[Metabolic steatotic liver disease: the move towards an inclusive definition]. / Maladie métabolique stéatosique du foie : vers une définition inclusive.

Steatotic liver disease is the most common liver pathology worldwide, comprises a wide range of liver diseases linked to metabolic dysfunction, excessive alcohol consumption, drug reactions and infectious and genetic origins. Following several years of deliberation, the major liver disease societies have recently adopted a new nomenclature and updated diagnostic criteria for steatotic liver diseases, aimed at better reflecting our evolving understanding of their pathophysiology. This article summarizes these newly adopted designations, explores the basis for these nomenclatures, presents recent epidemiological data and discusses new diagnostic criteria and recent advances in therapeutic approaches for steatotic liver disease.

La maladie stéatosique du foie est la pathologie hépatique actuelle la plus répandue mondialement, englobant un spectre de maladies hépatiques liées au métabolisme, à la consommation d'alcool, à des réactions médicamenteuses et des origines infectieuses et génétiques. À la suite de plusieurs années de délibérations, les principales sociétés spécialisées dans les maladies du foie ont récemment adopté une nouvelle nomenclature et des critères diagnostiques actualisés pour les maladies stéatosiques du foie, visant à mieux refléter notre compréhension évolutive de leur physiopathologie. Cet article résume ces nouvelles désignations adoptées, explore les fondements de ces nomenclatures, présente les récentes données épidémiologiques et discute des nouveaux critères diagnostiques et des avancées récentes dans les approches thérapeutiques des maladies stéatosiques du foie.

Variable Intrafamilial Expression of ABCB4 Disease.

Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a rare cholestatic liver disease with autosomal recessive inheritance caused by mutations in the ABCB4 gene. The clinical presentation of PFIC3 varies significantly, displaying incomplete penetrance without clear genotype-phenotype correlations. As such, the suitability of living-related liver donation for children with advanced disease has been questioned. We report here the long-term follow-up of a patient with PFIC3 resulting in decompensated cirrhosis at 11 years who successfully underwent living donor liver transplantation from his father, who carried the same ABCB4 homozygous mutation.

[Residual risk of liver disease after hepatitis C virus eradication]. / Risque résiduel d'hépatopathie après éradication du virus de l'hépatite C par les antiviraux directs.

Treatment of hepatitis C has known major progress thanks to direct-acting antivirals resulting in the healing, defined by a viral clearance (sustained virological response [SVR]), in the vast majority of patients. However, there is a residual risk of progressive liver damage in a minority of patients, potentially leading to complications such as liver decompensation, hepatocellular carcinoma and/or death. This article discusses the current knowledge of residual liver disease after treatment, the impact of comorbidities and the factors potentially predicting patients at risk of complications and warranting surveillance.

Le traitement de l'hépatite C a connu des progrès majeurs grâce aux antiviraux directs, permettant la guérison des patients, définie par une réponse virologique soutenue dans la grande majorité des cas. Il existe cependant un risque résiduel de progression de la maladie hépatique pour une faible proportion de patients pouvant entraîner un risque de complications majeures, de type décompensation cirrhotique, carcinome hépatocellulaire et/ou décès. Dans cet article, nous traitons des connaissances actuelles concernant le risque résiduel d'hépatopathie après traitement, de l'impact des comorbidités mais également des facteurs permettant d'identifier les patients à risque de complication et justifiant une surveillance.

NAFLD and MAFLD as emerging causes of HCC: A populational study.

BACKGROUND & AIMS: There are conflicting data regarding the epidemiology of hepatocellular carcinoma (HCC) arising in the context of non-alcoholic and metabolic-associated fatty liver disease (NAFLD and MAFLD). We aimed to examine the changing contribution of NAFLD and MAFLD, stratified by sex, in a well-defined geographical area and highly characterised HCC population between 1990 and 2014. METHODS: We identified all patients with HCC resident in the canton of Geneva, Switzerland, diagnosed between 1990 and 2014 from the prospective Geneva Cancer Registry and assessed aetiology-specific age-standardised incidence. NAFLD-HCC was diagnosed when other causes of liver disease were excluded in cases with type 2 diabetes, metabolic syndrome, or obesity. Criteria for MAFLD included one or more of the following criteria: overweight/obesity, presence of type 2 diabetes mellitus, or evidence of metabolic dysregulation. RESULTS: A total of 76/920 (8.3%) of patients were diagnosed with NAFLD-HCC in the canton of Geneva between 1990 and 2014. Between the time periods 1990-1994 and 2010-2014, there was a significant increase in HCC incidence in women (standardised incidence ratio [SIR] 1.83, 95% CI 1.08-3.13, p = 0.026) but not in men (SIR 1.10, 95% CI 0.85-1.43, p = 0.468). In the same timeframe, the proportion of NAFLD-HCC increased more in women (0-29%, p = 0.037) than in men (2-12%, p = 0.010) while the proportion of MAFLD increased from 21% to 68% in both sexes and from 7% to 67% in women (p <0.001). From 2000-2004 to 2010-2014, the SIR of NAFLD-HCC increased to 1.92 (95% CI 0.77-5.08) for men and 12.7 (95% CI 1.63-545) in women, whereas it decreased or remained stable for other major aetiologies of HCC. CONCLUSIONS: In a populational cohort spanning 25 years, the burden of NAFLD and MAFLD associated HCCs increased significantly, driving an increase in HCC incidence, particularly in women. LAY SUMMARY: Hepatocellular carcinoma (HCC) is the most common type of liver cancer, increasingly arising in patients with liver disease caused by metabolic syndrome, termed non-alcoholic fatty liver disease (NAFLD) or metabolic-associated fatty liver disease (MAFLD). We assessed all patients with HCC between 1990 and 2014 in the canton of Geneva (western Switzerland) and found an increase in all HCC cases in this timeframe, particularly in women. In addition, we found that HCC caused by NAFLD or MAFLD significantly increased over the years, particularly in women, possibly driving the increase in overall HCC cases.