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1. Effects of Age on Treatment of Chronic Hepatitis C with Direct Acting Antivirals

Author

Alexandre Pariente, Jean-Pierre Arpurt, Andre-Jean Remy, Isabelle Rosa-Hezode, Xavier Causse, Frederic Heluwaert, Gilles Macaigne, Jean Henrion, Christophe Renou, Matthieu Schnee, Hatem Salloum, Severine Hommel, Christophe Pilette, Ramuntxo Arotcarena, Georges Barjonet, Hortensia Lison, Frangois Bourhis, Vincent Jouannaud, Arnaud Pauwels, Yann Le-Bricquir, Edmond Geagea, Bertrand Condat, Marie-Pierre Ripault, David Zanditenas, Stephanie de Montigny-Lenhardt, Helene Labadie, Bertrand Tissot, Eric Maringe, Jean-Frangois Cadranel, Herve Hagege, and Bruno Lesgourgues

Subjects
Sustained Virological Response, Hospitals, General, Comorbidities, Prospective, Patients-reported outcomes, Specialties of internal medicine, RC581-951
Abstract

Introduction and aim: Data on the efficacy and tolerance of interferon-free treatment in chronic hepatitis C (CHC) in elderly patients are limited in phase II-III trials. Material and methods: A prospective cohort of adult patients with CHC treated in French general hospitals. Results: Data from 1,123 patients, distributed into four age groups, were analyzed. Of these, 278 were > 64 years old (fourth quartile) and 133 were > 73 years old (tenth decile). Elderly patients weighed less, were more frequently treatment-experienced women infected with genotype 1b or 2, while they less frequently had genotype 3 or HIV coinfection, but had more frequent comorbidities and drug consumption. Half of the patients had cirrhosis, whatever their ages. The main treatment regimens were sofosbuvir/ledipasvir (37.8%), sofosbuvir/daclatasvir (31.8%), sofosbuvir/simeprevir (16.9%), sofosbuvir/ribavirin (7.8%); ribavirin was given to 24% of patients. The overall sustained virological response (SVR) rate was 91.0 % (95% CI: 89.292.5%) with no difference according to age. Logistic regression of the independent predictors of SVR were albumin, hepatocellular carcinoma and treatment regimen, but not age. The rate of severe adverse events (66 in 59/1062 [5.6%] patients) tended to be greater in patients older than 64 years of age (21/261,8.1%), but the only independent predictors of SAE by logistic regression were cirrhosis and baseline hemoglobin. Patient-reported overall tolerance was excellent in all age groups, and patient-reported fatigue decreased during and after treatment, independent of age. Conclusions: The high efficacy and tolerance of interferon-free regimens is confirmed in elderly patients in real-life conditions.

Published
2019
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2. The PRSS3P2 and TRY7 deletion copy number variant modifies risk for chronic pancreatitis

Author

Emmanuelle Masson, Maren Ewers, Sumit Paliwal, Kiyoshi Kume, Virginie Scotet, David N. Cooper, Vinciane Rebours, Louis Buscail, Karen Rouault, Amandine Abrantes, Lina Aguilera Munoz, Jérémie Albouys, Laurent Alric, Xavier Amiot, Isabelle Archambeaud, Solène Audiau, Laetitia Bastide, Julien Baudon, Guy Bellaiche, Serge Bellon, Valérie Bertrand, Karine Bideau, Kareen Billiemaz, Claire Billioud, Sabine Bonnefoy, Corinne Borderon, Barbara Bournet, Estelle Breton, Mathias Brugel, Guillaume Cadiot, Marine Camus, Marine Carpentier-Pourquier, Patrick Chamouard, Ulriikka Chaput, Jian-Min Chen, Franck Cholet, Dragos Marius Ciocan, Christine Clavel, Benoit Coffin, Laura Coimet-Berger, Simona Cosconea, Isabelle Creveaux, Adrian Culetto, Oussama Daboussi, Louis De Mestier, Thibault Degand, Christelle D'engremont, Bernard Denis, Solène Dermine, null Desgrippes, Augustin Drouet D'Aubigny, Raphaël Enaud, Alexandre Fabre, Claude Férec, Dany Gargot, Eve Gelsi, Elena Gentilcore, Rodica Gincul, Emmanuelle Ginglinger-Favre, Marc Giovannini, Cécile Gomercic, Hannah Gondran, Thomas Grainville, Philippe Grandval, Denis Grasset, Stéphane Grimaldi, Sylvie Grimbert, Hervé Hagege, Sophie Heissat, Olivia Hentic, Anne Herber-Mayne, Marc Hervouet, Solene Hoibian, Jérémie Jacques, Bénédicte Jais, Mehdi Kaassis, Stéphane Koch, Elodie Lacaze, Joël Lacroute, Thierry Lamireau, Lucie Laurent, Xavier Le Guillou, Marc Le Rhun, Sarah Leblanc, Philippe Levy, Astrid Lievre, Diane Lorenzo, Frédérique Maire, Kévin Marcel, Jacques Mauillon, Stéphanie Morgant, Driffa Moussata, Nelly Muller, Sophie Nambot, Bertrand Napoleon, Anne Olivier, Maël Pagenault, Anne-laure Pelletier, Olivier Pennec, Fabien Pinard, Mathieu Pioche, Bénédicte Prost, Lucille Queneherve, Noemi Reboux, Samia Rekik, Ghassan Riachi, Barbara Rohmer, Bertrand Roquelaure, Isabelle Rosa Hezode, Florian Rostain, Jean-Christophe Saurin, Laure Servais, Roxana Stan-Iuga, Clément Subtil, Jérémy Tanneche, Charles Texier, Lucie Thomassin, David Tougeron, Lucine Vuitton, Timothée Wallenhorst, Marc Wangerme, Hélène Zanaldi, Frank Zerbib, Seema Bhaskar, Kazuhiro Kikuta, G Venkat Rao, Shin Hamada, D Nageshwar Reddy, Atsushi Masamune, Giriraj Ratan Chandak, and Heiko Witt

Subjects
Hepatology, Endocrinology, Diabetes and Metabolism, Gastroenterology
Abstract

PRSS1 and PRSS2 constitute the only functional copies of a tandemly-arranged five-trypsinogen-gene cluster (i.e., PRSS1, PRSS3P1, PRSS3P2, TRY7 and PRSS2) on chromosome 7q35. Variants in PRSS1 and PRSS2, including missense and copy number variants (CNVs), have been reported to predispose to or protect against chronic pancreatitis (CP). We wondered whether a common trypsinogen pseudogene deletion CNV (that removes two of the three trypsinogen pseudogenes, PRSS3P2 and TRY7) might be associated with CP causation/predisposition.We analyzed the common PRSS3P2 and TRY7 deletion CNV in a total of 1536 CP patients and 3506 controls from France, Germany, India and Japan by means of quantitative fluorescent multiplex polymerase chain reaction.We demonstrated that the deletion CNV variant was associated with a protective effect against CP in the French, German and Japanese cohorts whilst a trend toward the same association was noted in the Indian cohort. Meta-analysis under a dominant model yielded a pooled odds ratio (OR) of 0.68 (95% confidence interval (CI) 0.52-0.89; p = 0.005) whereas an allele-based meta-analysis yielded a pooled OR of 0.84 (95% CI 0.77-0.92; p = 0.0001). This protective effect is explicable by reference to the recent finding that the still functional PRSS3P2/TRY7 pseudogene enhancers upregulate pancreatic PRSS2 expression.The common PRSS3P2 and TRY7 deletion CNV was associated with a reduced risk for CP. This finding provides additional support for the emerging view that dysregulated PRSS2 expression represents a discrete mechanism underlying CP predisposition or protection.

Published
2023
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3. Combination of fibrates with obeticholic acid is able to normalise biochemical liver tests in patients with difficult-to-treat primary biliary cholangitis

Author

Pietro Invernizzi, Dominique Larrey, Thomas Berg, Christine Silvain, Christina Weiler-Normann, Rodolphe Anty, Cervoni Jp, Albert Parés, Cynthia Levy, Olivier Chazouillères, Laurent Lam, Christophe Bureau, Isabelle Rosa-Hezode, Palak J. Trivedi, Christoph Schramm, Nora Cazzagon, Laurent Alric, Vincent Leroy, Alexandra Heurgué, Frederik Nevens, Jérôme Dumortier, Pierre Antoine Soret, Olivier Roux, Marco Carbone, Fabrice Carrat, Pascal Potier, Lena Smets, Christophe Corpechot, Gestionnaire, Hal Sorbonne Université, Centre de Référence des Maladies Rares - Maladies Inflammatoires des Voies Biliaires et Service d’Hépatologie [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Centre de Recherche Saint-Antoine (CRSA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Service de santé publique [CHU Saint-Antoine], University Hospitals Leuven [Leuven], Leipzig University, Università degli Studi di Milano-Bicocca = University of Milano-Bicocca (UNIMIB), Centre Hospitalier Universitaire [Grenoble] (CHU), University Hospitals Birmingham [Birmingham, Royaume-Uni], Azienda Ospedale Università di Padova = Hospital-University of Padua (AOUP), University Hospital Hamburg-Eppendorf, Universitaetsklinikum Hamburg-Eppendorf = University Medical Center Hamburg-Eppendorf [Hamburg] (UKE), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées, Centre Hospitalier Intercommunal de Créteil (CHIC), Centre Hospitalier Universitaire de Reims (CHU Reims), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Hôpital Edouard Herriot [CHU - HCL], Hospices Civils de Lyon (HCL), Centre Hospitalier Régional d'Orléans (CHRO), Centre de référence des Maladies Vasculaires du Foie [Paris] (FILFOIE), Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre hospitalier universitaire de Poitiers (CHU Poitiers), Centre Hospitalier Universitaire de Nice (CHU Nice), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), University of Miami Leonard M. Miller School of Medicine (UMMSM), Clinic Barcelona Hospital Universitari, Soret, P, Lam, L, Carrat, F, Smets, L, Berg, T, Carbone, M, Invernizzi, P, Leroy, V, Trivedi, P, Cazzagon, N, Weiler-Normann, C, Alric, L, Rosa-Hezode, I, Heurgue, A, Cervoni, J, Dumortier, J, Potier, P, Roux, O, Silvain, C, Bureau, C, Anty, R, Larrey, D, Levy, C, Pares, A, Schramm, C, Nevens, F, Chazouilleres, O, and Corpechot, C

Subjects
Liver Cirrhosis, medicine.medical_specialty, Cholagogues and Choleretics, Bilirubin, [SDV]Life Sciences [q-bio], Chenodeoxycholic Acid, Gastroenterology, chemistry.chemical_compound, Retrospective Studie, Internal medicine, Chenodeoxycholic acid, medicine, Humans, Pharmacology (medical), Cholagogues and Choleretic, ComputingMilieux_MISCELLANEOUS, Retrospective Studies, Bezafibrate, Fenofibrate, Hepatology, Liver Cirrhosis, Biliary, business.industry, Fibric Acids, Ursodeoxycholic Acid, Biliary, Obeticholic acid, Retrospective cohort study, Odds ratio, eye diseases, Ursodeoxycholic acid, Fibric Acid, [SDV] Life Sciences [q-bio], chemistry, business, Human, medicine.drug
Abstract

Background: Obeticholic acid (OCA) and fibrates are second-line therapies for patients with primary biliary cholangitis (PBC) with an inadequate response to ursodeoxycholic acid (UDCA). Aim: To know whether OCA and fibrates, administered together in combination with UDCA, have additive beneficial effects in patients with difficult-to-treat PBC. Methods: PBC patients treated for ≥3months with UDCA, OCA and fibrates (bezafibrate or fenofibrate) due to failure of either second-line therapy were included in a multicentre, uncontrolled retrospective cohort study. Changes in biochemical liver tests and pruritus were analysed using a generalised linear mixed-effect model. Results: Among 58 patients included, half received OCA as second-line and fibrates as third-line therapy (Group OCA-Fibrate), while the other half had the inverse therapeutic sequence (Group Fibrate-OCA). The mean duration of triple therapy was 11months (range 3-26). Compared to dual therapy, triple therapy was associated with a significant gain in alkaline phosphatase (ALP) reduction: 22% per first year (95% CI 12%-31%), an effect that was stronger in OCA-Fibrate than in Fibrate-OCA group. Triple therapy was associated with a 3.4 (95% CI 1.4-8.2) odds ratio (OR) of reaching normal ALP and with a significant decrease in gamma-glutamyl transpeptidase (GGT), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin. The ORs of achieving the Paris-2 and Toronto criteria of adequate biochemical response were 6.8 (95% CI 2.8-16.7) and 9.2 (95% CI 3.4-25.1) respectively. Finally, triple therapy significantly improved pruritus in OCA-Fibrate but not in Fibrate-OCA group. Conclusions: Triple therapy with UDCA, OCA and fibrates is able to normalise biochemical liver tests and improve pruritus in patients with difficult-to-treat PBC.

Published
2021
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4. [Chronic abdominal pain due to bowel ischemia in a patient with Leiden factor V mutation]

Author

Ariane, Chryssostalis, Hervé, Hagège, Isabelle, Rosa-Hezode, Philippe, Cattan, Isabelle, De Lacroix-Szmania, Patrick, Cabanis, Nazanin, Bayani, Issam, Abd Alsamad, and Michel, Chousterman

Subjects
Adult, Intestinal Diseases, Ischemia, Anticoagulants, Factor V, Humans, Point Mutation, Female, Abdominal Pain, Activated Protein C Resistance
Abstract

Leiden Factor V mutation, associated with resistance to activated protein C, is a prothrombotic state found in 20% of the patients with a first episode of deep-vein thrombosis. We report the case of a 30-Year-old woman with a history of intermittent abdominal pain who developed small bowel infarction requiring extensive small bowel resection. Biological search for prothrombotic disorder showed resistance to activated protein C due to homozygosity for the factor V Leiden mutation. Long-term anticoagulant therapy was initiated. Unexplained abdominal pain may be due to venous mesenteric ischemia, which can be associated with factor V Leiden mutation.

Published
2004

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