study of consecutive paediatric and adult patients in a tertiary centre between 2018 and 2019, who underwent ultrasound, liver (LSM) and spleen stiffness (SSM) measurement. CFLD was defined according to physical examination, liver tests and ultrasound findings. PSVD was likely if there were PH signs in the absence of advanced chronic liver disease (CF-ACLD, LSM <10 kPa). A historical cohort was used to validate the prognostic significance of the new definitions. Fifty (27.5%) patients met CFLD criteria. At least one sign of PH was found in 47 (26%) patients, but most (81%) had LSM <10 kPa and were likely to have PSVD; only 9 (5%) had CF-ACLD. PSVD and CFLD (LSM <10 kPa) co-existed in most (23/36) cases. In the historical cohort (n = 599 patients), likely PSVD and CFLD+PH were independently associated with a 2-fold and 3.5-fold increase in mortality compared to patients without PH, respectively. In 34 patients with SSM, values <21 and >50 kPa accurately diagnosed specific signs of PH. PSVD is the prevailing cause of PH in CF patients. We developed a new diagnostic algorithm based on clinical and elastosonography criteria to classify liver involvement in patients with CF.

Predictive value of liver and spleen stiffness measurement based on two-dimensional shear wave elastography for the portal vein pressure in patients with compensatory viral cirrhosis.

This study aimed to explore the predictive value of liver and spleen stiffness measurement based on two-dimensional shear wave elastography for the portal vein pressure in patients with compensatory viral cirrhosis. From January 2017 to August 2019, 107 patients with compensatory viral cirrhosis and 76 patients with viral hepatitis were enrolled as cirrhosis group and hepatitis group, respectively. Patient data were obtained during admission, and this study was a review and analysis of patient data. Liver stiffness measurement (LSM), spleen stiffness measurement (SSM), portal vein diameter and spleen thickness were compared between the two groups, and their diagnostic value for compensatory viral cirrhosis was analyzed. According to the hepatic vein pressure, the cirrhosis group patients were divided into non-hypertensive group (no portal hypertension, hepatic venous pressure gradient (HVPG) < 5 mmHg), mild group (mild portal hypertension, 5 mmHg ≤ HVPG ≤ 10 mmHg) and severe group (clinically significant portal hypertension group, HVPG > 10 mmHg). LSM, SSM, portal vein diameter and spleen thickness of the three groups were compared, and the correlation between SSM and hepatic vein pressure was analyzed. LSM, SSM, portal vein diameter and spleen thickness in the cirrhosis group were higher than those in hepatitis group (all P<0.05). The area under the curve (AUC) of combined detection was larger than that of LSM, SSM and spleen thickness detection alone in liver cirrhosis diagnosis (all P<0.05). LSM, SSM, portal vein diameter and spleen thickness increased with the increase of hepatic vein pressure in patients with liver cirrhosis (all P<0.05). LSM, SSM, portal vein diameter and spleen thickness were all positively correlated with hepatic vein pressure (P<0.05). ROC curve showed that AUC of combined detection was greater than that of LSM, SSM, portal vein diameter and spleen thickness alone detection in the diagnosis of clinically significant portal hypertension (all P<0.05). The increase of LSM, SSM, portal vein diameter and spleen thickness were the influencing factors for hepatic vein pressure rising (all P<0.05). There was an increase of LSM and SSM in patients with compensatory viral cirrhosis, which were positively correlated with hepatic venous pressure, and combined index detection has diagnostic and predictive value for the change of portal venous pressure.