Transjugular liver biopsy (TJLB) is usually performed when a percutaneous liver biopsy (PLB) is contraindicated. TJLB is an invasive procedure and the patient's tolerance may be variable. To compare patient tolerance and quality of the biopsy sample between PLB and TJLB. A total of 143 patients underwent a liver biopsy; of these, 75 underwent TJLB and 68 underwent PLB. To evaluate patient tolerance, we used a visual analog scale that scored the intensity of the symptoms. The length of the biopsy sample and the total number of portal tracts per biopsy were also determined for assessment of biopsy quality. The biopsy sample length was similar in both groups (18.88 ± 8.83 mm on PLB vs. 18.26 ± 10.30 mm on TJLB). No differences were found in the number of portal tracts between the two groups (10.43 ± 8.25 on TJLB vs. 12 ± 10.09 on PLB). Fewer complications were observed in the TJLB group compared with the PLB group (P=0.002).Further, higher degree of pain was reported by patients who underwent PLB compared with patients who underwent TJLB (3.18 ± 3.17 vs. 1.19 ± 2.07); as such, there was a greater need for analgesics on PLB. TJLB and PLB techniques provide similar quality of tissue samples; however, TJLB is less painful and therefore better tolerated by patients.

Background & Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) imposes significant healthcare burdens. Early detection of advanced fibrosis and cirrhosis in MASLD is essential due to their unfavourable outcomes. This multi-level random-effects meta-analysis aimed to provide the best evidence for the diagnostic accuracy of two-dimensional shear wave elastography (2D-SWE) in detecting liver fibrosis in biopsy-proven MASLD. Approach & Results: Systematic search in PubMed/MEDLINE, Embase, Scopus, Web of Science, LILACS, and Cochrane Library electronic databases for full-text articles published in any language up to the 26^th of February 2024. Included studies reported liver stiffness measurement (LSM) by 2D-SWE and used histological diagnosis as gold standard. A linear mixed-effects multiple thresholds model was employed, and summary estimates for sensitivity (Se), specificity (Sp), and summary area under the curve (sAUC) were computed. 20 observational studies (SuperSonic Imagine, General Electric Healthcare, Canon Medical Systems) fulfilled the inclusion criteria, comprising 2223 participants with biopsy-proven MASLD. The prevalence of mild fibrosis (F1), significant fibrosis (F2), advanced fibrosis (F3), and cirrhosis (F4) was 30.0%, 18.5%, 17.9%, and 10.9%, respectively. The sAUCs [95%CI] in detecting ≥F1, ≥F2, ≥F3, and F4 for all ultrasound machines considered together were 0.82 [0.16-0.98], 0.82 [0.76-0.88], 0.86 [0.77-0.93], and 0.89 [0.80-0.95], respectively. The optimal cut-off values were 6.432 kPa for ≥F1, 8.174 kPa for ≥F2, 9.418 kPa for ≥F3, and 11.548 kPa for F4, respectively. Conclusions: Our meta-analysis identified optimised cut-offs for fibrosis staging by 2D-SWE in etiology-specific chronic liver diseases (MASLD), with excellent diagnostic performance, underscoring the potential for standardising cut-off values. Export

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a societal burden due to the lack of effective treatment and incomplete pathophysiology understanding. This review explores the intricate connections among liver sinusoidal endothelial cells (LSECs), platelets, neutrophil extracellular traps (NETs), and coagulation disruptions in MASLD pathogenesis. In MASLD’s early stages, LSECs undergo capillarization and dysfunction due to excessive dietary macronutrients and gut-derived products. Capillarization leads to ischemic changes in hepatocytes, triggering pro-inflammatory responses in Kupffer cells (KCs) and activating hepatic stellate cells (HSCs). Capillarized LSECs show a pro-inflammatory phenotype through adhesion molecule overexpression, autophagy loss, and increased cytokines production. Platelet interaction favors leucocyte recruitment, NETs formation, and liver inflammatory foci. Liver fibrosis is facilitated by reduced nitric oxide, HSC activation, profibrogenic mediators, and increased angiogenesis. Moreover, platelet attachment, activation, α-granule cargo release, and NETs formation contribute to MASLD progression. Platelets foster fibrosis and microthrombosis, leading to parenchymal extinction and fibrotic healing. Additionally, platelets promote tumor growth, epithelial–mesenchymal transition, and tumor cell metastasis. MASLD’s prothrombotic features are exacerbated by insulin resistance, diabetes, and obesity, manifesting as increased von Willebrand factor, platelet hyperaggregability, hypo-fibrinolysis, and a prothrombotic fibrin clot structure. Improving LSEC health and using antiplatelet treatment appear promising for preventing MASLD development and progression.

Introduction: Mortality from variceal bleeding remains high despite the therapeutic progress in severe cirrhosis. Understanding the predictive factors of failure to control bleeding (FTB) and mortality will lead to better future therapies. Comorbidities are thought to be important prognostic...

Background & Aims: Obesity proved to favor clinical decompensation in patients with cirrhosis. Our aim was to investigate if metabolic syndrome (MS) in cirrhotic patients represents a risk factor for decompensation.Methods: 704 cirrhotics, included in a MS prevalence study were considered for evaluation; 121 patients were excluded because they did not complete the follow-up and 303 because they were decompensated at the start of the study. The remaining 280 were followed-up for a median period of 28.1±18 months. Patients were censored at the end of follow-up or at occurrence of a liver related event (LRE). Liver related events were considered the following: decompensation (ascites, variceal bleeding, hepatorenal syndrome, jaundice, encephalopathy), hepatocellular carcinoma, portal vein thrombosis and infections.Results: All MS criteria except the abdominal circumference were significantly different between decompensated and compensated patients. HDL-cholesterol levels were lower in decompensated patients. Among the 280 patients who completed the follow-up, 85 (30%) presented LREs. Ascites was the most frequent event. In the univariate analysis of the MS criteria we found a trend to significance of an inverse correlation between MS and LREs. There was no significant difference between patients with or without MS regarding survival free of LREs, 76.7% and 66.5%, respectively. None of the MS criteria reached the level of significance in discriminating patients with and without LREs.Conclusions: In short term, presence of MS was not a risk factor for LREs. In short term, liver function and lower nutritional status influenced the prognosis. In decompensated patients, the MS defining criteria are not applicable.Abbreviations: BMI: body mass index; EV: esophageal varices; HR: hazard ration; HVPG: hepatic venous pressure gradient; LRE: liver related event; MS: metabolic syndrome; PHT: portal hypertension; WC: waist circumference.