Journal of Hepatology

Check our September issue! This month's cover features the article "Comparison of non-contrast abbreviated MRI and ultrasound as surveillance modalities for HCC" by Dong Hwan Kim, Jeong Hee Yoon et al. (https://bit.ly/3yJhR8Z) Full issue here: https://bit.ly/36khmDF EASL | The Home of Hepatology

Angiocrine signaling in sinusoidal homeostasis and liver diseases The hepatic sinusoids are composed of liver sinusoidal endothelial cells (LSECs), which are surrounded by hepatic stellate cells (HSCs) and contain liver-resident macrophages called Kupffer cells, and other patrolling immune cells. All these cells communicate with each other and with hepatocytes to maintain sinusoidal homeostasis and a spectrum of hepatic functions under healthy conditions. Sinusoidal homeostasis is disrupted by metabolites, toxins, viruses, and other pathological factors, leading to liver injury, chronic liver diseases, and cirrhosis. Alterations in hepatic sinusoids are linked to fibrosis progression and portal hypertension. LSECs are crucial regulators of cellular crosstalk within their microenvironment via angiocrine signaling. This review discusses the mechanisms by which angiocrine signaling orchestrates sinusoidal homeostasis, as well as the development of liver diseases. Here, we summarise the crosstalk between LSECs, HSCs, hepatocytes, cholangiocytes, and immune cells in health and disease and comment on potential novel therapeutic methods for treating liver diseases. Full review here: https://bit.ly/4gd5aUz EASL | The Home of Hepatology

Genetics meets diet: unveiling how personalized nutrition may impacts steatotic siver disease Steatotic liver disease (SLD) is affected by genetics and diet. This study, analyzed data from 21,619 UK Biobank participants, examining dietary patterns, genetic variants (PNPLA3-rs738409-G, TM6SF2-rs58542926-T), and a hepatic steatosis polygenic risk score (PRS). They found that a Mediterranean diet and high intake of fruits, vegetables, and legumes were linked to lower liver fat content (LFC), while higher red/processed meat intake and genetic factors were associated with higher LFC. Dietary impacts were more pronounced in those with higher genetic risk, suggesting personalized dietary counseling could be especially beneficial. Find it here: https://bit.ly/4g1bGOa EASL | The Home of Hepatology

WHAT IS YOUR DIAGNOSIS ❓ A 47-year-old overweight woman (BMI 29) was evaluated for elevated transaminases (AST 146 IU/L , ALT 170 IU/L, normal GGT & AP). Current medication nimesulide. Previous DILI (5 years ago) attributed to amoxicillin-clavulanate. ANA 1/160, HbsAg and anti-HCV negative. 👨🔬A liver biopsy was performed. 🤔What is your diagnosis? 1️⃣ Drug-induced liver injury 2️⃣ Alcohol-related liver disease 3️⃣ Autoimmune hepatitis 4️⃣ Metabolic dysfunction-associated steatotic liver disease Full case here👉https://bit.ly/3ANgQ05 EASL | The Home of Hepatology

Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD)❕ ✔ This joint EASL-EASD-EASO guideline provides an update on definitions, prevention, screening, diagnosis and treatment for MASLD. Find the full text here 👉 https://bit.ly/3XeJnFc EASL | The Home of Hepatology

Loss of the ciliary gene Pkd1l1 contributes to biliary atresia pathology Biliary atresia, a pediatric cholangiopathy, is the most common indication for pediatric liver transplantation worldwide. Its etiology is multifactorial, occurring in isolation or with congenital anomalies. This study, shows that PKD1L1 gene variants, identified in syndromic cases, contribute to biliary atresia pathology. Pkd1l1-deficient mice exhibited congenital anomalies, including malrotation and heterotaxy, ductular reaction, periportal fibrosis, and hypertrophic and fibrotic extrahepatic bile ducts with delayed biliary drainage. Moreover, reduced primary cilia and altered ciliogenesis gene expression were observed in cholangiocytes. Full text here: https://lnkd.in/d72hdwg9 EASL | The Home of Hepatology

WHAT IS YOUR DIAGNOSIS ❓ A 27-year old man is admitted to the hospital with fever, jaundice, elevated transaminses (> 2000 IU/L), LDH (> 1000 IU/L) and progressive anemia. 👨🔬On physical examination splenomegaly. - Viral hepatitis serologies were negative. - A liver biopsy was performed. 🤔What is your diagnosis? 1️⃣ Adult-onset Still’s disease 2️⃣ Epstein-Barr virus infection 3️⃣ Drug-induced liver injury 4️⃣ Hepatosplenic T-cell lymphoma Full case here👉https://lnkd.in/dnWd5NpT EASL | The Home of Hepatology

How to predict decompensation and mortality in patients with alcohol-related liver disease (ALD)? Patients with ALD face significant risks of disease progression and adverse outcomes. Liver stiffness measurement (LSM) is recommended for prognostication and monitoring. This study, shows that LSM is useful for ALD prognosis. Elevated baseline LSM (>10 kPa) was linked to a 19-fold increased risk of decompensation. LSM changes over two years correlated with decompensation and death, with higher LSM indicating worse outcomes. #OpenAccess here: https://lnkd.in/dQmv4c8a Maja Thiele Aleksander Krag EASL | The Home of Hepatology

Developing and validating clinical prediction models in hepatology – An overview for clinicians Prediction models are everywhere in clinical medicine. We use them to assign a diagnosis or a prognosis, and there have been continuous efforts to develop better prediction models. It is important to understand the fundamentals of prediction modelling, thus, we herein describe nine steps to develop and validate a clinical prediction model with the intention of implementing it in clinical practice: Determine if there is a need for a new prediction model; define the purpose and intended use of the model; assess the quality and quantity of the data you wish to develop the model on; develop the model using sound statistical methods; generate risk predictions on the probability scale (0-100%); evaluate the performance of the model in terms of discrimination, calibration, and clinical utility; validate the model using bootstrapping to correct for the apparent optimism in performance; validate the model on external datasets to assess the generalisability and transportability of the model; and finally publish the model so that it can be implemented or validated by others. @OpenAccess here: https://lnkd.in/d88G6f4b Rickard Strandberg EASL | The Home of Hepatology

Novel animal model of extrahepatic cholangiocarcinoma The PTEN-AKT pathway is frequently disrupted in extrahepatic cholangiocarcinoma (eCCA). This study, shows that conditional knockout mice with targeted deletion of the Pten gene in extrahepatic biliary epithelial cells replicate the progression from sclerosing cholangitis-like lesions to dysplasia, ultimately leading to eCCA. Notably, Trp53 inactivation hastened disease progression. Both genetic and pharmacological strategies aimed at reducing AURKA expression, which is elevated in both human and mouse eCCA, effectively mitigated disease progression. Full text here: https://lnkd.in/dDgT-M9b EASL | The Home of Hepatology