Impact of Keratins 8 and 18 Genetic Variants on the Severity of Alcoholic Liver Disease.

Alcohol-related liver disease (ALD) affects ∼30% of heavy drinkers and is characterized by liver steatosis, fibrosis, and steatohepatitis. The aggregation of keratins 8 (KRT8) and 18 (KRT18) plays a key role in the formation of Mallory-Denk bodies, a hallmark of ALD. Circulating levels of KRT18 fragments are elevated during ALD, and several KRT8/18 genetic variants have been linked to an increased risk of liver disease. In this study, we explored the relationship between the histologic features of ALD and genetic variants of KRT8/18 in 106 severe patients with ALD from the Hôpitaux Universitaires de Genève. We found a significant over-representation of several KRT8 (rs2070910, rs137898974, rs1065306) and KRT18 (rs17120866, rs1492241) variants located in the noncoding regions of these genes. Increased circulating level of keratins 18 fragments were associated with rs17120866 and alcoholic hepatitis. The combination of several KRT18 variants appeared associated with a poorer prognosis. These results highlight the possible role of KRT18 variants in ALD.

[New oncological indications for liver transplantation]. / Nouvelles indications oncologiques à la transplantation hépatique.

Transplantation oncology represents a specificity of liver transplantation. Hepatocellular carcinoma is now an accepted indication with very good long-term results. Cholangiocarcinoma, hepatic -metastases from colorectal cancer and neuroendocrine tumors are emerging indications with outcome superior to those that can be achieved with systemic treatments in very selected patients.

La transplantation pour des indications oncologiques représente une particularité exclusive de la transplantation hépatique. Le carcinome hépatocellulaire est désormais une indication confirmée par de très bons résultats à long terme. Le cholangiocarcinome, les métastases hépatiques du cancer colorectal et neuro­endocrine représentent des indications émergentes avec des ­résultats supérieurs à ceux obtenus avec les traitements systémiques, sous réserve d'une rigoureuse sélection des patients.

[Population screening for hepatic fibrosis : who to screen, why and how ?] / Dépistage de la fibrose hépatique dans la population.

The development of liver fibrosis is the consequence of histological remodeling of the liver parenchyma, reflecting chronic inflammatory liver disease or hepatocyte necrosis. These tissue modifications result in structural changes to the extracellular matrix, predisposing to progression to cirrhosis and hepatocellular carcinoma, whatever the underlying etiology. Recent data demonstrate the potential benefits of screening for hepatic fibrosis, in particular in order to detect and treat the cause of the underlying liver disease as early as possible, which could ultimately lead to the many known complications in cirrhotic patients. Early identification of the population at risk of hepatic fibrosis should precede screening, which may be initiated in the primary care physician's office and continued at a later stage by the specialist.

L'apparition d'une fibrose hépatique est souvent la conséquence d'une atteinte inflammatoire chronique du foie ou d'une ­nécrose hépatocytaire. Ces modifications tissulaires ont pour conséquence un changement structurel de la matrice extracellulaire, prédisposant à la progression vers une cirrhose ainsi qu'un carcinome hépatocellulaire, quelle que soit l'étiologie sous-jacente. Des données récentes démontrent le bénéfice ­potentiel du dépistage de la fibrose hépatique, afin de détecter et traiter au plus tôt la cause de la maladie ­hépatique sous-jacente qui pourrait, à terme, conduire aux nombreuses complications connues chez le patient cirrhotique. Une identification précoce de la population à risque de fibrose hépatique peut être initié au cabinet du médecin de premier recours et se poursuivre ultérieurement chez le ­spécialiste.

[Liver transplantation in adults : choosing the appropriate candidate and timing]. / Quel patient adresser à un centre de transplantation hépatique ?

Liver transplantation is the best treatment option for patients with end-stage liver failure, as well as for various oncological (hepatic or extrahepatic), metabolic and genetic indications. Cirrhosis and its complications represent the most frequent indication for transplantation. This treatment option should be considered for cirrhotic patients with significant liver failure, the development of hepatocellular carcinoma or when complications linked to portal hypertension appear. In view of the limited availability of organs and a waiting time on the list estimated at around one year in Switzerland, careful assessment of the risk-benefit ratio and correct timing of evaluation in a transplant center are crucial to optimize the benefits of this procedure.

La transplantation du foie est la meilleure option thérapeutique pour les patients atteints d'une insuffisance hépatique terminale ainsi que pour différentes indications oncologiques (hépatiques ou extrahépatiques), métaboliques et génétiques. La cirrhose et ses complications représentent l'indication la plus fréquente à la transplantation. Celle-ci doit être évoquée chez un patient cirrhotique en cas d'insuffisance hépatique marquée, d'apparition d'un carcinome hépatocellulaire ou lors de complications liées à l'hypertension portale. Vu la disponibilité limitée des organes et d'un temps d'attente en liste de transplantation pouvant être supérieur à un an en Suisse, l'évaluation du rapport bénéfices-risques de la transplantation ainsi que du meilleur moment pour un bilan pré-greffe permet d'optimiser les bénéfices de cette intervention.

[Updated recommandations for the follow-up of a patient with cirrhosis]. / Actualisation du suivi d'un patient atteint de cirrhose.

A close collaboration between the general practitioner and the gastroenterologist is necessary to optimize the management of a patient with cirrhosis, a frequent and serious complication of chronic liver diseases. Both the treatment of the etiological factor of liver disease and the surveillance of potential complications of cirrhosis are key issues in the proper management of cirrhosis. Preventive measures aim at keeping the patient in a compensated form of cirrhosis which is associated with a better survival. We address here the updated management strategies regarding the most frequent complications of cirrhosis.

La prise en charge d'un patient atteint de cirrhose implique une collaboration étroite entre le médecin généraliste et le spécialiste, combine le traitement de la maladie causale ainsi que la mise en place d'une surveillance des complications pouvant occasionner une décompensation avec un impact pronostique négatif. Nous passons en revue les principales situations cliniques de la cirrhose pour lesquelles des recommandations actualisées ont pour but d'améliorer la prise en charge de cette maladie fréquente grevée d'une importante morbimortalité.

Final safety and efficacy results from a 106 real-world patients registry with an ascites-mobilizing pump.

BACKGROUND AND AIMS: Patients with cirrhotic refractory ascites ineligible for transjugular intrahepatic shunt (TIPSS) have limited treatment options apart from repeated large volume paracentesis. The alfapump® is an implantable device mobilizing ascites from the peritoneal cavity to the bladder, from where it can be excreted. The aim of this observational cohort study was to prospectively investigate safety and efficacy of the device in a real-world cohort with cirrhotic refractory ascites and contraindications for TIPSS. METHODS: A total of 106 patients received an implant at 12 European centres and were followed up for up to 24 months. Complications, device deficiencies, frequency of paracentesis, clinical status and survival were recorded prospectively. RESULTS: Approximately half of the patients died on-study, about a quarter was withdrawn because of serious adverse events leading to explant, a sixth were withdrawn because of liver transplant or recovery, and nine completed follow-up. The most frequent causes of on-study death and complication-related explant were progression of liver disease and infection. The device reduced the requirement for large-volume paracentesis significantly, with more than half of patients not having required any post-implant. Survival benefits were not observed. Device-related reinterventions were predominantly caused by device deficiencies. A post-hoc comparison of the first 50 versus the last 50 patients enrolled revealed a decreased reintervention rate in the latter, mainly related to peritoneal catheter modifications. CONCLUSIONS: The device reduced paracentesis frequency in a real-world setting. Technical complications were successfully decreased by optimization of management and device modification (NCT01532427).

[Polycystic liver disease]. / Polykystoses hépatiques.

Polycystic liver disease (PLD) includes three entities in adults : biliary hamartomas which develop as a result of ductal plate malformation, autosomal dominant polycystic liver disease (ADPLD) and autosomal dominant polycystic kidney disease (ADPKD) which occur in the setting of genetic disorders. Hamartomas are asymptomatic and benign. PLD are marked by a steady growth of cysts over time, clinically silent in the majority of cases. Symptomatic forms mainly affect women due to the influence of estrogens on the growth of cysts therefore estrogen treatments are contraindicated in this setting. Diagnosis is based on imaging. Complications are rare but must be identified early in order to offer appropriate care in an expert center.

Les polykystoses hépatiques (PKH) de l'adulte regroupent les hamartomes biliaires, conséquence d'une malformation congénitale de la plaque ductale, la polykystose hépatorénale autosomique dominante (PKHRAD) et la polykystose hépatique isolée (PKHI), de cause génétique. Les hamartomes sont asymptomatiques et bénins. Les PKH sont marquées par une croissance régulière des kystes au fil du temps, silencieuse dans la majorité des cas. Les formes symptomatiques concernent majoritairement les femmes, la croissance des kystes étant influencée par les œstrogènes. De ce fait, les traitements œstrogéniques doivent être proscrits. Le diagnostic repose sur l'imagerie. Les complications sont rares mais doivent être identifiées précocement afin de proposer une prise en charge adaptée en centre expert.

[Advances in gastroenterology and hepatology 2021]. / Gastroentérologie et hépatologie.

Among the recent advances in gastroenterology, colonoscopy with artificial intelligence is associated with a better quality of screening. In refractory UC, Ozanimod seems to be an interesting salvage treatment, which still needs to be validated by Swissmedic. Among the direct-acting anticoagulants, Rivaroxaban is more frequently associated with GI bleeding. The classification of oesophageal motor disorders has been recently revised, the Chicago v4.0 classification should be applied in diagnostic management. The use of Semaglutide seems to show very promising results in the management of metabolic steatosis. SARS-CoV-2 infection can be complicated by biliary tract disease, which can progress to hepatocellular failure.

Parmi les récentes avancées en gastroentérologie, la coloscopie couplée à une intelligence artificielle est associée à un dépistage de meilleure qualité. Lors de rectocolite hémorragique réfractaire, l'ozanimod semble être un traitement de sauvetage intéressant, qui doit encore être validé par Swissmedic. Parmi les anticoagulants à action directe, le rivaroxaban est plus fréquemment associé aux hémorragies digestives. La classification des troubles moteurs de l'œsophage a fait l'objet d'une révision récente, la classification de Chicago v4.0 doit être appliquée dans la prise en charge diagnostique. L'utilisation du sémaglutide semble montrer des résultats très prometteurs dans la prise en charge de la stéatose métabolique. L'infection par le virus à SARS-CoV-2 peut se compliquer d'une atteinte des voies biliaires, pouvant évoluer jusqu'à l'insuffisance hépatocellulaire.

Hepatic Alveolar Echinococcosis.

Hepatic alveolar echinococcosis (HAE) is a rare but severe zoonosis caused by the pseudotumoral intrahepatic development of the larval stage of the tapeworm Echinococcus multilocularis. HAE is present only in the Northern Hemisphere, predominantly in China. Currently, there is a significant resurgence of cases in historically endemic areas associated with emergence of HAE in countries not previously concerned. Today, in European countries, HAE is often discovered by chance; however, clinicians should be made aware of opportunistic infections that progressively emerged recently as a result of therapeutic or pathological immunosuppression. Ultrasonography is the key first-line diagnostic procedure, with specific serology providing confirmation in 95% of the cases. Albendazole, only parasitostatic, is the mainstay for treatment. Surgical resection, if feasible, is the gold standard for treatment, and more patients are currently eligible for this option because of an earlier diagnosis. The prognosis has considerably improved but remains poor in countries where access to care is less favorable.

Genetic Variation in HSD17B13 Reduces the Risk of Developing Cirrhosis and Hepatocellular Carcinoma in Alcohol Misusers.

BACKGROUND AND AIMS: Carriage of rs738409:G in patatin-like phospholipase domain containing 3 (PNPLA3) is associated with an increased risk for developing alcohol-related cirrhosis and hepatocellular carcinoma (HCC). Recently, rs72613567:TA in hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13) was shown to be associated with a reduced risk for developing alcohol-related liver disease and to attenuate the risk associated with carriage of PNPLA3 rs738409:G. This study explores the risk associations between these two genetic variants and the development of alcohol-related cirrhosis and HCC. APPROACH AND RESULTS: Variants in HSD17B13 and PNPLA3 were genotyped in 6,171 participants, including 1,031 with alcohol-related cirrhosis and HCC, 1,653 with alcohol-related cirrhosis without HCC, 2,588 alcohol misusers with no liver disease, and 899 healthy controls. Genetic associations with the risks for developing alcohol-related cirrhosis and HCC were determined using logistic regression analysis. Carriage of HSD17B13 rs72613567:TA was associated with a lower risk for developing both cirrhosis (odds ratio [OR], 0.79; 95% confidence interval [CI], 0.72-0.88; P = 8.13 × 10-6 ) and HCC (OR, 0.77; 95% CI, 0.68-0.89; P = 2.27 × 10-4 ), whereas carriage of PNPLA3 rs738409:G was associated with an increased risk for developing cirrhosis (OR, 1.70; 95% CI, 1.54-1.88; P = 1.52 × 10-26 ) and HCC (OR, 1.77; 95% CI, 1.58-1.98; P = 2.31 × 10-23 ). These associations remained significant after adjusting for age, sex, body mass index, type 2 diabetes, and country. Carriage of HSD17B13 rs72613567:TA attenuated the risk for developing cirrhosis associated with PNPLA3 rs738409:G in both men and women, but the protective effect against the subsequent development of HCC was only observed in men (ORallelic , 0.75; 95% CI, 0.64-0.87; P = 1.72 × 10-4 ). CONCLUSIONS: Carriage of variants in PNPLA3 and HSD17B13 differentially affect the risk for developing advanced alcohol-related liver disease. A genotypic/phenotypic risk score might facilitate earlier diagnosis of HCC in this population.

[Update on cystic echinococcosis of the liver]. / Actualités sur l'échinococcose kystique hépatique.

Hepatic cystic echinococcosis (HCE), is a cosmopolitan parasitic zoonosis. Autochtonous HCE cases are rare and the majority of cases are imported from endemic areas. It induces the development in the liver of Echinococcus granulosus larvae. Extrahepatic localizations are also possible. Cyst development is slow with an often-late diagnosis. In Switzerland, HCE discovery is usually fortuitous, during an abdominal radiological examination. More rarely, an acute clinical picture reveals a complication that can be severe or even fatal. The diagnosis is based on ultrasound findings that allows cyst characterization according to the WHO classification. This guides the therapeutic choice: simple monitoring, albendazole therapy, percutaneous procedures or surgery.

L'échinococcose kystique hépatique (EKH) est une zoonose parasitaire cosmopolite. Les cas d'EKH autochtones sont rares et la majorité est importée par des patients originaires de zones d'endémie. L'EKH est due au développement dans le foie de la larve d'Echinococcus granulosus. Des localisations extrahépatiques sont également possibles. Son évolution est lente avec un diagnostic fréquemment tardif. En Suisse, celui-ci est souvent fortuit, à l'occasion d'un examen radiologique abdominal. Plus rarement, un tableau clinique aigu et bruyant révèle une complication qui peut être sévère, voire mortelle. Le diagnostic basé sur l'échographie permet la caractérisation du kyste selon la classification de l'OMS. Celle-ci guide le choix thérapeutique: surveillance simple, traitement par albendazole, gestes percutanés ou chirurgie.

Abdominal Surgery in Patients With Idiopathic Noncirrhotic Portal Hypertension: A Multicenter Retrospective Study.

In patients with idiopathic noncirrhotic portal hypertension (INCPH), data on morbidity and mortality of abdominal surgery are scarce. We retrospectively analyzed the charts of patients with INCPH undergoing abdominal surgery within the Vascular Liver Disease Interest Group network. Forty-four patients with biopsy-proven INCPH were included. Twenty-five (57%) patients had one or more extrahepatic conditions related to INCPH, and 16 (36%) had a history of ascites. Forty-five procedures were performed, including 30 that were minor and 15 major. Nine (20%) patients had one or more Dindo-Clavien grade ≥ 3 complication within 1 month after surgery. Sixteen (33%) patients had one or more portal hypertension-related complication within 3 months after surgery. Extrahepatic conditions related to INCPH (P = 0.03) and history of ascites (P = 0.02) were associated with portal hypertension-related complications within 3 months after surgery. Splenectomy was associated with development of portal vein thrombosis after surgery (P = 0.01). Four (9%) patients died within 6 months after surgery. Six-month cumulative risk of death was higher in patients with serum creatinine ≥ 100 µmol/L at surgery (33% versus 0%, P < 0.001). An unfavorable outcome (i.e., either liver or surgical complication or death) occurred in 22 (50%) patients and was associated with the presence of extrahepatic conditions related to INCPH, history of ascites, and serum creatinine ≥ 100 µmol/L: 5% of the patients with none of these features had an unfavorable outcome versus 32% and 64% when one or two or more features were present, respectively. Portal decompression procedures prior to surgery (n = 10) were not associated with postoperative outcome. Conclusion: Patients with INCPH are at high risk of major surgical and portal hypertension-related complications when they harbor extrahepatic conditions related to INCPH, history of ascites, or increased serum creatinine.

Gene signature-MELD score and alcohol relapse determine long-term prognosis of patients with severe alcoholic hepatitis.

BACKGROUND: The gene-signature-model for end stage liver disease (gs-MELD) score has been shown to be a strong predictor of 6-month survival in severe alcoholic hepatitis (AH). Currently, only a few studies have evaluated the long-term prognosis of patients with severe AH. AIM: To assess the prognostic value of the gs-MELD score at 5 years in patients with severe AH. METHODS: Forty-eight consecutive patients with AH (25 males, median age 52 years [95% IC: 48-56]) were included. RESULTS: The median gs-MELD score was 2.6 (95% CI: 2.2-3.0). According to the gs-MELD score, 22 patients (46%) were considered to have a poor prognosis. During a median follow-up of 29 months (95% CI: 4-43), 19 patients (40%) were abstinent and 24 patients (50%) died. At 5 years, rates of survival were 61% (95% CI: 41-81) and 26% (95% CI: 11-55) in patients with low and high gs-MELD scores (P = .001), and 81% (95% CI: 58-96) and 22% (95% CI: 10-47) in abstainers and in consumers (P < .001) respectively. In multivariable competing risk regression modelling, gs-MELD score (subdistribution hazard ratio: 5.78, 95% CI: 2.17-15.38, P < .001) and recurrent alcohol consumption (subdistribution hazard ratio: 12.18, 95% CI: 3.16-46.95, P < .001) were independently associated with 5-year mortality. CONCLUSIONS: Both gs-MELD score and alcohol consumption drive AH long-term prognosis. The gs-MELD score may guide the development of molecularly targeted therapies in AH.

[Efficacy of new therapies]. / Hépatite D†: efficacité des nouvelles thérapies.

Hepatitis D virus causes chronic hepatitis D. The virus is defective, meaning it requires simultaneous presence of hepatitis B virus within the hepatocytes to complete its viral cycle. Globally, 15 to 20 millions people are estimated to be chronically co-infected by hepatitis B and D viruses. Current therapy remains limited to pegylated interferon alfa, which has an unsatisfactory success rate, several contraindications and many side effects. Drugs directly targeting the hepatitis D virus life cycle are being developed with promising results. These drugs target viral entry into hepatocytes, virion assembly or secretion from infected hepatocytes. This article provides an overview of the newly developed therapies and their efficacy.

L'hépatite D chronique est une infection causée par le virus de l'hépatite D, un virus défectueux nécessitant l'infection concomitante des hépatocytes par le virus de l'hépatite B. On estime que 15 à 20 millions d'individus dans le monde pourraient être co-infectés chroniquement par ces deux virus. Le seul traitement disponible est l'interféron alfa pégylé dont l'efficacité est encore insatisfaisante avec des effets indésirables fréquents. Des thérapies ciblant le virus de l'hépatite D sont en développement avec des résultats prometteurs. Parmi eux, les inhibiteurs de l'entrée du virus dans l'hépatocyte, de son assemblage ou encore de sa sécrétion. Cet article fait le point sur les thérapies en développement et leur efficacité.

[NASH: new terminology and what else is new in 2020]. / NASH†: nouvelle terminologie et nouveautés en 2020.

Non-alcoholic fatty liver disease (NAFLD) includes a spectrum of hepatic pathology ranging from non-alcoholic fatty liver, non-alcoholic steatohepatitis (NASH) occasionally complicated with hepatic fibrosis or even cirrhosis. In order to propose a diagnosis with positive criteria, a panel of experts recently proposed the use of an alternative nomenclature, metabolic-dysfunction-associated fatty liver disease (MAFLD) whose use remains debated. In addition, in Switzerland and elsewhere, there is strong epidemiological growth of NAFLD. The next years will probably see the approval of new therapies for NAFLD/NASH but, at present, management remains focused on lifestyle interventions and joint monitoring by the primary care physician and, when necessary, the specialist.

La stéatopathie non alcoolique (NAFLD) comprend un spectre de pathologies allant de la stéatose hépatique non alcoolique à la stéatohépatite non alcoolique (NASH) parfois compliquée d'une fibrose hépatique, voire d'une cirrhose. Afin de proposer un diagnostic avec des critères positifs, un panel d'experts a récemment proposé l'utilisation d'une nomenclature alternative, la stéatopathie associée à la dysfonction métabolique (Metabolic-Dysfunction-Associated Fatty Liver Disease, MAFLD) dont l'utilisation reste discutée. D'autre part, la NAFLD est en pleine croissance épidémiologique en Suisse comme ailleurs. Les prochaines années vont probablement voir l'approbation de nouvelles thérapeutiques pour la NAFLD/NASH mais, à l'heure actuelle, la prise en charge reste centrée sur les mesures hygiéno-diététiques et le suivi conjoint par le médecin de premier recours et, si nécessaire, par le spécialiste.

Combination of Gene Expression Signature and Model for End-Stage Liver Disease Score Predicts Survival of Patients With Severe Alcoholic Hepatitis.

BACKGROUND & AIMS: Patients with severe alcoholic hepatitis (AH) have a high risk of death within 90 days. Corticosteroids, which can cause severe adverse events, are the only treatment that increases short-term survival. It is a challenge to predict outcomes of patients with severe AH. Therefore, we developed a scoring system to predict patient survival, integrating baseline molecular and clinical variables. METHODS: We obtained fixed liver biopsy samples from 71 consecutive patients diagnosed with severe AH and treated with corticosteroids from July 2006 through December 2013 in Brussels, Belgium (derivation cohort). Gene expression patterns were analyzed by microarrays and clinical data were collected for 180 days. We identified gene expression signatures and clinical data that are associated with survival without liver transplantation at 90 and 180 days after initiation of corticosteroid therapy. Findings were validated using liver biopsies from 48 consecutive patients with severe AH treated with corticosteroids, collected from March 2010 through February 2015 at hospitals in Belgium and Switzerland (validation cohort 1) and in liver biopsies from 20 patients (9 received corticosteroid treatment), collected from January 2012 through May 2015 in the United States (validation cohort 2). RESULTS: We integrated data on expression patterns of 123 genes and the model for end-stage liver disease (MELD) scores to assign patients to groups with poor survival (29% survived 90 days and 26% survived 180 days) and good survival (76% survived 90 days and 65% survived 180 days) (P < .001) in the derivation cohort. We named this assignment system the gene signature-MELD (gs-MELD) score. In validation cohort 1, the gs-MELD score discriminated patients with poor survival (43% survived 90 days) from those with good survival (96% survived 90 days) (P < .001). The gs-MELD score also discriminated between patients with a poor survival at 180 days (34% survived) and a good survival at 180 days (84% survived) (P < .001). The time-dependent area under the receiver operator characteristic curve for the score was 0.86 (95% confidence interval 0.73-0.99) for survival at 90 days, and 0.83 (95% confidence interval 0.71-0.96) for survival at 180 days. This score outperformed other clinical models to predict survival of patients with severe AH in validation cohort 1. In validation cohort 2, the gs-MELD discriminated patients with a poor survival at 90 days (12% survived) from those with a good survival at 90 days (100%) (P < .001). CONCLUSIONS: We integrated data on baseline liver gene expression pattern and the MELD score to create the gs-MELD scoring system, which identifies patients with severe AH, treated or not with corticosteroids, most and least likely to survive for 90 and 180 days.

Biomarkers for acute kidney injury in decompensated cirrhosis: A prospective study.

AIM: Acute kidney injury (AKI) is a frequent complication in cirrhotic patients. As serum creatinine is a poor marker of renal function in this population, we aimed to study the utility of several biomarkers in this context. METHODS: A prospective study was conducted in hospitalized patients with decompensated cirrhosis. Serum creatinine (SCr), Cystatin C (CystC), NGAL and urinary NGAL, KIM-1, protein, albumin and sodium were measured on three separate occasions. Renal resistive index (RRI) was obtained. We analyzed the value of these biomarkers to determine the presence of AKI, its aetiology [prerenal, acute tubular necrosis (ATN), or hepatorenal (HRS)], its severity and a composite clinical outcome at 30 days (death, dialysis and intensive care admission). RESULTS: We included 105 patients, of which 55 had AKI. SCr, CystC, NGAL (plasma and urinary), urinary sodium and RRI at inclusion were independently associated with the presence of AKI. SCr, CystC and plasma NGAL were able to predict the subsequent development of AKI. Pre-renal state showed lower levels of SCr, NGAL (plasma and urinary) and RRI. ATN patients had high levels of NGAL (plasma and urinary) as well as urinary protein and sodium. HRS patients presented an intermediate pattern. All biomarkers paralleled the severity of AKI. SCr, CystC and plasma NGAL predicted the development of the composite clinical outcome with the same performance as the MELD score. CONCLUSIONS: In patients with decompensated cirrhosis, early measurement of renal biomarkers provides valuable information on AKI aetiology. It could also improve AKI diagnosis and prognosis.

[Liver transplantation and acute failure in chronic liver disease]. / Transplantation hépatique et défaillance aiguë lors d'hépatopathie chronique.

Acute cirrhotic decompensation is characterized by a rapid and sudden deterioration of hepatocellular function. It may be associated with secondary failure of one or more organs. The definition and understanding of a complex cirrhotic decompensation with multi-organ damage, is still poorly defined. This entity is currently called Acute on Chronic Liver Failure (ACLF). Depending on the number of affected organs, decompensation is classified into 4 stages, from 0 to 4. Mortality is proportional to the number of failed organs, with mortality from 50 % to 80 % at 30 days when 3 or more organs are affected. The interest of liver transplantation in the most severe forms, which has been debated for a long time, seems to be a safe alternative with good results in well selected patients.

La décompensation cirrhotique aiguë est caractérisée par une péjoration rapide et brutale de la fonction hépatocellulaire. Elle peut être associée à une défaillance secondaire d'un ou plusieurs organes. La définition et la compréhension d'une décompensation cirrhotique complexe avec atteinte multi-organes sont encore mal définies. Cette entité est actuellement appelée Acute on Chronic Liver Failure (ACLF). Selon le nombre d'organes affectés, la décompensation est classifiée en 4 stades, de 0 à 4. La mortalité est proportionnelle au nombre d'organes défaillants, avec une mortalité de 50 à 80 % à 30 jours lors d'atteinte de 3 organes ou plus. La transplantation hépatique dans les formes les plus graves, longtemps débattue, semble être une alternative sûre et avec de bons résultats, chez des patients bien sélectionnés.

Quantification of Liver Surface Nodularity at CT: Utility for Detection of Portal Hypertension.

Purpose To determine whether quantification of liver surface nodularity (LSN) provides an estimate of the presence of clinically significant portal hypertension (CSPH) in patients with cirrhosis. Materials and Methods This retrospective study included a training cohort (n = 189) and separate external validation cohort (n = 78), both composed of patients with cirrhosis who underwent abdominal CT and hepatic venous pressure gradient (HVPG) measurement between 2010 and 2016. The LSN score, liver and spleen volumes, liver-to-spleen volume ratio, platelet count to spleen diameter ratio, Iranmanesh score, aspartate amino transferase-to-platelet ratio index, and Fibrosis-4 index were derived from CT images and serum laboratories. The accuracy of the various tests for predicting CSPH was evaluated with area under the receiver operating characteristic curve (AUROC) and compared by using the DeLong test. Student t test and Pearson correlation coefficient were used. Results One hundred eighty-nine patients were analyzed (119 men [mean age ± standard deviation, 57 years ± 11; range, 29-81 years] and 70 women [mean age, 61 years ± 10; range, 34-83 years]; overall mean age, 58 years ± 10; range, 29-83 years). A total of 102 patients (54%) had CSPH. LSN score correlated with HVPG (r = 0.75; P < .001). Patients with CSPH had a higher LSN score than did those without CSPH (3.2 ± 0.6 vs 2.4 ± 0.3; P < .001). A cutoff value of 2.8 had a positive predictive value of 88% for CSPH; the AUROC of LSN was 0.88 ± 0.03. This was higher than that of other available noninvasive tests (DeLong, all P < .001). In the validation cohort, LSN score of 2.8 had a positive predictive value of 86% for CSPH; the AUROC was 0.87 ± 0.04. Conclusion The CT-based liver surface nodularity score demonstrated high diagnostic performance for detecting clinically significant portal hypertension and outperformed multiple other noninvasive tests. © RSNA, 2018 Online supplemental material is available for this article.