Thrombose de la veine porte révélant une hyperhomocystéinémie (revue de la littérature à propos de 2 observations)

La thrombose de la veine porte, souvent d origine multifactorielle, peut résulter de facteurs locaux ou généraux. Parmi eux, les affections prothrombotiques générales occupent une place importante, de par leur fréquence et leur conséquence sur la prise en charge thérapeutique. Les conclusions discordantes des études sur l hyperhomocystéinémie, un de ses états thrombogènes, ne permettent pas d établir son rôle certain dans la thrombose de la veine porte. L hyperhomocystéinémie, d origine génétique ou acquise, apparait comme un facteur de risque modéré de thrombose veineuse à l inverse de la mutation MTHFR C677T, non considérée comme tel. Aucune étude n a démontré de réduction du risque de récidive thrombotique chez les patients bénéficiant d une supplémentation vitaminique abaissant l homocystéinémie. Le traitement de la thrombose de la veine porte associera le traitement anticoagulant et la prévention primaire et secondaire des hémorragies digestives dues à l hypertension portale.TOULOUSE3-BU Santé-Centrale (315552105) / SudocSudocFranceF

Modélisation des différentes techniques chirurgicales.

National audienc

Plasma hypercoagulability in the presence of thrombomodulin but not of activated protein C in patients with cirrhosis

Plasma hypercoagulability in the presence of thrombomodulin but not of activated protein C in patients with cirrhosi

Assessment of Malnutrition, Sarcopenia and Frailty in Patients with Cirrhosis: Which Tools Should We Use in Clinical Practice?

This article belongs to the Special Issue Nutrition in Liver Cirrhosis and Liver TransplantationMalnutrition is a common comorbidity in patients with cirrhosis. Its prognostic value is indisputable as it greatly affects the evolution of liver diseases. It has a major impact on both morbi-mortality before and after liver transplantation. Being now integrated in the definition of malnutrition and recognized as a new entity in the international classification of diseases, physicians have taken great interest in sarcopenia. Its negative consequences on the fate of patients with cirrhosis are well-demonstrated. The concept of frailty has recently been enlarged to chronic liver diseases as symptoms of impaired global physical functioning. In this article, we will discuss the definitions of malnutrition and emphasize its links with sarcopenia and frailty. We will show the relevance of frailty and sarcopenia in the course of liver diseases. The emerging role of muscle depletion on the cardiorespiratory system will also be highlighted. The importance of body composition will be demonstrated and the main tools reviewed. Finally, we adapted the definition of malnutrition to patients with cirrhosis based on the assessment of sarcopenia together with reduced food intakes

3D Digital Model of the Pelvic System for Better Understanding of Anatomical Theories of Pelvic Organ Support.

International audienc

Pathophysiological aspects of cystocele with a 3D finite elements model

International audienc

Intraindividual variability over time of thrombin generation in patients with cirrhosis

International audienceBackground: Patients with cirrhosis are at high risk of thrombotic events, including portal vein thrombosis and venous thromboembolism. In such patients, hypercoagula-bility is not detected by conventional coagulation tests, but only by the thrombin generation assay (TGA) that integrates the role of pro-and anticoagulant factors. However, TGA use to predict clinical events depends on thrombin generation vari-ability over time.Objectives: The aim of this study was to compare TGA intraindividual variability over time in patients with cirrhosis and in healthy controls. Methods: Blood samples were prospectively collected from 34 healthy controls and 52 patients with cirrhosis at week 0 (inclusion), 6, and 12. TGA was performed with the calibrated automated thrombogram method, tissue factor (5 pM), phospholipids, and with and without thrombomodulin (4 nM) or activated protein C (1 nM). Results: When TGA was performed with thrombomodulin, endogenous thrombin po-tential in patients with cirrhosis was higher compared with controls and increased with cirrhosis severity. Stability over time of all thrombin generation parameters was excellent in healthy controls, good in Child-Turcotte-Pugh (CTP)-A patients, and poor in CTP-B/C patients (severe cirrhosis). In CTP-B/C patients, the phenotype was more variable because one-third of patients switched to normal or hypercoagulability during the 3-month follow-up.Conclusion: A study with longer monitoring is needed to correlate the hypercoagulable phenotype of patients with cirrhosis with the occurrence of thrombotic events

Natural History of Recurrent Alcohol‐Related Cirrhosis After Liver Transplantation: Fast and Furious

International audienceAlcohol-related liver disease (ALD) is one of the main indications for liver transplantation (LT). Severe alcohol relapse can rapidly lead to recurrent alcohol-related cirrhosis (RAC) for the graft. The aim of this study was to describe the natural history of RAC and the overall survival after LT and after an RAC diagnosis. From 1992 to 2012, 812 patients underwent primary LT for ALD in 5 French transplant centers. All patients with severe alcohol relapse and an RAC diagnosis on the graft were included. The diagnosis of cirrhosis was based on the analysis of liver biopsy or on the association of clinical, biological, radiological, and/or endoscopic features of cirrhosis. RAC was diagnosed in 57/162 patients (35.2%) with severe alcohol relapse, and 31 (54.4%) of those patients had at least 1 episode of liver decompensation. The main types of decompensation were ascites (70.9%), jaundice (58.0%), and hepatic encephalopathy (9.6%). The cumulative probability of decompensation was 23.8% at 5 years, 50.1% at 10 years, and 69.9% at 15 years after LT. During the follow-up, 36 (63.2%) patients died, the main cause of death being liver failure (61.1%). After diagnosis of cirrhosis, the survival rate was 66.3% at 1 year, 37.8% at 5 years, and 20.6% at 10 years. In conclusion, RAC is associated with a high risk of liver decompensation and a poor prognosis. Prevention of severe alcohol relapse after LT is a major goal to improve patient survival

Specificities of Hepatocellular Carcinoma Developed on Non Alcoholic Fatty Liver Disease in Absence of Cirrhosis Revealed by Tissue 1H-NMR Spectroscopy

SESSION 6 - CANCER-RELATED MALNUTRITION, METABOLISM, DYSIMMUNITYBackground and aims:Epidemiologic studies suggest that NAFLD increases the risk of Hepato-Cellular Carcinoma (HCC),even in non-cirrhotic NAFLD. This underlying disease is reported in up to 40% HCC.To get insights into the biology of HCC in non-cirrhotic NAFLD and seek for putative cancer pathways, we performed metabolomics in HCC associated with cirrhosis and non-cirrhotic NAFLD.Methods:Metabolomics was performed using 1H-NMR Spectroscopy. The analysis included 28 pairs of HCC tissue and distant Non-Involved Tissue (NIT) collected from patients undergoing hepatectomy. HCC was associated with cirrhosis (n = 9), normal liver (n=6) or NAFLD (n = 13).Results:In HCC versus NIT, statistical analyses showed high level of lactate and phosphocholine and low level of glucose. Multivariate analysis of HCC groups showed increased level of β-hydroxybutyrate in HCC-Cirrhosis and increased level of glutamine in HCC-NAFLD. OPLS-DA models of HCC-cirrhosis vs NIT (either normal tissue or cirrhosis) and HCC-NAFLD vs NIT (either normal tissue or NAFLD) were constructed before comparing them in shared and unique structure (SUS) plots. From SUS-plots, HCC-Cirrhosis was characterized by high levels of β-hydroxybutyrate, tyrosine and phenylalanine, whereas HCC-NAFLD was characterized by high levels of glutamine/glutamate. Glutamine Synthetase (GS) immuno-staining was correlated with the NMR-spectroscopy glutamine quantification.Conclusion:This study provides evidence of metabolic specificities of HCC associated with non-cirrhotic NAFLD versus HCC associated with cirrhosis. These alterations could suggest activation of glutamine synthetase pathway in HCC-NAFLD and mitochondrial dysfunction in HCC-cirrhosis, that may be part of specific carcinogenic processe