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LINKED CONTENT: This article is linked to Hassanein et al papers. To view these articles, visit https://doi.org/10.1111/apt.18054 and https://doi.org/10.1111/apt.18128. [ABSTRACT FROM AUTHOR]

Background & Aims: Liver stiffness measured with 2‐dimensional shear wave elastography by Supersonic Imagine (2DSWE‐SSI) is well‐established for fibrosis diagnostics, but non‐conclusive for portal hypertension. Methods: We performed an individual patient data meta‐analysis of 2DSWE‐SSI to identify clinically significant portal hypertension (CSPH), severe portal hypertension and large varices in cirrhosis patients, using hepatic venous pressure gradient and upper endoscopy as reference. We used meta‐analytical integration of diagnostic accuracies with optimized rule‐out (sensitivity‐90%) and rule‐in (specificity‐90%) cut‐offs. Results: Five studies from seven centres shared data on 519 patients. After exclusion, we included 328 patients. Eighty‐nine (27%) were compensated and 286 (87%) had CSPH. 2DSWE‐SSI < 14 kPa ruled out CSPH with a summary AUROC (sROC), sensitivity and specificity of 0.88, 91% and 37%, and correctly classified 85% of patients, with minimal between‐study heterogeneity. The false negative rate was 60%, of which decompensated patients accounted for 78%. 2DSWE‐SSI ≥ 32 kPa ruled in CSPH with sROC, sensitivity, specificity and correct classifications of 0.83, 47%, 89% and 55%. In a subgroup analysis, the 14 kPa cut‐off showed consistent sensitivity and higher specificity for patients with compensated cirrhosis, without ascites, viral aetiology or BMI < 25 kg/m2. 2DSWE‐SSI ruled out severe portal hypertension and large varices with fewer correctly classified and lower sROC, and with minimal benefit for ruling in. Conclusion: Liver stiffness using 2‐dimensional shear wave elastography below 14 kPa may be used to rule out clinically significant portal hypertension in cirrhosis patients, but this would need validation in populations of compensated liver disease. 2DSWE‐SSI cannot predict varices needing treatment. [ABSTRACT FROM AUTHOR]

Background & Aims: Several non‐invasive tests (NITs) have been developed to diagnose oesophageal varices (EV), including the recent Baveno VI criteria to rule out high‐risk varices (HRV). Spleen stiffness measurement (SSM) with the standard FibroScan® (SSM@50Hz) has been evaluated. However, the EV grading could be underestimated because of a ceiling threshold (75 kPa) of the SSM@50Hz. The aims were to evaluate SSM by a novel spleen‐dedicated FibroScan® (SSM@100Hz) for EV diagnosis compared with SSM@50Hz, other validated NITs and Baveno VI criteria. Methods: This prospective multicentre study consecutively enrolled patients with chronic liver disease; blood data, endoscopy, liver stiffness measurement (LSM), SSM@50Hz and SSM@100Hz were collected. Results: Two hundred and sixty patients met inclusion criteria. SSM@100Hz success rate was significantly higher than that of SSM@50Hz (92.5% vs 76.0%, P <.001). SSM@100Hz accuracy for the presence of EV (AUC = 0.728) and HRV (AUC = 0.756) was higher than in other NITs. SSM@100Hz AUC for large EV (0.782) was higher than SSM@50Hz (0.720, P =.027). AUC for HRV with SSM@100Hz (0.780) was higher than with LSM (0.615, P <.001). The spared endoscopy rate of Baveno VI criteria (8.1%) was significantly increased by the combination to SSM@50Hz (26.5%) or SSM@100Hz (38.9%, P <.001 vs others). The missed HRV rate was, respectively, 0% and 4.7% for combinations. Conclusions: SSM@100Hz is a new performant non‐invasive marker for EV and HRV providing a higher accuracy than SSM@50Hz and other NITs. The combination of Baveno VI criteria and SSM@100Hz significantly increased the spared endoscopy rate compared to Baveno VI criteria alone or combined with SSM@50Hz. Clinical trial number: NCT02180113. [ABSTRACT FROM AUTHOR]

Portal hypertension is the strongest predictor of hepatic decompensation and death in patients with cirrhosis. However, its discriminatory accuracy in patients with nonalcoholic fatty liver disease (NAFLD) has been challenged because hepatic vein catheterization may not reflect the real portal vein pressure as accurately as in patients with other etiologies. We aimed to evaluate the relationship between hepatic venous pressure gradient (HVPG) and presence of portal hypertension–related decompensation in patients with advanced NAFLD (aNAFLD). Multicenter cross-sectional study included 548 patients with aNAFLD and 444 with advanced RNA-positive hepatitis C (aHCV) who had detailed portal hypertension evaluation (HVPG measurement, gastroscopy, and abdominal imaging). We examined the relationship between etiology, HVPG, and decompensation by logistic regression models. We also compared the proportions of compensated/decompensated patients at different HVPG levels. Both cohorts, aNAFLD and aHVC, had similar baseline age, gender, Child-Pugh score, and Model for End-Stage Liver Disease score. Median HVPG was lower in the aNAFLD cohort (13 vs 15 mmHg) despite similar liver function and higher rates of decompensation in aNAFLD group (32% vs 25%; P =.019) than in the aHCV group. For any of the HVPG cutoff analyzed (<10, 10–12, or 12 mmHg) the prevalence of decompensation was higher in the aNAFLD group than in the aHCV group. Patients with aNAFLD have higher prevalence of portal hypertension–related decompensation at any value of HVPG as compared with aHCV patients. Longitudinal studies aiming to identify HVPG thresholds able to predict decompensation and long-term outcomes in aNAFLD population are strongly needed. [ABSTRACT FROM AUTHOR]

Background & Aims Liver stiffness ( LS), spleen stiffness ( SS) and serum markers have been proposed to non-invasively assess portal hypertension or oesophageal varices ( EV) in cirrhotic patients. We aimed to evaluate the performance of a stepwise algorithm that combines Lok score with LS and SS for diagnosing high-risk EV ( HREV) and to compare it with other already-validated non-invasive methods. Methods We performed a cross-sectional study including 136 consecutive compensated cirrhotic patients with various aetiologies, divided into training (90) and validation (46) set. Endoscopy was performed within 6 months from inclusion for EV screening. Spleen diameter was assessed by ultrasonography. LS and SS were measured using Fibroscan. Lok score, platelet count/spleen diameter ratio, LSM-spleen diameter to platelet ratio score and oesophageal varices risk score ( EVRS) were calculated and their diagnostic accuracy for HREV was assessed. The algorithm classified patients as having/not-having HREV. Its performance was tested and compared in both groups. Results In the training set, all variables could select patients with HREV with moderate accuracy, the best being LSPS ( AUROC = 0.818; 0.93 sensitivity; 0.63 specificity). EVRS, however, was the only independent predictor of HREV ( OR = 1.521; P = 0.032). The algorithm correctly classified 69 (76.66%) patients in the training set ( P < 0.0001) and 36 (78.26%) in the validation one. In the validation group, the algorithm performed slightly better than LSPS and EVRS, showing 100% sensitivity and negative predicted value. Conclusion The stepwise algorithm combining Lok score, LS and SS could be used to select patients at low risk of having HREV and who may benefit from more distanced endoscopic evaluation. [ABSTRACT FROM AUTHOR]

Based on platelets and liver stiffness measurements, the Baveno VI criteria (B6C), the expanded B6C (EB6C), and the ANTICIPATE score can be used to rule out varices needing treatment (VNT) in patients with compensated chronic liver disease. We aimed to improve these tests by including data on the ratio of platelets to liver stiffness. In a retrospective analysis of data from 10 study populations, collected from 2004 through 2018, we randomly assigned data from 2368 patients with chronic liver disease of different etiologies to a derivation population (n = 1579; 15.1% with VNT, 50.2% with viral hepatitis, 28.9% with nonalcoholic fatty liver disease, 20.8% with alcohol-associated liver disease, with model for end-stage liver disease scores of 9.5 ± 3.0, and 93.0% with liver stiffness measurements ≥10 kPa) or a validation population (n = 789). Test results were compared with results from a sequential algorithm (VariScreen). VariScreen incorporated data on platelets or liver stiffness measurements and then the ratio of platelets to liver stiffness measurement, adjusted for etiology, patient sex, and international normalized ratio. In the derivation population, endoscopies were spared for 23.9% of patients using the B6C (VNT missed in 2.9%), 24.3% of patients using the ANTICIPATE score (VNT missed in 4.6%), 34.5% of patients using VariScreen (VNT missed in 2.9%), and 41.9% of patients using the EB6C (VNT missed in 10.9%). Differences in spared endoscopy rates were significant (P ≤.001), except for B6C vs ANTICIPATE and in missed VNT only for EB6C vs the others (P ≤.009). VariScreen was the only safe test regardless of sex or etiology (missed VNT ≤5%). Moreover, VariScreen secured screening without missed VNT in patients with model for end-stage liver disease scores higher than 10. This overall strategy performed better than a selective strategy restricted to patients with compensated liver disease. Test performance and safety did not differ significantly among populations. In a retrospective study of data from 2368 patients with chronic liver disease, we found that the B6C are safe whereas the EB6C are unsafe, based on missed VNT. The VariScreen algorithm performed well in patients with chronic liver disease of any etiology or severity. It is the only test that safely rules out VNT and can be used in clinical practice. [Display omitted] [ABSTRACT FROM AUTHOR]

INTRODUCTION: We aimed to explore the prevalence of portal hypertension in the most common etiologies of patients with compensated advanced chronic liver disease (cACLD) and develop classification rules, based on liver stiffness measurement (LSM), that could be readily used to diagnose or exclude clinically significant portal hypertension (CSPH) in clinical practice. METHODS: This is an international cohort study including patients with paired LSM/hepatic venous pressure gradient (HVPG), LSM ≥10 kPa, and no previous decompensation. Portal hypertension was defined by an HVPG >5 mm Hg. A positive predictive value ≥90% was considered to validate LSM cutoffs for CSPH (HVPG ≥10 mm Hg), whereas a negative predictive value ≥90% ruled out CSPH. RESULTS: A total of 836 patients with hepatitis C (n = 358), nonalcoholic steatohepatitis (NASH, n = 248), alcohol use (n = 203), and hepatitis B (n = 27) were evaluated. Portal hypertension prevalence was >90% in all cACLD etiologies, except for patients with NASH (60.9%), being even lower in obese patients with NASH (53.3%); these lower prevalences of portal hypertension in patients with NASH were maintained across different strata of LSM values. LSM ≥25 kPa was the best cutoff to rule in CSPH in alcoholic liver disease, chronic hepatitis B, chronic hepatitis C, and nonobese patients with NASH, whereas in obese NASH patients, the positive predictive value was only 62.8%. A new model for patients with NASH (ANTICIPATE-NASH model) to predict CSPH considering body mass index, LSM, and platelet count was developed, and a nomogram was constructed. LSM ≤15 kPa plus platelets ≥150 x 109/L ruled out CSPH in most etiologies. DISCUSSION: Patients with cACLD of NASH etiology, especially obese patients with NASH, present lower prevalences of portal hypertension compared with other cACLD etiologies. LSM ≥25 kPa is sufficient to rule in CSPH in most etiologies, including nonobese patients with NASH, but not in obese patients with NASH. [ABSTRACT FROM AUTHOR]

Esophageal varices (EVs) are among the most severe complications of cirrhosis, with a prevalence of 50% to 60% among cirrhotic patients. International guidelines therefore recommend that cirrhotic patients should be screened for the presence of EVs. The main objective of this study was to introduce a new spleen-dedicated FibroScan (Echosens, Paris, France) examination and to assess its performance in detecting large EVs (grade 2 and 3). This novel examination has been validated in simulation and phantom studies and has been used in a population of patients with chronic liver disease. The study described here suggests that the novel spleen-dedicated FibroScan examination performs better than the standard FibroScan for the detection of large EVs (area under the curve = 0.70 for the standard examination and 0.79 [p <0.01] for the spleen examination), but further clinical studies are needed to investigate the role of spleen stiffness in the management of cirrhotic patients. [ABSTRACT FROM AUTHOR]

Liver cirrhosis is a diffuse chronic liver disease affecting the entire liver. The fibrosis accumulation and distribution in the liver are known to be heterogeneous. „Localized" or „focal" cirrhosis is only anecdotically reported. Acute hepatitis E virus (HEV) infection is uncommon in western countries, especially in temperate climate areas and is very often missed or underdiagnosed. However, it may be responsible of up to 15% of acute-on-chronic liver failure cases. We present the case of a 35-year-old patient with a very uncommon association of Budd-Chiari syndrome secondary to hepatocellular carcinoma (HCC) developed on a noncirrhotic right liver lobe and secondary biliary cirrhosis of the left liver lobe, that further complicated with acute HEV infection leading to acute-on-chronic liver failure and death. [ABSTRACT FROM AUTHOR]

Multiple biliary hamartomas, also known as von Mayenburg complexes (VMC), are rare, benign malformations of the intrahepatic bile ducts. VMC are frequently incidental imaging findings and may mimic multifocal liver lesions, including metastases. The present case report is aimed to illustrate the distictive imaging and histopatological features of VMC. A 44-year-old male patient with no significant past medical history was admitted to our tertiary referral hospital for unintentional weight loss and fatigability. Laboratory workup evidenced no significant abnormalities and preserved liver function. Autoimmune and viral ethiologies of liver damage were excluded. Abdominal ultrasound revealed multiple hyperechoic liver lesions up to 5 mm each, scattered throughout the prenchyma with no signs of portal hypertension. Liver stiffness measured by 2D-share wave elastography was 5.2 kPa. Contrast-enhanced ultrasonography showed homogenous hepatic enhancement with no wash-out. Magnetic resonance cholangiopancreatography revealed disseminated subcentimetric cystic liver lesions without communication to the normal biliary tree. Percutaneous liver biopsy was performed and histological findings revealed irregular and disorganized dilated bile ducts with single layer cubic epithelium without cytological atypia, sorrounded by collagenous stroma, highly suggestive for the diagnosis of VMC. Here we reported the case of a patient with rare biliary hamartomas, highlighting the role of key imaging aspects combined with histological findings in establishing the diagnosis. biliary hamartoma, von Meyenburg complexes, percutaneous liver biopsy. [ABSTRACT FROM AUTHOR]

Background: The role of ultrasound (US) surveillance for transjugular intrahepatic portosystemic shunt (TIPS) dysfunction has long been a matter of debate, and clear-cut criteria have yet to be conventionally defined. To evaluate the role of US parameters in detecting hemodynamic TIPS dysfunction in the absence of clinical signs of decompensation. We included all the patients treated with TIPS for portal hypertension-related complications who had a scheduled TIPS revision within the first six weeks after the procedure, irrespective of the clinical and US variables. Clinical TIPS dysfunction (CD) was defined as the recurrence of variceal bleeding or inadequate control of ascites. Hemodynamic TIPS dysfunction (HD) was defined by a PPG exceeding ten mmHg at the first revision. Thus, we have comparatively analyzed the US parameters of 86 patients at TIPS placement and first TIPS revision. Recurrent variceal bleeding was the main indication for TIPS in 72 patients (83.7%). While 14 patients (16.3%) had intractable ascites as the main TIPS indication, 51 patients (59.3%) had ascites prior to TIPS. The rate of CD at the first revision was 2.7% (n=2/72) for variceal bleeding and 33% (n=17/51) for inadequate control of ascites. HD occurred in 44 cases (51.2%). Among the patients with CD for inadequate control of ascites, 13 also had HD. Patients with HD had a significantly lower PVV when compared to patients with a revision PPG below ten mmHg (36 ± 14.7 cm/s vs. 45.7 ± 19.2 cm/s, p=0.008). However, the discriminative capabilities of PVV in detecting HD were modest, with an AUROC of 0.655 for a cut-off value of 30.5 cm/s. Patients with HD also had a significant decrease in PVV at the first revision (-5.4 ± 20 cm/s), compared o patients without HD, which more frequently had an increase in PVV (+6.1 ± 20.9 cm/s), p=0.01. Patients with hemodynamic TIPS dysfunction had a significantly lower PVV and have shown a decreasing PVV compared to the baseline value. A low or decreasing PVV might be sufficient to prompt hepatic catheterization in the absence of clinical recurrence, given the substantially higher rate of clinically silent HD. [ABSTRACT FROM AUTHOR]

The article discusses study which investigated the accuracy of liver stiffness measurement (LSM) during direct acting antiviral (DAA) therapy to estimate clinically significant portal hypertension (CSPH) and to predict long-term outcome in compensated advanced chronic liver disease (cACLD) patients after obtaining sustained virologic response (SVR). Topics covered include a reduction of LSM during treatment, and the role of HPV-induced inflammation on hepatic vascular resistance.