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1. Diagnostic performance of FibroTest, SteatoTest and ActiTest in patients with NAFLD using the SAF score as histological reference

Author

Munteanu, M. Tiniakos, D. Anstee, Q. Charlotte, F. Marchesini, G. Bugianesi, E. Trauner, M. Romero Gomez, M. Oliveira, C. Day, C. Dufour, J.-F. Bellentani, S. Ngo, Y. Traussnig, S. Perazzo, H. Deckmyn, O. Bedossa, P. Ratziu, V. Poynard, T. Castille, J.-M. Langon, T. Lawlor, D. Marra, F. Sørensen, T. Tribelli, C. De Minicis, S. Burt, A.D. Gouw, A.S.H. Lackner, C. Schirmacher, P. Terracciano, L. Brain, J. Bury, Y. Cabibi, D. David, E. Losi, L. Montani, M. Pareja, M.J. Wendum, D. Wrba, F. Ziol, M. Thabut, D. Moussalli, J. Lebray, P. Rudler, M. Bismuth, F.I. Rosmorduc, O. Calmus, Y. Hartemann, A. Jacqueminet, S. Bruckert, E. Giral, P. Naveau, S. Perlemuter, G. Varsat, B. Mercadier, A. the FLIP Consortium the FibroFrance Group

Abstract

Background: Blood tests of liver injury are less well validated in non-alcoholic fatty liver disease (NAFLD) than in patients with chronic viral hepatitis. Aims: To improve the validation of three blood tests used in NAFLD patients, FibroTest for fibrosis staging, SteatoTest for steatosis grading and ActiTest for inflammation activity grading. Methods: We pre-included new NAFLD patients with biopsy and blood tests from a single-centre cohort (FibroFrance) and from the multicentre FLIP consortium. Contemporaneous biopsies were blindly assessed using the new steatosis, activity and fibrosis (SAF) score, which provides a reliable and reproducible diagnosis and grading/staging of the three elementary features of NAFLD (steatosis, inflammatory activity) and fibrosis with reduced interobserver variability. We used nonbinary-ROC (NonBinAUROC) as the main endpoint to prevent spectrum effect and multiple testing. Results: A total of 600 patients with reliable tests and biopsies were included. The mean NonBinAUROCs (95% CI) of tests were all significant (P < 0.0001): 0.878 (0.864–0.892) for FibroTest and fibrosis stages, 0.846 (0.830–0.862) for ActiTest and activity grades, and 0.822 (0.804–0.840) for SteatoTest and steatosis grades. FibroTest had a higher NonBinAUROC than BARD (0.836; 0.820–0.852; P = 0.0001), FIB4 (0.845; 0.829–0.861; P = 0.007) but not significantly different than the NAFLD score (0.866; 0.850–0.882; P = 0.26). FibroTest had a significant difference in median values between adjacent stage F2 and stage F1 contrarily to BARD, FIB4 and NAFLD scores (Bonferroni test P < 0.05). Conclusions: In patients with NAFLD, SteatoTest, ActiTest and FibroTest are non-invasive tests that offer an alternative to biopsy, and they correlate with the simple grading/staging of the SAF scoring system across the three elementary features of NAFLD: steatosis, inflammatory activity and fibrosis. © 2016 The Authors. Alimentary Pharmacology & Therapeutics published by John Wiley & Sons Ltd

Published
2016

2. Prognostic value of liver fibrosis biomarkers: A meta-analysis

Author

Poynard, Ngo, Y., Perazzo, H., Munteanu, M., Lebray, P., Moussalli, J., Thabut, D., Benhamou, Y., and Ratziu, V.

Subjects
Feature
Abstract

Aims and Methods: Several serum biomarkers such as FibroTest, aspartate transaminase-platelet ratio index (APRI), FIB-4, and liver stiffness measurement by FibroScan have been validated as alternatives to biopsy for the diagnosis of fibrosis in patients with chronic liver disease. This paper aims to assess the 5-year prognostic values of these biomarkers. A meta-analysis combined all published prognostic studies. Baseline biopsy and APRI data were used as references. Results: Only 3 biomarkers had several prognostic validations: FibroTest (4 studies; 2,396 patients), APRI (5 studies; 2,422 patients), and FIB-4 (3 studies; 1,184 patients). For the prediction of survival without liver-related death, the areas under the receiver operating characteristic curves (AUROCs) were 0.86 for biopsy (95% confidence interval [CI], 0.77–0.95), 0.88 for FibroTest (95% CI, 0.79–0.98), 0.73 for FIB-4 (95% CI, 0.62–0.85), and 0.66 for APRI (95% CI, 0.57–0.75). APRI had a significantly lower prognostic value versus biopsy, with a mean difference between AUROCs of –0.21 (95% CI, –0.33 to –0.10; P

3. Is antiviral treatment (IFN alpha and/or ribavirin) justified in cirrhosis related to hepatitis C virus? Société Royale Belge de Gastro-entérologie

Author

Poynard T, Moussalli J, Ratziu V, Thierry Thevenot, Regimbeau C, Opolon P, Horsmans Y, Brenard R, Closon M, Fevery J, and Hautekeete M

Subjects
Liver Cirrhosis, Male, Hepatitis C, Chronic, Antiviral Agents, Survival Analysis, Treatment Outcome, Belgium, Meta-Analysis as Topic, Practice Guidelines as Topic, Ribavirin, Humans, Drug Therapy, Combination, Female, Controlled Clinical Trials as Topic, Interferons, Randomized Controlled Trials as Topic
Abstract

To assess the benefit risk ratio of interferon and ribavirin in the treatment of patients with post hepatitis C cirrhosis we summarize the spontaneous over mortality of this disease, and made an overview of the randomized trials and of other controlled studies.In comparison to controls, patients with post hepatitis C cirrhosis have a 17 fold increase risk of dying from a liver disease that a control population, and a 6 fold increase from primary liver cancer. In France the hepatitis C epidemic which start in the sixties explains now the observed dramatic increase in mortality by primary liver cancer, both in men and women. Meta-analysis of randomized trials and controlled retrospective studies showed that interferon treatment is associated with a significant increase in ALT response at the end of the treatment, with a decrease in hepatocellular incidence as well as a decrease in mortality in comparison with controls. Very few data are published concerning ribavirin alone or in combination with interferon in patients with cirrhosis. Preliminary data suggest that this combination during 48 weeks permit to obtain in patients with compensated cirrhosis 20% of sustained virological response. The safety was acceptable but patients with low initial blood cells count must be carefully followed. In conclusion this overview clearly demonstrates a benefit-risk ratio in favor of treatment in patients with post hepatitis C cirrhosis by interferon.

6. Acute hepatitis during hypersensitivity syndrome due to midecamycin

Author

Thevenot, T., Philippe Mathurin, Martinez, F., Moussalli, J., Poynard, T., Opolon, P., and Chosidow, O.

Subjects
Drug Hypersensitivity, Male, Liver Function Tests, Biopsy, Acute Disease, Humans, Macrolides, Chemical and Drug Induced Liver Injury, Middle Aged, Leucomycins
Abstract

We report here the first case of symptomatic acute hepatic injury due to midecamycin in a 58-year-old man. The clinical picture was compatible with a hypersensitivity syndrome with cutaneous, renal and hepatic involvement. Liver eosinophil polynuclear infiltrate, hypereosinophilia and acute interstitial nephritis were consistent with the hypothesis of an immunoallergic mechanism.

8. Identification of an Endoglin Variant Associated With HCV-Related Liver Fibrosis Progression by Next-Generation Sequencing

Author

Frédégonde About, Stéphanie Bibert, Emmanuelle Jouanguy, Bertrand Nalpas, Lazaro Lorenzo, Vimel Rattina, Mohammed Zarhrate, Sylvain Hanein, Mona Munteanu, Beat Müllhaupt, David Semela, Nasser Semmo, Jean-Laurent Casanova, Ioannis Theodorou, Philippe Sultanik, Thierry Poynard, Stanislas Pol, Pierre-Yves Bochud, Aurélie Cobat, Laurent Abel, The Swiss Hepatitis C Cohort Study Group, The French ANRS HC EP 26 Genoscan Study Group, Francesco Negro, Antoine Hadengue, Laurent Kaiser, Laura Rubbia-Brandt, Darius Moradpour, Cristina Cellerai, Martin Rickenbach, Andreas Cerny, Gladys Martinetti, Jean-François Dufour, Meri Gorgievski, Virginie Masserey Spicher, Markus Heim, Hans Hirsch, Beat Helbling, Stephan Regenass, Raffaele Malinverni, Guenter Dollenmaier, Gieri Cathomas, University of Zurich, Cobat, Aurélie, Negro, Francesco, Hadengue, Antoine, Kaiser, Laurent, Rubbia-Brandt, Laura, Swiss Hepatitis C Cohort Study Group, French ANRS HC EP 26 Genoscan Study Group, Negro, F., Hadengue, A., Kaiser, L., Rubbia-Brandt, L., Moradpour, D., Cellerai, C., Rickenbach, M., Cerny, A., Martinetti, G., Dufour, J.F., Gorgievski, M., Spicher, V.M., Heim, M., Hirsch, H., Helbling, B., Regenass, S., Malinverni, R., Dollenmaier, G., Cathomas, G., Bousquet, L., Ngo, Y., Lebray, P., Moussalli, J., Benhamou, Y., Thabut, D., Vallet-Pichard, A., Fontaine, H., Mallet, V., Sogni, P., Trabut, J.B., Bourlière, M., Delfraissy, J.F., Imagine - Institut des maladies génétiques (IMAGINE - U1163), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Infectious Disease Service, Department of Internal Medicine, Université de Lausanne = University of Lausanne (UNIL), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Descartes - Paris 5 (UPD5), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Université de Montpellier (UM), Hôpital Universitaire de Réadaptation, de Rééducation et d'Addictologie du CHU de Nîmes [Grau-du-Roi] (CHU Nîmes), BioPredictive [Paris], University hospital of Zurich [Zurich], University of Bern, Bern University Hospital [Berne] (Inselspital), Laboratory of Human Genetics of Infectious Diseases (Necker Branch - INSERM U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Rockefeller University [New York], Centre d'Immunologie et des Maladies Infectieuses (CIMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie du système immunitaire (Inserm U1223), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Research Unit on Cardiovascular and Metabolic Diseases (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut de Cardiométabolisme et Nutrition = Institute of Cardiometabolism and Nutrition [CHU Pitié Salpêtrière] (IHU ICAN), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Hospitalier Universitaire Vaudois [Lausanne] (CHUV), and Génétique Humaine des Maladies Infectieuses (Inserm U980)

Subjects
0301 basic medicine, 2716 Genetics (clinical), lcsh:QH426-470, rare-variant association study, [SDV]Life Sciences [q-bio], 610 Medicine & health, ddc:616.07, Virus, 03 medical and health sciences, 0302 clinical medicine, 1311 Genetics, Fibrosis, TGF beta signaling pathway, Genetics, Medicine, HCV-related liver fibrosis, TGF-beta, endoglin, exome sequencing, Exome, Genetics (clinical), Exome sequencing, Genetic association, ddc:616, business.industry, Odds ratio, Brief Research Report, Endoglin, medicine.disease, 3. Good health, lcsh:Genetics, 030104 developmental biology, 10219 Clinic for Gastroenterology and Hepatology, 030220 oncology & carcinogenesis, 1313 Molecular Medicine, Immunology, Molecular Medicine, business
Abstract

International audience; Despite the astonishing progress in treating chronic hepatitis C virus (HCV) infection with direct-acting antiviral agents, liver fibrosis remains a major health concern in HCV infected patients, in particular due to the treatment cost and insufficient HCV screening in many countries. Only a fraction of patients with chronic HCV infection develop liver fibrosis. While there is evidence that host genetic factors are involved in the development of liver fibrosis, the common variants identified so far, in particular by genome-wide association studies, were found to have limited effects. Here, we conducted an exome association study in 88 highly selected HCV-infected patients with and without fibrosis. A strategy focusing on TGF-β pathway genes revealed an enrichment in rare variants of the endoglin gene (ENG) in fibrosis patients. Replication studies in additional cohorts (617 patients) identified one specific ENG variant, Thr5Met, with an overall odds ratio for fibrosis development in carriers of 3.04 (1.39-6.69). Our results suggest that endoglin, a key player in TGF-β signaling, is involved in HCV-related liver fibrogenesis.

Published
2019

9. Genome-Wide Association Study Identifies Variants Associated With Progression of Liver Fibrosis From HCV Infection

Author

Thierry Poynard, Beat Müllhaupt, Jean-Laurent Casanova, Stanislas Pol, Ioannis Theodorou, Zoltán Kutalik, Andrew H. Talal, Mona Munteanu, Raffaele Malinverni, Philippe Halfon, Pierre-Yves Bochud, Darius Moradpour, Markus H. Heim, Francesco Negro, Ira M. Jacobson, Charles M. Rice, Stéphanie Bibert, Bertrand Nalpas, Christian Bréchot, Jacob George, Laurence Bousquet, Etienne Patin, Laurent Abel, Hans H. Hirsch, Gladys Martinetti, Vijayaprakash Suppiah, Jean-François Dufour, Graeme J. Stewart, Andreas Cerny, Anne Boland, Julien Guergnon, David Semela, David R. Booth, Marc Bourlière, Emmanuelle Jouanguy, Laurent Argiro, Human genetics of infectious diseases: Complex predisposition (Equipe Inserm U1163), Imagine - Institut des maladies génétiques (IMAGINE - U1163), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller University [New York], Department of Medical Genetics, Université de Lausanne = University of Lausanne (UNIL), Université Pierre et Marie Curie - Paris 6 - UFR de Médecine Pierre et Marie Curie (UPMC), Université Pierre et Marie Curie - Paris 6 (UPMC), Infectious Disease Service, Department of Internal Medicine, Service d'hépatologie médicale [CHU Cochin], Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Génétique Humaine des Maladies Infectieuses (Inserm U980), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Biopredictive, Université Paris Descartes - Paris 5 (UPD5), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Génétique et immunologie des maladies parasitaires (GIMP), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Médecine générale, Assistance Publique - Hôpitaux de Marseille (APHM)-Hôpital Européen [Fondation Ambroise Paré - Marseille], Institut de Biologie François JACOB (JACOB), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), University hospital of Zurich [Zurich], University of Bern, Division of Gastroenterology and Hepatology, Institut für Medizinischediagnostik, Mikrobiologie, University of Bassel, School of Life Sciences, University of Technology Sydney (UTS), Pathogénèse et traitement de l'hépatite fulminante et du cancer du foie, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Weill Medical College of Cornell University [New York], Service d'hépatologie et de gastroentérologie [Hôpital Saint-Joseph - Marseille], Aix Marseille Université (AMU)-Hôpital Saint-Joseph [Marseille], Immunité et Infection, IFR113-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université de Lausanne (UNIL), University Hospital and University of Lausanne, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR113-Sorbonne Université (SU), Service d'Hépato-Gastro-Entérologie [CHU Pitié-Salpêtrière], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Swiss Hepatitis C Cohort Study Group, International Hepatitis C Genetics Consortium, French ANRS HC EP 26 Genoscan Study Group, Negro, F., Hadengue, A., Kaiser, L., Rubbia-Brandt, L., Moradpour, D., Cellerai, C., Rickenbach, M., Cerny, A., Martinetti, G., Dufour, J.F., Gorgievski, M., Masserey Spicher, V., Heim, M., Hirsch, H., Müllhaupt, B., Helbling, B., Regenass, S., Malinverni, R., Semela, D., Dollenmaier, G., Cathomas, G., Suppiah, V., Berg, T., Weltman, M., Abate, M.L., Spengler, U., Bassendine, M., Dore, G.J., Irving, W.L., Powell, E., Riordan, S., Ahlenstiehl, G., Stewart, G., Booth, D.R., George, J., Nalpas, B., Abel, L., Monteanu, M., Bousquet, L., Ngo, Y., Lebray, P., Moussalli, J., Benhamou, Y., Thabut, D., Vallet-Pichard, A., Fontaine, H., Mallet, V., Sogni, P., Trabut, J.B., Bourlière, M., Theodorou, I., Delfraissy, J.F., Poynard, T., Pol, S., Suppiah, Vijayaprakash, Patin, Etienne, Kutalik, Zoltan, Geurgnon, Julien, Bibert, Stephanie, and Laurent, Abel

Subjects
Liver Cirrhosis, Male, Hepatitis C, Chronic/complications/virology, Genome-wide association study, Apoptosis, genetic analysis, Hepacivirus, ddc:616.07, Liver disease, 0302 clinical medicine, Fibrosis, Risk Factors, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Apoptosis/genetics, risk factors, ddc:616, 0303 health sciences, Liver Disease, Gastroenterology, virus diseases, Genetic Analysis, Hepatitis C, 3. Good health, Phenotype, Cirrhosis, Disease Progression, 030211 gastroenterology & hepatology, Female, liver disease, Viral hepatitis, Adult, Genotype, Eye Proteins/genetics, Genome-Wide Association Study, Hepatitis C, Chronic/complications, Hepatitis C, Chronic/virology, Humans, Lipase/genetics, Liver Cirrhosis/genetics, Liver Cirrhosis/virology, Logistic Models, Membrane Proteins/genetics, Polymorphism, Single Nucleotide, Proportional Hazards Models, Proto-Oncogene Proteins/genetics, Receptor Protein-Tyrosine Kinases/genetics, Ubiquitin-Protein Ligases/genetics, Young Adult, Ubiquitin-Protein Ligases, Single-nucleotide polymorphism, C-Mer Tyrosine Kinase, Biology, Article, 03 medical and health sciences, Proto-Oncogene Proteins, medicine, SNP, Eye Proteins, 030304 developmental biology, Hepatology, c-Mer Tyrosine Kinase, cirrhosis, Membrane Proteins, Receptor Protein-Tyrosine Kinases, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Lipase, Hepatitis C, Chronic, medicine.disease, Liver Cirrhosis/genetics/virology, digestive system diseases, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, Immunology
Abstract

BACKGROUND AIMS: Polymorphisms in IL28B were shown to affect clearance of hepatitis C virus (HCV) infection in genome wide association (GWA) studies. Only a fraction of patients with chronic HCV infection develop liver fibrosis a process that might also be affected by genetic factors. We performed a 2 stage GWA study of liver fibrosis progression related to HCV infection. METHODS: We studied well characterized HCV infected patients of European descent who underwent liver biopsies before treatment. We defined various liver fibrosis phenotypes on the basis of METAVIR scores with and without taking the duration of HCV infection into account. Our GWA analyses were conducted on a filtered primary cohort of 1161 patients using 780650 single nucleotide polymorphisms (SNPs). We genotyped 96 SNPs with P values

Published
2012

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