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Academic literature on the topic 'Maladie du foie liée à l’alcool'
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Journal articles on the topic "Maladie du foie liée à l’alcool"
Émile, Carole. "Stéatoses hépatiques métaboliques et maladies du foie liées à l’alcool." Option/Bio 32, no. 631-632 (April 2021): 18–20. http://dx.doi.org/10.1016/s0992-5945(21)00076-3.
Full textGuglielmi, Stefano, Diana Ollo, Nicolas Goossens, and Laurent Spahr. "Maladie hépatique liée à l’alcool : nouvelles recommandations européennes de prise en charge." Revue Médicale Suisse 14, no. 616 (2018): 1500–1505. http://dx.doi.org/10.53738/revmed.2018.14.616.1500.
Full textPélisse-Jamet, Claude. "Hépatite de Rubarth et CIVD chez un chiot." Le Nouveau Praticien Vétérinaire canine & féline 18, no. 80 (2021): 61–63. http://dx.doi.org/10.1051/npvcafe/80061.
Full textBrousse, G. "Le plaisir n’est-il que dans le gène : où en sommes-nous de l’interaction gène-individu-environnement dans les addictions ?" European Psychiatry 30, S2 (November 2015): S13. http://dx.doi.org/10.1016/j.eurpsy.2015.09.043.
Full textHilal, Fahd, Jérôme Jeanblanc, and Mickaël Naassila. "Intérêt et mécanismes d’action de la kétamine dans le traitement de l’addiction à l’alcool – Revue des études cliniques et précliniques." Biologie Aujourd’hui 217, no. 3-4 (2023): 161–82. http://dx.doi.org/10.1051/jbio/2023028.
Full textThéron, Alexandre, Anne-Charlotte Teyssier, Aziz Abgaou, and Anne Sirvent. "Les complications de la greffe de cellules souches hématopoïétiques chez l'enfant." Médecine Intensive Réanimation, November 22, 2023. http://dx.doi.org/10.37051/mir-00188.
Full textDissertations / Theses on the topic "Maladie du foie liée à l’alcool"
Ntandja, Wandji Line Carolle. "Caractérisation de la fibrose dans l'hépatite alcoolique et décryptage des mécanismes liant cette fibrose au défaut du compartiment hépatocytaire." Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS024.
Full textBackground and Aims: Therapeutic options available in alcohol-related hepatitis (AH) remain limited and are mainly based on steroids. Unfortunately, steroids only improve short-term survival and almost 40% of patients do not respond to steroids. In the latter case, only early liver transplantation, offered in selected patients, can improve patient survival. However, in the context of graft shortage, the development of new drugs is urgent, and this requires a better understanding of the pathophysiology of AH. Our team identified in patients with severe AH a profound defect in liver regeneration partly related to an overactivation of YAP in the hepatocytes of these patients. Furthermore, our team also observed a different composition of the extracellular matrix (ECM) in the livers of patients with AH (compared to that of patients with alcohol-related cirrhosis), with an enrichment of the latter in laminin. The therapeutic axis focusing on fibrosis seems to be an interesting option since the degree of fibrosis is a key prognostic factor in these patients. In addition, the alteration of innate and acquired immunityin patients with AH is associated with an increased risk of infection, which impacts their survival. The objectives of this thesis were to identify new strategies to improve the outcome of patients with AH. Using a fundamental approach, we aimed to identify new therapeutic targets by focusing in particular on fibrogenesis in AH and its potential link with altered hepatocytes. Using a clinical approach, we aimed to improve the detection and management of infections (pneumopathy) in patients with severe AH. Method: Using livers from patients transplanted for severe AH not responding to steroids (n=22) or for decompensated alcohol-related cirrhosis without AH (Cirrh, n=24), we evaluated the distribution of fibrosis and YAP by immunostaining. We also assessed the composition of the extracellular matrix (ECM) by proteomic analysis (bulk and spatial proteomics) and RTPCR. We also developed liver organoids (which preserve the phenotypic characteristics of native livers) from the livers of patients with AH or Cirrh. The latter were cocultured with human primary hepatic myofibroblasts in order to evaluate their activation (expression of α-SMA, COL1A1, PDGFRα, etc.) and proliferation (expression of cyclin D1, BrDU). In order to evaluate the impact of YAP overactivation in hepatocytes on the activation of myofibroblasts, we cultured the latter with transduced Cirrh organoids with an active YAP (in order to mimicorganoids derived from AH livers) or with conditioned media collected from wells containing transduced (YAP medium) or not transduced hepatocytes (CTRL medium) with activated YAP. Results: AH livers presented with both perilobular (as in Cirrh livers) and specifically intralobular fibrosis. Bulk proteomics and PCR showed a specific ECM protein signature (e.g.laminin A2 was increased while vitronectin was decreased in AH). Spatial proteomics showed that the ECM composition between intralobular and perilobular areas was different in AH than in Cirrh livers. AH organoids overexpressed YAP. In the 3D model, AH organoids induced greater activation and proliferation of cocultured myofibroblasts. YAP-transduced Cirrh organoids induced changes in myofibroblasts similar to those observed in AH. YAP medium also induced increased myofibroblast activation and proliferation. Lung infections were the most frequently observed infections on patient admission. History of tobacco (active or passive), the presence of grade ≥2 hepatic encephalopathy and the severity of liver disease (MELD score > 21) were associated with the presence of lung infectionat admission. Lung infection was associated with a reduced access to steroids and a worst prognosis 30 days after admission. Furthermore, after the beginning of steroids, lung infections were more frequent in patients not responding to steroids and were associated with poorer survival [...]
Papillon, Charles-Antoine. "Les microARNs comme biomarqueurs de la maladie du foie liée à l'alcool : de la préclinique à la clinique." Thesis, Amiens, 2019. http://www.theses.fr/2019AMIE0021.
Full textAlcohol-related liver disease (ALD) is a spectrum of disorders which appears after chronic alcohol consumption. ALD has a quiet development until advanced forms as cirrhosis or hepatocellular carcinoma (HCC), both characterized by a high mortality rate. The lack of early clinical symptoms induces a late diagnostic in 50-60% of HCC cases. Late diagnostic cases have a poor prognosis and a 5-year survival rate of 11-16 months. New following-up tools allowing an early diagnostic and a better prognosis appear necessary. Over the recent years, a lot of interest has been accorded to microRNAs in that matter for various diseases, as miRNAs are small epigenetics factors find stable in blood circulation. During this thesis, we have studied some miRNAs selected from literature for their link to HCC, and assessed feasibility and relevance of a circulating miRNAs quantification protocol for ALD follow-up. We observed in a cellular model of chronic alcohol exposure an overproduction of all studied miRNAs. In an animal model of chronic alcohol exposure we observed variations of miRNAs that can be linked to given treatments. At last, we observed a significant increase of all miRNAs in serum of patients suffering from ALD and HCC-related to alcohol. Those results demonstrated the feasibility of such a protocol and the potential of these miRNAs as biomarkers for the follow-up of ALD cases
Delacôte, Claire. "Vers une meilleure compréhension de la maladie du foie liée à l'alcool et des facteurs influençant sa progression : approche de modélisation." Thesis, Lille 2, 2020. http://www.theses.fr/2020LIL2S029.
Full textIn France, excessive alcohol consumption is the leading cause of cirrhosis and hepatocellular carcinoma (HCC), ahead of viral hepatitis and metabolic syndrome. In 2016, there were nearly 10,500 deaths by cirrhosis or HCC, despite a significant decrease in per capita alcohol consumption since 1960 (26L in 1960, 11.7L in 2017).Alcohol drinkers are at risk of developing alcohol-related liver disease (ALD). It progresses from the initial stage of steatosis to more advanced stages of fibrosis and cirrhosis, which may lead to complications: decompensation and HCC. ALD is an asymptomatic disease prior to the onset of complications, and many patients are diagnosed late with life-threatening consequences.Implementing early actions targeting excessive alcohol drinkers could help to reduce liver morbidity and mortality through the avoidance or earlier diagnosis of complications. The evaluation of the possible benefit of such public health actions requires, on the one hand, knowledge of the different stages leading to the development of complications and, on the other hand, knowledge of the impact of risk factors on progression, in order to be able to determine the populations to target. Among the risk factors identified, the metabolic syndrome plays an important role. Thus, in order to understand the mechanisms of evolution of ALD, it is necessary to study in parallel those leading to non-alcoholic fatty liver disease (NAFLD).The natural history of ALD is still poorly described, especially for the stages preceding cirrhosis. Mathematical modeling provides a conceptual framework to overcome the ethical issues that would arise from a cohort study of the evolution of ALD.The main objective of this work is to mathematically reconstruct the natural history of ALD and to predict the associated morbidity and mortality. The secondary objectives are to estimate the incidence of this pathology and to identify the at-risk population. For this purpose, we developed a Markov model that simulates the trajectory of cohorts of individuals from the moment they start at-risk alcohol consumption until their death. It integrates the main risk factors described as associated with the progression of ALD in the literature (sex, age, overweight and obesity, amount of alcohol, genetic polymorphism). Unknown parameters of progression are estimated by a back-calculation method.Three steps were necessary to supply and calibrate this model : 1) characterize mortality by decompensated cirrhosis and HCC related to alcohol consumption or metabolic syndrome from data provided by the French National Hospital Discharge database; 2) set up a Markov model on hospitalization data of excessive consumers to estimate the progression of fibrosis; 3) implement a Markov model on survey data from the general French population to estimate the process of entry into at-risk alcohol consumption or the onset of overweight and obesity.In conclusion, this work is the first to characterize the progression of ALD in the general French population. It is based on robust epidemiological data to which new insights are provided. The developed tools could be used to test the impact of public health policies that could be implemented in populations most likely to develop liver damage